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Vol.1, No.1, 1-3 (2013)Pain Studies and Treatment doi:10.4236/pst.2013.11001Case report: Effect of immunoglobulin on pain in Post-Polio Syndrome—Three case reportsLars Werhagen*, Kristian BorgDivision of Rehabilitation Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Danderyd, Sweden; *Corresponding Author:Received 8 February 2013; revised 11 March 2013; accepted 3 April 2013Copyright © 2013 Lars Werhagen, Kristian Borg. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.ABSTRACTStudy design: Case reports. Setting: University hospital setting. Objective: To analyze the effect of intravenous immunoglobulin on neuropathic and nociceptive pain in three patients with Post- Polio Syndrome (PPS). Materials and Methods: Three patients with PPS and pain who received treatment with 90 g IvIg are described. Results: Before treatment one of the patients had pure neuropathic pain and the other two had a com- bination of neuropathic and nociceptive pain. There was no effect on pain in the patient with pure neuropathic pain and only effect on the nociceptive pain in the patients with a combina- tion of neuropathic and nociceptive pain. Dis- cussion: Pain is one of the most common sym- ptoms in PPS. Previous studies have shown an effect on pain in PPS patients receiving IvIg. The results of the present study point to that the ef- fect on pain is limited to nociceptive pain and that there is no effect on neuropathic pain which leads to increased knowledge of characteriza- tion of responders of IvIg treatment. Conclusion: IvIg treatment treatment reduces nociceptive but not neuropathic pain in PPS patients. Keywords:Post-Polio Syndrome; Pain; Immunoglobulin Treatment1. INTRODUCTIONPain is common in patients with Post-Polio Syndrome (PPS) and is present in a majority of patients [1-5]. The pain in PPS is in most cases nociceptive to its character but when neuropathic pain is present a concomitant dis- ease must be suspected [3]. PPS patients in the western world have reached an age where concomitant neurolo- gical disorders more often occur. Thus, neuropathic pain is anticipated to increase in PPS patients the coming years. Furthermore, pain is more common among fe- males than in males and the intensity of pain according to the V AS scale, as reported by PPS patients, is often high [3,6]. In a previous study we were able to show that treatment with intravenous immunoglobulin (IvIg) was effective and reduced nociceptive pain in seven out of ten PPS patients [7]. IvIg treatment, however, is costly and it is therefore of importance to thoroughly character- ize responders for the treatment.In this case report we describe three patients with PPS and pain of different origin, neuropathic and nociceptive, who reacted differently to IvIg. Thus, this gives more information to the background of the effect of IvIg in PPS, particularly for pain, and increase the knowledge of the different clinical features of responders on IvIg.2. METHODSA description of the patients appears in Table 1. PPS was defined according to the criteria of March of Dimes [8]. Before acceptance for treatment all three patients underwent a thorough neurological and general examina- tion to confirm the PPS diagnosis. Medical investigation revealed no diagnosis constituting exclusion of treatment with IvIg in any of the patients. Immediately before and six month after treatment the patients underwent an ex- amination by the physician responsible for the treatment, one of the authors. At the same time they were inter- viewed according to a specific questionnaire about the presence of pain, its intensity, character and localization, their social and working situation, walking aids, paresis and its localization and the presence of concomitant dis- orders.Pain was classified according to the International As- sociation for the Study of Pain (IASP). A pain was clas- sified as neuropathic if present in an area with sensory disturbances to pin-prick and light touch and without relation to joint movements and/or infection. A pain wasL. Werhagen, K. Borg / Pain Studies and Treatment 1 (2013) 1-32Table 1. Gender, age at polio infection, actual age, marital and working status, pares at its localization, the use of walking aids and concomitant diseases in the three PPS patients who underwent treatment with intravenous immunoglobulin (IvIg).Patient number GenderAge atpolioAge attreatmentMaritalstatusWorkingstatusParesisWalkingaidsConcomitant disease1 Female 1 year 58 years Married Retired Legs No Cervical disc herniation2 Female 5 years 65 years Divorced Retired Legs 2 crutches Lumbar disc herniation3 Female 5 years 63 years Married Retired Legs No Polyneuropathyclassified as nociceptive when aching in an area with signs of inflammation and painful joint movements were described. The intensity of the pain was measured with the Visual Analogue Scale (V AS) 0 - 100 before and after treatment. The patients received a total of 90 g of IvIg (Xepol, Grifols, Barcelona, Spain) during three consecu- tive days.3. CASE REPORTS3.1. Case Number 1A 58-year-old married and retired woman. She con- tracted poliomyelitis at the age of one year. Initially she suffered from paresis and weakness of her left leg. She recovered and lived a normal life. Fifteen years previous to this study she experienced weakness of her legs. Neu- rological examination revealed a light to moderate pare- sis of both legs but she was able to walk unaided. She was diagnosed with PPS. In addition, she suffered from severe pain in her right arm. This pain was classified as neuropathic and the pain intensity before treatment was 80/100 (Table 2). Investigation with MRT revealed a cervical disc hernia.She had no effect on her pain after IvIg treatment and was referred to a pain clinic.3.2. Case Number 2A 65-year-old retired and divorced woman. She con- tracted poliomyelitis at the age of 5 years. She was ini- tially paretic in both legs but was, however, able to live a normal life and walked without aids. Around ten years previous to this study she became weaker in her legs and she was diagnosed with PPS. She walked with two crut- ches and for longer distances she used a wheel-chair. In 1983 she underwent surgery due to a disc hernia at L4/L5 level and was re-operated in 1993. She suffered from pain in her left leg classified as neuropathic and pain in her feet, back and arms classified as nociceptive. After treatment with IvIg the pain decreased from V AS 75 to 25. Her neuropathic pain was only slightly decreased.3.3. Case Number 3A 63-year-old retired and married woman. She con- tracted poliomyelitis at the age of 5 years. She recovered fully but 20 years previous to this study she experienced problem with balance and weakness of the legs. However, she was able to walk without aids. At the post-polio out- patient clinic she was diagnosed with PPS. 2002 she was diagnosed with polymyalgia rheumatica, and polyneuro- pathy on a vascular basis. She underwent treatment with prednisolone. When examined she suffered from a pain in her lower legs classified as neuropathic and pain in back and thighs classified as nociceptive. She had under- gone treatment with Gabapentin for her neuropathic pain without any effect. The intensity of pain according to V AS was 40 - 90/100 before and 15 - 40/100 after IvIg treatment. Six month after treatment her pain was classi- fied as pure neuropathic pain.4. DISCUSSIONThe three patients of the present study demonstrate that IvIg was effective when pain with classified as no- ciceptive but not when classified as neuropathic. In all three patients a concomitant disease was present, in two patient’s disc herniation and in the third patient the back- ground to the neuropathic pain was polyneuropathy. This point to that the effect of IvIg in PPS is not primarily directed to pain but to the background to the pain. The background for the neuropathic pain is a direct effect on nervous structures either due to an external pressure as in disc herniation or due to metabolic factors as in poly- neuropathy. However, the background for the nociceptive pain is not clear. Pain from joint and muscles is a com- mon complaint in PPS patients. However, the pain has not been analyzed thoroughly. One possible background for nociceptive pain in PPS may be inflammation. An in- flammatory process in PPS has been described both in cerebrospinal fluid and in peripheral blood [4,9-12]. IvIg has been reported to decrease the inflammatory process and in parallel a clinical effect including decrease of pain was found [4,10-14]. Furthermore, Melin et al. (K. Borg 2012, personal communication) showed an increase of prostaglandin antibodies in blood vessels of muscle in PPS patients which may be one underlying cause of muscle pain in PPS. Thus, one might speculate that the finding of the present study, a decrease of nociceptive pain as a result of IvIg treat ent, is due to the dampen-mL. Werhagen, K. Borg / Pain Studies and Treatment 1 (2013) 1-33 Table 2. Pain its character and intensity according to the Visual Analogue Scale (V AS) before and after treatment with intravenous immunoglobulin (IvIg) in the three PPS patients.Patient number Classification of pain beforetreatmentV AS before treatmentClassification of pain aftertreatmentV AS aftertreatment1 Neuropathic 80 Neuropathic80 2 Nociceptiveneuropathic 75 Neuropathic 253 Nociceptive neuropathic 40 - 90 Neuropathic 15 - 40ing of an inflammatory reaction. In order to confirm these studies with larger patient materials are required. Besides the low number of patients reported in the pre- sent study this study can be critized in other ways. The classification of pain is difficult and the patients are in age when concomitant diseases are commonly found. However, the patients were before and after treatment examined by the same physician and interviewed ac- cording to a structured questionnaire and no other con- comitant disorder was found. However, with the back- ground of the results of this and other studies it is of im- portance to further analyze pain in PPS adequately and to further develop criteria for selection of PPS for treatment with IvIg based on clinical and molecular data. REFERENCES[1]Gonzalez, H., Olsson, T. and Borg, K. (2010) Manage-ment of postpolio syndrome. The Lancet Neurology, 9,634-642. doi:10.1016/S1474-4422(10)70095-8[2]Trojan, D.A. and Cashman, N.R. (2005) Post-poliomye-litis syndrome. Muscle Nerve, 31, 6-19.doi:10.1002/mus.20259[3]Werhagen, L. and Borg, K. (2010) Analysis of long-standing nociceptive and neuropathic pain in patients withpost-polio syndrome. Journal of Neurology, 257, 1027- 1031. doi:10.1007/s00415-010-5456-0[4]Farbu, E., Rekand, T., Vik-Mo, E., Lygren, H., Gilhus,N.E. and Aarli, J.A. (2007) Post-polio syndrome patientstreated with intravenous immunoglobulin: A double- blinded randomized controlled pilot study. European Jour-nal of Neurology, 14, 60-65.doi:10.1111/j.1468-1331.2006.01552.x[5]Willén, C. and Grimby, G. (1998) Pain, physical activity,disability in individuals with late effects of polio. Ar-chives of Physical Medicine and Rehabilitation, 79, 915-919. doi:10.1016/S0003-9993(98)90087-9[6]Widar, M. and Ahlström, G. (1999) Pain in persons withpost-polio. The Swedish version of the MultidimensionalPain Inventory (MPI). Scandinavian Journal of CaringScience, 13, 33-40.[7]Werhagen, L. and Borg, K. (2011) Effect of intravenousimmunoglobulin on pain in patients with post-polio syn- drome. Journal of Rehabilitation Medicine, 43, 1038- 1040. doi:10.2340/16501977-0884[8]March of Dimes. Post-polio syndrome: Identifying bestpractice in diagnosis and care./downloads/PostPolio.pdf[9]Gonzalez, H., Khademi, M., Andersson, M., Wallström,E., Borg, K. and Olsson, T. (2002) Prior poliomyelitis—Evidence of cytokine production in the central nervous system. Journal of the Neurological Sciences, 205, 9-13.doi:10.1016/S0022-510X(02)00316-7[10]Gonzalez, H., Khademi, M., Andersson, M., Piehl, F.,Wallström, E., et al. (2004) Prior poliomyelitis—IvIg treat- ment reduces proinflammatory cytokine production. Jour-nal of Neuroimmunology, 150, 139-144.doi:10.1016/j.jneuroim.2004.01.010[11]Fordyce, C.B., Gagne, D., Jalili, F., alatab, S., Arnold,D.L., Da Costa, D., Sawoszczuk, S., Bodner, C., Shapiro,S., Collet, J.-P., Robinson, A., Le Cruguel, J.-P., Lapierre, Y., Bar-Or, A. and Trojan, D.A. (2008) Elevated serum in-flammatory markers in post-poliomyelitis syndrome. Jour-nal of Neurological Sciences, 271, 80-86.doi:10.1016/j.jns.2008.03.015[12]Gonzalez, H., Khademi, M., Borg, K. and Olsson, T.(2012) Intravenous immunoglobulin treatment of the post- polio syndrome: Sustained effects on quality of life vari- ables and cytokine expression after one year follow-up.Journal of Neuroinflammation, 9, 167.doi:10.1186/1742-2094-9-167[13]Gonzalez, H., Stibrant-Sunnerhagen, K., Sjöberg, I., Ka-panoides, G., Olsson, T. and Borg, K. (2006) Intravenous immunoglobulin for post-polio syndrome: A randomised controlled trial. Lancet Neurology, 5, 493-500.doi:10.1016/S1474-4422(06)70447-1[14]Kaponides, G., Gonzalez, H., Olsson, H. and Borg, K.(2006) Effect of intravenous immunoglobulin in patients with post-polio syndrome—An uncontrolled pilot study.Journal of Rehabilitation Medicine, 38, 138-140.doi:10.1080/16501970500441625。

2004 ADA 糖尿病指南

Standards of Medical Care in Diabetes A MERICAN D IABETES A SSOCIATIOND iabetes is a chronic illness that re-quires continuing medical care andpatient self-management education to prevent acute complications and to re-duce the risk of long-term complications. Diabetes care is complex and requires that many issues,beyond glycemic control,be addressed.A large body of evidence exists that supports a range of interventions to improve diabetes outcomes.These standards of care are intended to provide clinicians,patients,research-ers,payors,and other interested persons with the components of diabetes care, treatment goals,and tools to evaluate the quality of care.While individual prefer-ences,comorbidities,and other patient factors may require modiﬁcation of goals, targets that are desirable for most patients with diabetes are provided.These stan-dards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information,refer to Bode(Ed.):Medical Management of Type1 Diabetes(1),Zimmerman(Ed.):Medical Management of Type2Diabetes(2),and Klingensmith(Ed):Intensive Diabetes Management(3).The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes.A grading system(Table1),developed by the American Diabetes Association(ADA) and modeled after existing methods,was utilized to clarify and codify the evidence that forms the basis for the recommenda-tions.The level of evidence that supports each recommendation is listed after eachrecommendation using the letters A,B,C,or E.CLASSIFICATION,DIAGNOSIS,ANDSCREENINGClassiﬁcationIn1997,the ADA issued new diagnosticand classiﬁcation criteria(4);in2003,modiﬁcations were made regarding thediagnosis of impaired fasting glucose(IFG)(5).The classiﬁcation of diabetesincludes four clinical classes:●Type1diabetes(results from␤-cell de-struction,usually leading to absoluteinsulin deﬁciency).●Type2diabetes(results from a progres-sive insulin secretory defect on thebackground of insulin resistance).●Other speciﬁc types of diabetes(due toother causes,e.g.,genetic defects in␤-cell function,genetic defects in insu-lin action,diseases of the exocrine pan-creas,drug or chemical induced).●Gestational diabetes mellitus(GDM)(diagnosed during pregnancy).DiagnosisCriteria for the diagnosis of diabetes innonpregnant adults are shown in Table2.Three ways to diagnose diabetes are avail-able,and each must be conﬁrmed on asubsequent day unless unequivocalsymptoms of hyperglycemia are present.Although the75-g oral glucose tolerancetest(OGTT)is more sensitive and mod-estly more speciﬁc than fasting plasmaglucose(FPG)to diagnose diabetes,it ispoorly reproducible and rarely performedin practice.Because of ease of use,accept-ability to patients,and lower cost,theFPG is the preferred screening and diag-nostic test.It should be noted that the vastmajority of people who meet diagnosticcriteria for diabetes by OGTT,but not byFPG,will have an A1C valueϽ7.0%.Theuse of the A1C for the diagnosis of diabe-tes is not recommended at this time.Hyperglycemia not sufﬁcient to meetthe diagnostic criteria for diabetes is cate-gorized as either IFG or impaired glucosetolerance(IGT),depending on whether itis identiﬁed through FPG or an OGTT:●IFGϭFPG100mg/dl(5.6mmol/l)to125mg/dl(6.9mmol/l)●IGTϭ2-h plasma glucose140mg/dl(7.8mmol/l)to199mg/dl(11.0mmol/l)Recently,IFG and IGT have been ofﬁ-cially termed“pre-diabetes.”Both catego-ries,IFG and IGT,are risk factors forfuture diabetes and cardiovascular dis-ease(CVD).Recent studies have shownthat modest weight loss and regular phys-ical activity can reduce the rate of progres-sion of IGT to type2diabetes(6–8).Drugtherapy(metformin[8],acarbose[9],andorlistat[10]and troglitazone[no longerclinically available][11])has been shownto be effective in reducing progression todiabetes,though generally not as effec-tively as intensive lifestyle interventions.ScreeningGenerally,people with type1diabetespresent with acute symptoms of diabetesand markedly elevated blood glucose lev-els.Type2diabetes is frequently not di-agnosed until complications appear,andapproximately one-third of all peoplewith diabetes may be undiagnosed.Al-though the burden and natural history ofdiabetes is well known and although thereis good evidence for beneﬁt from treatingcases diagnosed in the context of usualclinical care,there are no randomized tri-als demonstrating the beneﬁts of earlydiagnosis through screening of asymp-tomatic individuals(12).Nevertheless,there is sufﬁcient indirect evidence to jus-●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●The recommendations in this paper are based on the evidence reviewed in the following publication: Standards of care for diabetes(Technical Review).Diabetes Care17:1514–1522,1994.Originally approved1988.Most recent review/revision,October2003.Abbreviations:ABI,ankle-brachial index;ARB,angiotensin receptor blocker;CAD,coronary artery disease;CHD,coronary heart disease;CSII,continuous subcutaneous insulin injection;CVD,cardiovascular disease;FPG,fasting plasma glucose;GCT,glucose challenge test;DCCB,dihydropyridine calcium channel blocker;DCCT,Diabetes Control and Complications Trial;DKA,diabetic ketoacidosis;DRS,Diabetic Retinopathy Study;ECG,electrocardiogram;eGFR,estimated GFR;ESRD,end-stage renal disease;ETDRS, Early Treatment Diabetic Retinopathy Study;GDM,gestational diabetes mellitus;GFR,glomerularﬁltration rate;HRC,high-risk characteristic;IFG,impaired fasting glucose;IGT,impaired glucose tolerance;MNT, medical nutrition therapy;NPDR,nonproliferative diabetic retinopathy;OGTT,oral glucose tolerance test; PAD,peripheral arterial disease;PDR,proliferative diabetic retinopathy;PPG,postprandidial plasma glu-cose;SMBG,self-monitoring of blood glucose;UKPDS,U.K.Prospective Diabetes Study.©2004by the American Diabetes Association.P O S I T I O N S T A T E M E N Ttify opportunistic screening in a clinical setting of individuals at high risk.Criteria for testing for diabetes in asymptomatic, undiagnosed adults are listed in Table3. The recommended screening test for non-pregnant adults is the FPG.The OGTT is more sensitive for the diagnosis of diabe-tes and pre-diabetes,but is impractical and expensive as a screening procedure.The incidence of type2diabetes in children and adolescents has increased dramatically in the last decade.Consis-tent with screening recommendations for adults,only children and youth at in-creased risk for the presence or the devel-opment of type2diabetes should be tested(13)(Table4).Detection and diagnosis of GDM Risk assessment for GDM should be un-dertaken at theﬁrst prenatal visit.Women with clinical characteristics consistentwith a high risk for GDM(those withmarked obesity,personal history of GDM,glycosuria,or a strong family history ofdiabetes)should undergo glucose testingas soon as possible(14).An FPGՆ126mg/dl or a casual plasma glucoseՆ200mg/dl meets the threshold for the diagno-sis of diabetes and needs to be conﬁrmedon a subsequent day unless unequivocalsymptoms of hyperglycemia are present.High-risk women not found to have GDMat the initial screening and average-riskwomen should be tested between24and28weeks of gestation.Testing should fol-low one of two approaches:●One-step approach:perform a diagnos-tic100-g OGTT●Two-step approach:perform an initialscreening by measuring the plasma orserum glucose concentration1h after a50-g oral glucose load(glucose chal-lenge test[GCT])and perform a diag-nostic100-g OGTT on that subset ofwomen exceeding the glucose thresh-old value on the GCT.When the two-step approach is used,a glucosethreshold valueՆ140mg/dl identiﬁesϳ80%of women with GDM,and theyield is further increased to90%by us-ing a cutoff ofՆ130mg/dl.●Diagnostic criteria for the100-g OGTTare as follows:Ն95mg/dl fasting,Ն180mg/dl at1h,Ն155mg/dl at2h,andՆ140mg/dl at3h.Two or more ofthe plasma glucose values must be metor exceeded for a positive diagnosis.The test should be done in the morningafter an overnight fast of8–14h.Thediagnosis can be made using a75-g glu-cose load,but that test is not as wellTable1—ADA evidence grading system for clinical practice recommendationsLevel ofevidence DescriptionA Clear evidence from well-conducted,generalizable,randomized controlled trials that are adequately powered including:●Evidence from a well-conducted multicenter trial●Evidence from a meta-analysis that incorporated quality ratings in the analysis●Compelling nonexperimental evidence,i.e.,“all or none”rule developed by Center for Evidence Based Medicine at OxfordSupportive evidence from well-conducted randomized controlled trials that are adequately powered including:●Evidence from a well-conducted trial at one or more institutions●Evidence from a meta-analysis that incorporated quality ratings in the analysisB Supportive evidence from well-conducted cohort studies●Evidence from a well-conducted prospective cohort study or registry●Evidence from a well-conducted prospective cohort study●Evidence from a well-conducted meta-analysis of cohort studiesSupportive evidence from a well-conducted case-control studyC Supportive evidence from poorly controlled or uncontrolled studies●Evidence from randomized clinical trials with one or more major or three or more minor methodologicalﬂaws that couldinvalidate the results●Evidence from observational studies with high potential for bias(such ascase series with comparison to historical controls)●Evidence from case series or case reportsConﬂicting evidence with the weight of evidence supporting the recommendationE Expert consensus or clinical experienceTable2—Criteria for the diagnosis of diabetes1.Symptoms of diabetes and a casual plasma glucose200mg/dl(11.1mmol/l).Casual is deﬁned as any time of day without regard to timesince last meal.The classic symptoms of diabetes include polyuria,polydipsia,and unexplained weight loss.OR2.FPG126mg/dl(7.0mmol/l).Fasting is deﬁned as no caloric intake for at least8h.OR3.2-h PG200mg/dl(11.1mmol/l)during an OGTT.The test should be performed as described by the World Health Organization(4a),using a glucose load containing the equivalent of75-g anhydrous glucose dissolved in water.In the absence of unequivocal hyperglycemia,these criteria should be conﬁrmed by repeat testing on a different day.The OGTT is not recommended for routine clinical use,but may be required in the evaluation of patients with IFG(see text)or when diabetes is still suspected despite a normal FPG.Position Statementvalidated for detection of at-risk infants or mothers as the100-g OGTT.●Low-risk status requires no glucose testing,but this category is limited to those women meeting all of the follow-ing characteristics:•AgeϽ25years.•Weight normal before pregnancy.•Member of an ethnic group with alow prevalence of GDM.•No known diabetes inﬁrst-degreerelatives.•No history of abnormal glucose tol-erance.•No history of poor obstetric out-come.Recommendations●The FPG is the preferred test to screen for and diagnose diabetes in children and nonpregnant adults.(E)●Screen for diabetes in high-risk,asymp-tomatic,undiagnosed adults and chil-dren within the health care setting.(E)●In those with pre-diabetes(IFG/IGT), lifestyle modiﬁcation should bestrongly recommended and progres-sion of glycemic abnormalities followedby screening at least yearly.(A)●Screen for diabetes in pregnancy usingrisk factor analysis and screening testsas noted;the OGTT is the preferredscreening test in pregnancy.(E)INITIAL EVALUATIONA complete medical evaluation should beperformed to classify the patient,detectthe presence or absence of diabetes com-plications,assist in formulating a manage-ment plan,and provide a basis forcontinuing care.If the diagnosis of diabe-tes has already been made,the evaluationshould review the previous treatment andthe past and present degrees of glycemicboratory tests appropriate tothe evaluation of each patient’s generalmedical condition should be performed.A focus on the components of compre-hensive care(Table5)will assist thehealth care team to ensure optimal man-agement of the patient with diabetes.MANAGEMENTPeople with diabetes should receivemedical care from a physician-coordi-nated team.Such teams may include,but are not limited to,physicians,nurse practitioners,physician’s assis-tants,nurses,dietitians,pharmacists,andmental health professionals with exper-tise and a special interest in diabetes.It isessential in this collaborative and inte-grated team approach that individualswith diabetes assume an active role intheir care.The management plan should be for-mulated as an individualized therapeuticalliance among the patient and family,thephysician,and other members of thehealth care team.Any plan should recog-nize diabetes self-management educationas an integral component of care.In de-veloping the plan,consideration shouldbe given to the patient’s age,school orwork schedule and conditions,physicalactivity,eating patterns,social situationand personality,cultural factors,andpresence of complications of diabetes orTable3—Criteria for testing for diabetes in asymptomatic adult individuals1.Testing for diabetes should be considered in all individuals at age45years and above,particularly in those with a BMI25kg/m2*,and,ifnormal,should be repeated at3-year intervals.2.Testing should be considered at a younger age or be carried out more frequently in individuals who are overweight(BMI25kg/m2*)andhave additional risk factors:●are habitually physically inactive●have aﬁrst-degree relative with diabetes●are members of a high-risk ethnic population(e.g.,African American,Latino,Native American,Asian American,Paciﬁc Islander)●have delivered a baby weighingϾ9lb or have been diagnosed with GDM●are hypertensive(140/90mmHg)●have an HDL cholesterol level35mg/dl(0.90mmol/l)and/or a triglyceride level250mg/dl(2.82mmol/l)●have PCOS●on previous testing,had IGT or IFG●have other clinical conditions associated with insulin resistance(e.g.PCOS or acanthosis nigricans)●have a history of vascular disease*May not be correct for all ethnic groups.PCOS,polycystic ovary syndrome.Table4—Testing for type2diabetes in children●CriteriaOverweight(BMIϾ85th percentile for age and sex,weight for heightϾ85th percentile,or weightϾ120%of ideal for height)PlusAny two of the following risk factors:Family history of type2diabetes inﬁrst-or second-degree relativeRace/ethnicity(Native American,African American,Latino,Asian American,Paciﬁc Islander)Signs of insulin resistance or conditions associated with insulin resistance(acanthosis nigricans,hypertension,dyslipidemia,or PCOS)●Age of initiation:age10years or at onset of puberty,if puberty occurs at a younger age●Frequency:every2years●Test:FPG preferredClinical judgment should be used to test for diabetes in high-risk patients who do not meet these criteria.PCOS,polycystic ovary syndrome.Standards of Medical Careother medical conditions.A variety of strategies and techniques should be used to provide adequate education and devel-opment of problem-solving skills in the various aspects of diabetes management.Implementation of the management planrequires that each aspect is understoodand agreed on by the patient and the careproviders and that the goals and treat-ment plan are reasonable.Glycemic controlGlycemic control is fundamental to themanagement of diabetes.Prospective ran-domized clinical trials such as the Diabe-tes Control and Complications TrialTable5—Components of the comprehensive diabetes evaluationMedical history●Symptoms,results of laboratory tests,and special examination results related to the diagnosis of diabetes●Prior AIC records●Eating patterns,nutritional status,and weight history;growth and development in children and adolescents●Details of previous treatment programs,including nutrition and diabetes self-management education,attitudes,and health beliefs●Current treatment of diabetes,including medications,meal plan,and results of glucose monitoring and patients’use of data●Exercise history●Frequency,severity,and cause of acute complications such as ketoacidosis and hypoglycemia●Prior or current infections,particularly skin,foot,dental,and genitourinary infections●Symptoms and treatment of chronic eye;kidney;nerve;genitourinary(including sexual),bladder,and gastrointestinal function(includingsymptoms of celiac disease in type1diabetic patients);heart;peripheral vascular;foot;and cerebrovascular complications associated with diabetes●Other medications that may affect blood glucose levels●Risk factors for atherosclerosis:smoking,hypertension,obesity,dyslipidemia,and family history●History and treatment of other conditions,including endocrine and eating disorders●Assessment for mood disorder●Family history of diabetes and other endocrine disorders●Lifestyle,cultural,psychosocial,educational,and economic factors that might inﬂuence the management of diabetes●Tobacco,alcohol,and/or controlled substance use●Contraception and reproductive and sexual historyPhysical examination●Height and weight measurement(and comparison to norms in children and adolescents)●Sexual maturation staging(during pubertal period)●Blood pressure determination,including orthostatic measurements when indicated,and comparison to age-related norms●Fundoscopic examination●Oral examination●Thyroid palpation●Cardiac examination●Abdominal examination(e.g.,for hepatomegaly)●Evaluation of pulses by palpation and with auscultation●Hand/ﬁnger examination●Foot examination●Skin examination(for acanthosis nigricans and insulin-injection sites)●Neurological examination●Signs of diseases that can cause secondary diabetes(e.g.,hemochromatosis,pancreatic disease)Laboratory evaluation●A1C●Fasting lipid proﬁle,including total cholesterol,HDL cholesterol,triglycerides,and LDL cholesterol●Test for microalbuminuria in type1diabetic patients who have had diabetes for at least5years and in all patients with type2diabetes;some advocate beginning screening of pubertal children before5years of diabetes●Serum creatinine in adults(in children if proteinuria is present)●Thyroid-stimulating hormone(TSH)in all type1diabetic patients;in type2if clinically indicated●Electrocardiogram in adults,if clinically indicated●Urinalysis for ketones,protein,sedimentReferrals●Eye exam,if indicated●Family planning for women of reproductive age●MNT,as indicated●Diabetes educator,if not provided by physician or practice staff●Behavioral specialist,as indicated●Foot specialist,as indicated●Other specialties and services as appropriatePosition Statement(DCCT)(15)and the U.K.Prospective Di-abetes Study(UKPDS)(16,17)have shown that improved glycemic control is associated with sustained decreased rates of retinopathy,nephropathy,and neu-ropathy(18).In these trials,treatment regimens that reduced average A1C to ϳ7%(ϳ1%above the upper limits of normal)were associated with fewer long-term microvascular complications;how-ever,intensive control was found to increase the risk of severe hypoglycemia and weight gain(19,20).Epidemiological studies support the potential of intensive glycemic control in the reduction of CVD (15–20).Recommended glycemic goals for nonpregnant individuals are shown in Ta-ble6.A major limitation to the available data are that they do not identify the op-timum level of control for particular pa-tients,as there are individual differences in the risks of hypoglycemia,weight gain, and other adverse effects.Furthermore, with multifactorial interventions,it is un-clear how different components(e.g.,ed-ucational interventions,glycemic targets, lifestyle changes,and pharmacological agents)contribute to the reduction of complications.There are no clinical trialdata available for the effects of glycemiccontrol in patients with advanced compli-cations,the elderly(Ն65years of age),oryoung children(Ͻ13years of age).Lessstringent treatment goals may be appro-priate for patients with limited life expect-ancies,in the very young or older adults,and in individuals with comorbid condi-tions.Severe or frequent hypoglycemia isan indication for the modiﬁcation of treat-ment regimens,including setting higherglycemic goals.More stringent goals(i.e.,a normalA1C,Ͻ6%)can be considered in individ-ual patients based on epidemiologicalanalyses that suggest that there is no lowerlimit of A1C at which further loweringdoes not reduce risk of complications,atthe risk of increased hypoglycemia(par-ticularly in those with type1diabetes).However,the absolute risks and beneﬁtsof lower targets are unknown.The risksand beneﬁts of an A1C goal ofϽ6%arecurrently being tested in an ongoing study(ACCORD[Action to Control Cardiovas-cular Risk in Diabetes])in type2diabetes(21).Elevated postchallenge(2-h OGTT)glucose values have been associated withincreased cardiovascular risk indepen-dent of FPG in some epidemiologicalstudies.Postprandial plasma glucose(PPG)levelsϾ140mg/dl are unusual innondiabetic individuals,although largeevening meals can be followed by plasmaglucose values up to180mg/dl.There arenow pharmacological agents that primar-ily modify PPG and thereby reduce A1Cin parallel.Thus,in individuals who havepremeal glucose values within target butwho are not meeting A1C targets,consid-eration of monitoring PPG1–2h after thestart of the meal and treatment aimed atreducing PPG valuesϽ180mg/dl maylower A1C.However,it should be notedthat the effect of these approaches on mi-cro-or macrovascular complications hasnot been studied(22).For information on glycemic controlfor women with GDM,refer to the ADAposition statement“Gestational DiabetesMellitus”(14).For information on glyce-mic control during pregnancy in womenwith preexisting diabetes,refer to MedicalManagement of Pregnancy Complicated byDiabetes(3rd ed.)(23).Referral for diabetes managementFor a variety of reasons,some people withdiabetes and their health care providersdo not achieve the desired goals of treat-ment(Table6).In such instances,addi-tional actions suggested includeenhanced diabetes self-management edu-cation,comanagement with a diabetesteam,change in pharmacological therapy,initiation of or increase in self-monitoringof blood glucose(SMBG),more frequentcontact with the patient,and referral to anendocrinologist.Intercurrent illnessThe stress of illness frequently aggravatesglycemic control and necessitates morefrequent monitoring of blood glucose andurine or blood ketones.A vomiting illnessaccompanied by ketosis may indicate di-abetic ketoacidosis(DKA),a life-threatening condition that requiresimmediate medical care to prevent com-plications and death;the possibility ofDKA should always be considered(24).Marked hyperglycemia requires tempo-rary adjustment of the treatment programand,if accompanied by ketosis,frequentinteraction with the diabetes care team.The patient treated with oral glucose-lowering agents or medical nutrition ther-apy(MNT)alone may temporarily requireTable6—Summary of recommendations for adults with diabetesGlycemic controlAICϽ7.0%*Preprandial plasma glucose90–130mg/dl(5.0–7.2mmol/l)Postprandial plasma glucose†Ͻ180mg/dl(Ͻ10.0mmol/l)Blood pressureϽ130/80mmHgLipids‡LDLϽ100mg/dl(Ͻ2.6mmol/l)TriglyceridesϽ150mg/dl(Ͻ1.7mmol/l)HDLϾ40mg/dl(Ͼ1.1mmol/l)§Key concepts in setting glycemic goals:●Goals should be individualized●Certain populations(children,pregnant women,and elderly)require special considerations●Less intensive glycemic goals may be indicatedin patients with severe or frequenthypoglycemia●More stringent glycemic goals(i.e.a normalA1C,Ͻ6%)may further reduce complicationsat the cost of increased risk of hypoglycemia(particularly in those with type1diabetes)●Postprandial glucose may be targeted if AICgoals are not met despite reaching preprandialglucose goals*Referenced to a nondiabetic range of4.0–6.0%using a DCCT-based assay.†Postprandial glucose mea-surements should be made1-2h after the beginning of the meal,generally peak levels in patients withdiabetes.‡Current NCEP/ATP III guidelines suggest that in patients with triglycerides200mg/dl,the“non-HDL cholesterol”(total cholesterol minus HDL)be utilized.The goal is130mg/dl(61).§For women,it has been suggested that the HDL goal be increased by10mg/dl.Standards of Medical Careinsulin.Adequateﬂuid and caloric intake must be assured.Infection or dehydration is more likely to necessitate hospitaliza-tion of the person with diabetes than the person without diabetes.The hospitalized patient should be treated by a physician with expertise in the management of dia-betes,and recent studies suggest that achieving very stringent glycemic control may reduce mortality in the immediate postmyocardial infarction period(25). Aggressive glycemic management with insulin may reduce morbidity in patients with severe acute illness(26).For information on management of patients in the hospital,refer to the ADA position statement titled“Hyperglycemic Crises in Diabetes”(24).Recommendations●Lowering A1C has been associated witha reduction of microvascular and neu-ropathic complications of diabetes.(A)●Develop or adjust the management plan to achieve normal or near-normal glycemia with an A1C goal ofϽ7%.(B)●More stringent goals(i.e.,a normal A1C,Ͻ6%)can be considered in indi-vidual patients.(B)●Lowering A1C may lower the risk of myocardial infarction and cardiovascu-lar death.(B)●Aggressive glycemic management with insulin may reduce morbidity in pa-tients with severe acute illness,periop-eratively and following myocardial infarction.(B)●Less stringent treatment goals may be appropriate for patients with a history of severe hypoglycemia,patients with limited life expectancies,very young children or older adults,and individu-als with comorbid conditions.(E)ASSESSMENT OF GLYCEMIC CONTROLTechniques are available for health pro-viders and patients to assess the effective-ness of the management plan on glycemic control.SMBGThe ADA’s consensus statements on SMBG provide a comprehensive review of the subject(27,28).Major clinical trials assessing the impact of glycemic control on diabetes complications have included SMBG as part of multifactorial interven-tions,suggesting that SMBG is a compo-nent of effective therapy.SMBG allows patients to evaluate their individual re-sponse to therapy and assess whether gly-cemic targets are being achieved.Resultsof SMBG can be useful in preventing hy-poglycemia and adjusting medications,MNT,and physical activity.The frequency and timing of SMBGshould be dictated by the particular needsand goals of the patients.Daily SMBG isespecially important for patients treatedwith insulin to monitor for and preventasymptomatic hypoglycemia.For mostpatients with type1diabetes and preg-nant women taking insulin,SMBG is rec-ommended three or more times daily.Theoptimal frequency and timing of SMBGfor patients with type2diabetes is notknown but should be sufﬁcient to facili-tate reaching glucose goals.When addingto or modifying therapy,type1and type2diabetic patients should test more oftenthan usual.The role of SMBG in stablediet-treated patients with type2diabetesis not known.Because the accuracy of SMBG is in-strument-and user-dependent(29),it isimportant for health care providers toevaluate each patient’s monitoring tech-nique,both initially and at regular inter-vals thereafter.In addition,optimal use ofSMBG requires proper interpretation ofthe data.Patients should be taught how touse the data to adjust food intake,exer-cise,or pharmacological therapy toachieve speciﬁc glycemic goals.Healthprofessionals should evaluate at regularintervals the patient’s ability to use SMBGdata to guide treatment.Recommendations●SMBG is an integral component of dia-betes therapy.(B)●Include SMBG in the managementplan.(E)●Instruct the patient in SMBG and rou-tinely evaluate the patient’s techniqueand ability to use data to adjust therapy.(E)A1CBy performing an A1C test,health provid-ers can measure a patient’s average glyce-mia over the preceding2–3months(29)and,thus,assess treatment efﬁcacy.A1Ctesting should be performed routinely inall patients with diabetes,ﬁrst to docu-ment the degree of glycemic control atinitial assessment and then as part of con-tinuing care.Since the A1C test reﬂectsmean glycemia over the preceding2–3months,measurement approximately ev-ery3months is required to determinewhether a patient’s metabolic control hasbeen reached and maintained within thetarget range.Thus,regular performanceof the A1C test permits detection of de-partures from the target(Table6)in atimely fashion.For any individual patient,the frequency of A1C testing should bedependent on the clinical situation,thetreatment regimen used,and the judg-ment of the clinician.Glycemic control is best judged bythe combination of the results of the pa-tient’s SMBG testing(as performed)andthe current A1C result.The A1C shouldbe used not only to assess the patient’scontrol over the preceding2–3monthsbut also as a check on the accuracy of themeter(or the patient’s self-reported re-sults)and the adequacy of the SMBG test-ing schedule.Table7contains thecorrelation between A1C levels and meanplasma glucose levels based on data fromthe DCCT(30).Recommendations●Perform the A1C test at least two timesa year in patients who are meeting treat-ment goals(and who have stable glyce-mic control)and quarterly in patientswhose therapy has changed or who arenot meeting glycemic goals.(E)MNTMNT is an integral component of diabetesmanagement and diabetes self-manage-ment education.A review of the evidenceand detailed information can be found inthe ADA technical review and positionstatement in this area(31,32).Peoplewith diabetes should receive individual-ized MNT as needed to achieve treatmentgoals,preferably provided by a registereddietitian familiar with the components ofTable7—Correlation between A1C level andmean plasma glucose levels(30)AIC(%)Mean plasma glucosemg/dl mmol/l61357.571709.5820511.5924013.51027515.51131017.51234519.5Position Statement。

肾脏小体积占位的自然史和临床处理

肾脏小体积占位的自然史和临床处理李应龙;曾凯;王勤章【摘要】随着现代影像学技术的迅速发展以及人们健康意识的增强,肾脏小体积占位(SRMs)的检出率越来越高,并以2％～3％的速度逐年增加.由于对于SRMs自然史的研究尚不十分明确,绝大部分肿物一经诊断都会及时行手术干预,而术后病理诊断发现部分肿物为分化较好的肾细胞癌,仅有20％～25％的恶性肿瘤具有潜在侵袭性.目前,肾部分切除术或肾癌根治术是SRMs的标准治疗方法,同时腹腔镜手术、机器人及消融术的发展,对肾脏小肿物的处理手段也有了更多的选择.然而对于高龄、存在较高手术风险的患者进行积极的影像学监测随访也是一种可选择的处理方式.【期刊名称】《现代泌尿外科杂志》【年(卷),期】2016(021)005【总页数】5页(P329-333)【关键词】肾脏小体积占位;自然史;治疗【作者】李应龙;曾凯;王勤章【作者单位】新疆石河子大学医学院第一附属医院泌尿外科,新疆石河子832008;新疆石河子大学医学院第一附属医院泌尿外科,新疆石河子832008;新疆石河子大学医学院第一附属医院泌尿外科,新疆石河子832008【正文语种】中文【中图分类】R737.11·专家论坛·肾脏小体积占位(small renal masses，SRMs)是指通过影像学检查发现的最大直径≤4 cm的肾脏实质性占位。

肾肿瘤的检出率正以每年2%～2.5%的速度增加，部分原因归结于频繁的影响学检查。

虽然肾肿瘤各临床分期发病率均有所上升，但SRMs的发病率上升尤为显著。

由于目前对SRMs自然病程缺乏足够的认识，当前其处理方式还存在较大争议。

在美国已将积极监测作为处理SRMs的初选治疗方案，但在我国仍以肾部分切除术或肾癌根治术作为治疗肾肿瘤的标准方案。

我们结合自身临床经验及复习相关文献对SRMs的自然病程及处理方式作以下简要介绍。

了解SRMs的生物学特性和自然病程有助于预测肿瘤的生长速度和转移的潜能，对选择最佳的治疗方法和确定最合理的治疗干预时间十分重要。

葛森疗法——精选推荐

葛森疗法葛森疗法我们知道，现代医疗⽆法治愈中晚期癌症、慢性病和疑难杂症。

⽽我们昨天向朋友们介绍的⾮常简单的巴德维疗法确能轻松地治愈这些疾病。

我们今天再向朋友们介绍⼀种能够治愈这些疾病的⾃然疗法——葛森疗法。

葛森疗法是德裔犹太⼈马克斯?葛森（Max Gerson，医学博⼠）最早于上世纪初解决严重偏头痛时发现的⾃然疗法。

葛森1958年出版了其最著名的⼀本书《癌症治疗—50位病例分析》，⽬前已经在全球50多个国家，⼏⼗种⽂字发⾏，葛森于1959年去世，去世之前发现是被别⼈下了砒霜。

与巴德维疗法⼀样，葛森疗法在全世界有⼤量的癌症、慢性病和疑难杂症治愈的实例。

我们仅将⼏个⽐较著名的摘要如下。

葛森博⼠最有名的患者是医疗传教⼠暨哲学家艾伯特?史怀哲博⼠。

史怀哲博⼠75岁时，只接受了6个星期的葛森疗法，就完全治好了他的糖尿病。

此后史怀哲博⼠⼜回到法属⾚道⾮洲的加彭兰巴雷内市，照顾了数千名⾮洲患者，获得1952年的诺贝尔和平奖，并持续⼯作⾄90岁以上。

在摆脱了糖尿病之后，史怀哲博⼠活到93岁。

葛森博⼠也顺便为史怀哲博⼠垂死的妻⼦海莲娜治好了结核病，让她继续活了28年。

他也治好了史怀哲博⼠19岁的⼥⼉雷娜的严重⽪肤病。

1992年，⽇本福岛县⽴医学⼤学的医科教授星野仁彦患了结肠癌。

在进⾏肿瘤切除⼿术时，发现癌细胞已经转移到肝脏。

在⼿术后的医疗照护期间，医师建议他进⾏多个疗程的化疗。

由于化疗医治结肠／直肠癌有明显的不良副作⽤，失败率也过⾼，肝癌转移的预后则更不乐观（97%的患者在接受化疗后死亡），因此星野教授拒绝进⾏化疗，改⽽⾃⾏着⼿实施葛森疗法。

⾄今，星野教授健康活过了⼆⼗多年，他的结肠癌和肝脏的转移都已经“治愈”。

英国王储查尔斯王⼦对葛森疗法评价说：“我知道有位被宣告得晚期癌症且即使接受化疗疗程也⽆法存活的病⼈转向求助葛森疗法。

令⼈⾼兴的是，7年后她仍然活得很好。

因此，与其抹去这样的经验，更重要的是，我们应该进⼀步去探讨这些治疗的益处。

关节镜下双滑轮结合双排缝线桥技术治疗肩袖损伤的效果及对肩关节功能恢复的影响

及家庭成员对患者的影响,导致结果可能存在偏倚,下一步将结合临床实践㊁采用多中心研究方法完善预测偏瘫患者康复效果不佳风险的列线图预测模型㊂综上所述,基于年龄㊁饮酒㊁高血压㊁康复训练开始时间以及居住环境构建的列线图预测模型,可较好地个体化预测康复训练效果不佳风险,有助于临床制定个体化干预方案,对改善康复训练效果有积极作用㊂ʌ参考文献ɔ[1]㊀Kuriakose D,Xiao Z.Pathophysiology and treatment ofstroke:present status and future perspectives[J].Int MolSci,2020,21(20):1-24.[2]㊀彭美娣,陈玉培,冯扣兰,等.急性缺血性脑卒中患者生活质量影响因素研究[J].交通医学,2022,36(5):532-534.[3]㊀Lou Y T,Yang J J,Ma Y F,et al.Effects of different acu-puncture methods combined with routine rehabilitation ongait of stroke patients[J].World Clin Cases,2020,8(24):6282-6295.[4]㊀Vluggen T P M M,van Haastregt J C M,Verbunt J A,et al.Feasibility of an integrated multidisciplinary geriatric rehabil-itation programme for older stroke patients:a process evalua-tion[J].BMC Neurol,2020,20(1):1-13.[5]㊀Shi R,Zhang T,Sun H,et al.Establishment of clinical pre-diction model based on the study of risk factors of stroke inpatients with type2diabetes mellitus[J].Front Endocrinol(Lausanne),2020,11(1):1-14.[6]㊀Sacco R L,Kasner S E,Broderick J P,et al.An updated def-inition of stroke for the21st century:a statement for health-care professionals from the American Heart Association/A-merican Stroke Association[J].Stroke,2013,44(7):2064-2089.[7]㊀Alex C.Activities of Daily Living(ADL)[M].Berlin germa-ny:springer netherlands,2014.19-20.[8]㊀Yan Q,Wang X,Zhang Y,et al.Analysis of influencing fac-tors of rehabilitation treatment effect in patients with first-episode stroke[J].Am Transl Res,2021,3(12):14046-14056.[9]㊀Yang C,Zhao J,Xie H,et al.Effects of early rehabilitationnursing intervention on nerve function and daily living in pa-tients with stroke hemiplegia[J].Am Transl Res,2021,13(10):11842-11850.[10]㊀Sun C,Li X,Song B,et al.A NADE nomogram to predictthe probability of6-month unfavorable outcome in Chinesepatients with ischemic stroke[J].BMC Neurol,2019,19(1):1-8.[11]㊀Zhou Z,Yin X,Niu Q,et al.Risk factors and a nomogramfor predicting intracranial hemorrhage in stroke patients un-dergoing thrombolysis[J].Neuropsychiatr Dis Treat,2020,16(1):1189-1197.[12]㊀Wang CY,Miyoshi S,Chen C H,et al.Walking ability andfunctional status after post-acute care for stroke rehabilita-tion in different age groups:a prospective study based onpropensity score matching[J].Aging(Albany NY),2020,12(11):10704-10714.[13]㊀Lv X,Chen H.Effect of virtual reality combined with intelli-gent exercise rehabilitation machine on the nursing recoveryof lower limb motor function of patients with hypertensivestroke[J].Healthc Eng,2022,2022(1):1-10. [14]㊀Lv Y,Zhang Q,Rong L,et al.Butylphthalide soft capsulescombined with modified tonic exercise therapy on neurologi-cal function and ability of daily living of patients with strokehemiplegia[J].Am Transl Res,2021,13(12):13803-13810.[15]㊀朱翠平.农村脑卒中偏瘫患者家庭康复护理干预的效果研究[J].护理管理杂志,2018,18(10):745-748.ʌ文章编号ɔ1006-6233(2023)09-1538-06关节镜下双滑轮结合双排缝线桥技术治疗肩袖损伤的效果及对肩关节功能恢复的影响张小钰,㊀马敬祖,㊀于㊀佳,㊀万㊀钧,㊀马㊀军(宁夏回族自治区人民医院,㊀宁夏㊀银川㊀750012)ʌ摘㊀要ɔ目的:探究关节镜下双滑轮和双排缝线桥联合技术治疗肩袖损伤(rotator cuff tears,RCT)的效果及对肩关节功能恢复的影响㊂方法:回顾性分析2018年7月至2022年6月于我院接受传统缝线桥技术治疗的52例RCT患者临床资料,纳入对照组,回顾性分析同期于我院接受关节镜下双滑轮结合双排缝线桥技术治疗的53例RCT患者临床资料,纳入观察组㊂比较两组患者手术指标,随访6个月㊃8351㊃ʌ基金项目ɔ宁夏回族自治区重点研发计划项目,(编号:2021BEG03050)ʌ通讯作者ɔ马㊀军后,比较两组患者治疗效果[愈合率㊁再撕裂率㊁视觉模拟评分(visual Analogue Scale,VAS)],术前和术后6个月关节活动度(前屈上举㊁体侧外旋㊁体侧内旋)㊁肩关节功能[美国肩肘外科协会评分(american Shoulder and Elbow Surgeons,ASES)㊁Constant-Murley评分(constant-Murley Score,CMS)㊁加州大学洛杉矶分校评分(university of California at Los Angeles,UCLA)],统计术后并发症发生情况㊂结果:两组患者手术时间㊁手术出血量㊁住院时间及疼痛缓解时间均差异无统计学意义(P均>0.05);术后6个月,两组患者VAS评分较术前降低,观察组低于对照组(P<0.05);前屈上举㊁体侧外旋㊁体侧内旋度数㊁ASES评分㊁UCLA评分及CMS评分均较术前升高,观察组高于对照组(P均<0.05)㊂结论:关节镜下双滑轮结合双排缝线桥技术在RCT治疗中效果显著,可加强RCT患者关节灵活度,有利于RCT患者肩关节功能恢复㊂ʌ关键词ɔ㊀肩袖损伤;㊀关节镜下双滑轮;㊀双排缝线桥;㊀肩关节功能;㊀关节灵活度ʌ文献标识码ɔ㊀A㊀㊀㊀㊀㊀ʌdoiɔ10.3969/j.issn.1006-6233.2023.09.023Effect of Arthroscopic Double Pulley Combined with Double Row Suture Bridge Technique on Rotator Cuff Tear and ItsInfluence on Shoulder Function RecoveryZHANG Xiaoyu,MA Jingzu,YU Jia,et al(The People's Hospital of Ningxia Hui Autonomous Region,Ningxia Yinchuan750012,China)ʌAbstractɔObjective:To explore the effect of combined technique of arthroscopic double pulley and double row suture bridge in the treatment of rotator cuff tear(RCT)and its influence on shoulder function re-covery.Methods:The clinical data of52patients with RCT who received traditional suture bridge technique in the hospital from July2018to June2022were retrospectively analyzed and the patients were included in control group.The clinical data of53patients with RCT who received arthroscopic double pulley combined with double row suture bridge technique in the hospital during the same period were retrospectively analyzed and the patients were enrolled as observation group.The surgical indicators,therapeutic effects[healing rate, re-tear rate,Visual Analogue Scale(VAS)]after6months of follow-up,the joint range of motion(forward flexion and upward lift,lateral external rotation,lateral internal rotation)and shoulder function[American Shoulder and Elbow Surgeons(ASES),Constant-Murley Score(CMS),University of California at Los An-geles(UCLA)]before surgery and at6months after surgery were compared between the two groups,and the postoperative complications were counted.Results:There were no significant differences in surgical time,sur-gical blood loss,hospital stay,and pain relief time between both groups(all P>0.05).At6months after sur-gery,VAS score in both groups was reduced compared to before the surgery,and the score in observation group was lower than that in control group(P<0.05).Forward flexion and upward lift,lateral external rota-tion,lateral internal rotation,ASES score,UCLA score and CMS score were enhanced compared with those before surgery,and the above indicators were higher in observation group than those in control group(all P< 0.05).Conclusion:Arthroscopic double pulley combined with double row suture bridge technique has a sig-nificant effect in the treatment of RCT,and it can enhance the joint flexibility of patients with RCT and is ben-eficial to shoulder function recovery in patients with RCT.ʌKey wordsɔ㊀Rotator cuff tear;㊀Arthroscopic double pulley;㊀Double row suture bridge;㊀Shoulder function;㊀Joint flexibility㊀㊀肩袖损伤(rotator cuff tears,RCT)由慢性劳损㊁间接暴力或退行性变等导致㊂据报道,60岁以上群体发病率为20%~30%,70岁以上群体则占50%左右[1]㊂RCT患者多伴有肩部疼痛㊁肌肉萎缩㊁肩关节活动受限等症状,随着病情加重将影响肱骨头稳定性,且大多高龄患者存在关节粘连现象,若不及时治疗[2]㊂临床㊃9351㊃上,小型肩袖损伤采用保守治疗,中㊁大㊁巨大型RCT 则需通过手术治疗缓解患者症状[3]㊂传统手术创伤大,不利于RCT患者术后康复㊂近年来,肩关节镜下手术趋于成熟,已成为肩袖损伤治疗的金标准 ,其修补方式主要包括内排缝合㊁双排缝合㊁双排缝线桥缝合及双滑轮结合缝线桥技术等,但目前尚未明确那种修补方法效果最佳[4]㊂本研究回顾性分析我院肩袖损伤患者临床资料,探究关节镜下双滑轮结合双排缝线桥技术在肩袖损伤中的治疗效果及对肩关节功能影响㊂报道如下㊂1㊀资料与方法1.1㊀一般资料:回顾性分析2018年7月至2022年6月于我院接受传统缝线桥技术治疗的52例RCT患者临床资料,纳入对照组,回顾性分析同期于我院接受关节镜下双滑轮结合双排缝线桥技术治疗的53例RCT 患者临床资料,纳入观察组㊂纳入标准:①经影像学确诊为RCT;②Cofield分型为中型㊁大型撕裂;③术后随访ȡ6个月㊂排除标准:①不可修复型肩袖撕裂者;②合并其他肩部疾病者;③术后无法康复训练者;④既往肩关节手术史者;⑤术后外伤导致再撕裂者;⑥治疗依从性差者;⑦精神异常或沟通障碍者;⑧临床资料不全者㊂患者一般资料差异无统计学意义(P>0.05)㊂见表1㊂表1㊀患者一般资料比较[ xʃs,n(%)]组别n性别男㊀㊀㊀㊀㊀女年龄(岁)症状持续时间(月)撕裂部位左肩㊀㊀㊀右肩撕裂程度中型㊀㊀㊀大型观察组5332(60.38)21(39.62)58.46ʃ6.137.94ʃ1.3828(52.83)25(47.17)36(67.92)17(32.08)对照组5228(53.85)24(46.15)58.84ʃ6.258.05ʃ1.4225(48.08)27(51.92)33(63.46)19(36.54)χ2/t0.4570.3150.4030.2370.232P0.4990.7540.6880.6260.6301.2㊀方法:两组患者术前均接受X射线㊁MRI㊁常规身体检查及感染预防㊂观察组:关节镜下双滑轮结合双排缝线桥㊂全麻后患者仰卧于手术台,肩部悬空,向前30度㊁向外45度牵引上肢,采用肩峰后㊁前㊁外三种不同路径放置关节镜,观察肩袖关节㊁盂肱关节㊁肱二头肌等处损伤情况及是否存在粘连,根据损伤程度,进行肱二头肌长头腱修整㊁回缩,清理肩袖间隙㊁上肱唇㊁肩峰下滑囊,松解关节粘连处㊂测定肩袖损伤形态㊁尺寸及厚度,清除损伤残端,松解肩袖,打磨肱骨足印区,清洁肩袖至止点,将2根内排锚钉(各带蓝㊁白色2根缝线)插入足印区内侧关节软骨边缘,缝合肩袖,将1根蓝线打结作为内排滑轮,然后向肩关节方向牵引,形成一个内排双轮滑,压紧肩袖,将1根蓝线和2根白线系于肱骨大结节远端,剪余线,清洗并封闭切口㊂对照组采用传统缝线桥技术㊂采用与观察组相同方法置入关节镜㊁修整㊁清理,在足印区肱骨关节软骨边缘置入2枚内排锚钉(各带2根缝线),用缝合器将其通过肩袖进行过线,将缝线打结,并固定与肌腱上,构成缝线桥,随后外排锚钉固定,剪余线,清洗并封闭切口㊂术后接受常规抗感染㊁止痛等处理,佩戴4~6周上肢外展支具,术后4周进行被动前屈㊁外展㊁内外旋等康复训练,术后4~6周活动达到正常范围者进行自主上肢肌肉训练,术后6周逐渐加强训练及关节协调训练,每次训练后可局部冰敷㊂术后1㊁3㊁6个月复查㊂1.3㊀观察指标:①手术指标:比较患者手术时间㊁手术出血量㊁住院时间㊂②治疗效果:统计随访期间患者愈合及再撕裂发生率,用视觉模拟评分(visual Analogue Scale,VAS)[5]评估疼痛程度,分数0~10分,分值越高,疼痛程度越强㊂③关节活动度:术前和术后6个月,采用量角器测量两组患者前屈上举㊁体侧外旋㊁体侧内旋的角度㊂④肩关节功能:术前和术后6个月,采用美国肩肘外科协会评分(american Shoulder and El-bow Surgeons,ASES)[6]㊁加州大学洛杉矶分校评分(u-niversity of California at Los Angeles,UCLA)[7]㊁Constant -Murley评分(constant-Murley Score,CMS)[8]评估, ASES含疼痛㊁生活功能,总分100分,分数与肩关节功能成正比,UCLA含肩关节前屈度㊁疼痛㊁功能㊁力量及治疗满意度,总分35分,分数与肩关节功能成正比, CMS含疼痛㊁肩关节活动角度㊁日常生活㊁肌力,总分100分,分数与肩关节功能成正比㊂⑤并发症:统计术后关节粘连㊁切口感染㊁神经血管损伤㊁骨折发生情况㊂1.4㊀统计学分析:采用SPSS19.0软件进行数据处理㊂㊃0451㊃计量资料年龄㊁症状持续时间㊁手术指标㊁VAS㊁ASES㊁UCLA及CMS评分以( xʃs)表示,组内比较行配对样本t检验,组间比较行独立样本t检验,计数资料性别㊁撕裂程度㊁撕裂部位以n(%)表示,采用χ2检验,P<0. 05表示差异有统计学意义㊂2㊀结㊀果2.1㊀患者手术指标比较:两组患者手术时间㊁手术出血量㊁住院时间差异均无统计学意义(P均>0.05)㊂见表2㊂表2㊀患者手术指标比较( xʃs)组别n手术时间(min)术中出血量(mL)住院时间(d)观察组5385.36ʃ6.7560.72ʃ5.84 5.12ʃ0.77对照组5284.03ʃ6.6162.11ʃ5.93 5.34ʃ0.82 t 1.020 1.210 1.417 P0.3100.2290.1592.2㊀患者治疗效果比较:观察组愈合率高于对照组,再撕裂率低于对照组(P均<0.05);术前,患者VAS评分差异无统计学意义(P均>0.05);术后6个月,患者VAS评分降低,观察组降幅大于对照组(P均<0.05)㊂见表3㊂表3㊀患者治疗效果比较[n(%), xʃs]组别n VAS评分㊀术前㊀㊀㊀㊀㊀术后6个月差值愈合再撕裂观察组53 5.94ʃ1.15 1.03ʃ0.31∗ 4.94ʃ0.6148(90.57)5(9.43)对照组52 5.81ʃ1.12 1.45ʃ0.43∗ 4.36ʃ0.5739(75.00)13(25.00) t/χ20.587 5.749 5.032 4.477 4.477 P0.559<0.001<0.0010.0340.034㊀㊀与同组术前比较,∗P<0.052.3㊀患者肩关节活动度比较:术前,患者前屈上举㊁体侧外旋㊁体侧内旋角度差异无统计学意义(P均>0.05);术后6个月,患者前屈上举㊁体侧外旋㊁体侧内旋角度均显著升高,观察升幅大于对照组(P均<0.05)㊂见表4㊂表4㊀患者肩关节活动度比较( xʃs,度)组别n前屈上举术前㊀㊀㊀术后6个月㊀㊀差值体侧外旋术前㊀㊀㊀术后6个月㊀㊀差值体侧内旋术前㊀㊀㊀术后6个月㊀㊀差值观察组5363.28ʃ6.42149.76ʃ15.13∗86.48ʃ7.2427.15ʃ3.1447.54ʃ5.66∗20.39ʃ2.12 4.15ʃ1.039.35ʃ2.43∗ 5.20ʃ1.14对照组5262.97ʃ6.51141.38ʃ14.75∗78.41ʃ6.9527.48ʃ3.3642.69ʃ5.23∗15.21ʃ1.63 4.21ʃ1.068.27ʃ2.24∗ 4.06ʃ1.07 t0.246 2.873 5.8250.520 4.55814.0170.294 2.367 5.281P0.8060.005<0.0010.604<0.001<0.0010.7690.020<0.001㊀㊀注:与同组术前比较,∗P<0.052.4㊀患者肩关节功能比较:术前,患者UCLA评分㊁CMS评分㊁ASES评分差异无统计学意义(P均>0.㊃1451㊃05);术后6个月,患者UCLA评分㊁CMS评分㊁ASES评分均显著升高,观察组升幅大于对照组(P均<0.05)㊂见表5㊂表5㊀患者肩关节功能比较( xʃs,分)组别n ASES评分术前㊀㊀㊀术后6个月㊀㊀差值UCLA评分术前㊀㊀㊀术后6个月㊀㊀差值CMS评分术前㊀㊀㊀术后6个月㊀㊀差值观察组5341.82ʃ4.5875.46ʃ6.92∗33.64ʃ3.2812.43ʃ1.7728.59ʃ2.25∗13.16ʃ1.3544.35ʃ5.2782.52ʃ8.76∗38.17ʃ4.06对照组5242.13ʃ4.6570.88ʃ6.67∗28.75ʃ2.9112.68ʃ1.8424.86ʃ2.17∗12.18ʃ1.3144.93ʃ5.5478.65ʃ8.24∗33.72ʃ4.18 t0.344 3.4528.0750.7108.644 3.7740.550 2.331 5.534P0.7310.001<0.0010.480<0.001<0.0010.5840.022<0.001㊀㊀注:与同组术前比较,∗P<0.052.5㊀两组患者并发症比较:两组患者均未有术后并发症发生㊂3㊀讨㊀论肩袖能够稳定肩关节㊁协调肩关节活动,创伤㊁慢性撞击㊁局部供血不足㊁磨损等因导致肩部肌肉机械性能降低,肩关节稳定性失衡,关节囊退行性变,引发肩部疼痛㊁功能损伤,严重影响患者日常生活[9]㊂老年人群尤其是长期重体力劳动者群体中该病发病率较高,且常伴有由炎症反应引起的粘连,进一步加重病情,降低患者肩关节活动能力,关节镜因其创伤小㊁术后疼痛轻㊁恢复快等优势已被广泛应用于肩袖损伤治疗㊂目前,临床上主要采用单排㊁双排㊁缝线桥等固定方式修复RCT,关节镜下双排缝线桥技术为一种新型修复方式,能够缩小肌腱与骨之间间隙,增加腱骨接触面积,进而增加固定效果,还可通过数条网状线阻断关节液渗入肌腱骨,有利于肩关节功能恢复㊂双滑轮结合双排缝线桥技术联合外排间断缝合与内排双轮滑技术,增加肌腱与骨的接触面积,增强肩袖修复的初始稳定性,促进肌腱修复[10]㊂本研究显示,两组患者手术指标均无显著性差异,但观察组愈合率高于对照组,再撕裂率及疼痛程度低于对照组,提示关节镜下双滑轮结合双排缝线桥技术能够提高RCT治疗效果,但对手术指标无明显影响㊂这可能是因为两组所用肩袖修复固定方式均是在关节镜下进行,该术创伤小,对病灶周围组织损伤小,能降低手术中的出血量,对病人的术后康复也有好处㊂,因此,两组患者手术时间㊁术中出血量及住院时间等无明显差异㊂但与传统缝线桥技术相比,双滑轮结合双排缝线桥技术改良内排锚钉缝线打结方式,与外排缝线桥技术相结合,将肩袖向骨面牵拉,使其充分接触,增强肩关节稳定性,且滑轮线可封闭关节,抑制关节液向腱骨面渗透,促进肌腱愈合㊂RCT修复后再撕裂因素包括肌腱与骨面未愈合㊁缝线断裂㊁锚钉松动㊁肌腱质量差及术后不当康复训练等,本研究中缝合术不仅能够增加固定强度,还能通过外锚钉缝合桥构成肩袖足印区网状固定,降低内排锚钉张力,缓解疼痛,避免组织缺血㊁坏死,促进肌腱愈合,减少肩袖再撕裂,此外,该术可以把压力转移到外侧锚钉,从而降低肌腱和缝线的剪切和收窄,降低再次撕裂的可能性[11]㊂本研究发现,观察组肩关节活动度大于对照组,且肩关节功能优于对照组,此结果与郭伟康等[12]研究结果一致㊂提示双滑轮结合双排缝线桥技术能够提高RCT患者肩关节活动度及功能㊂可能内排锚钉缝线打结可有效避免锚钉松动,同时结合外排缝线桥增加肌腱㊁骨接触,改善肩部稳定,促进术后功能恢复,为提高患者肩关节活动度打下良好基础,且接触面积增加能够使足印区覆盖充分㊁受压均匀,增强旋转力与抗剪切力,有利于术后康复训练,避免术后肩关节出现粘连㊁痉挛等促进肩关节功能恢复㊂综上所述,双滑轮结合双排缝线桥技术在肩袖损伤治疗中效果显著,能够减轻疼痛,提高肩关节活动度,促进肩关节功能恢复㊂ʌ参考文献ɔ[1]㊀张凯搏,唐新,李箭,等.2019年美国骨科医师学会(AAOS)肩袖损伤临床实践指南解读[J].中国运动医学杂志,2020,39(5):403-412.[2]㊀薛辉,周医斋,帖小佳,等.关节镜下松解术结合肩袖修复术治疗肩袖损伤合并冻结肩疗效分析[J].中国临床医生杂志,2020,48(4):469-472.[3]㊀朱周玮,刘旺鑫,孙晖晖,等.肩袖损伤治疗研究进展[J].新中医,2021,53(23):27-30.[4]㊀杨军,李志国,刘昭,等.关节镜下双排单滑轮缝线桥治疗全层肩袖损伤的临床效果分析[J].中国医刊,2022,57(7):771-774.[5]㊀严广斌.视觉模拟评分法[J].中华关节外科杂志(电子㊃2451㊃版),2014(2):273.[6]㊀Richards RR ,An KN ,Bigliani LU ,et al.A standardizedmethod for the assessment of shoulder function [J ].JShoul-der Elbow Surg ,1994,3(6):347-352.[7]㊀王少杰,石磊,张同恩,等.肩关节镜下肱二头肌长头肌腱转位增强修复巨大肩袖撕裂的疗效[J ].中华创伤杂志,2023,39(1):31-37.[8]㊀Conboy VB ,Morris RW ,Kiss J ,et al.An evaluation of theconstant -murley shoulder assessment [J ].Bone Joint SurgBr ,1996,78(2):229-232.[9]㊀Huntington L ,Coles -Black J ,Richardson M ,et al.The use ofsuturetape and suture -wire in arthroscopic rotator cuff re-pair :a comparative biomechanics study [J ].Injury ,2018,49(11):2047-2052.[10]㊀齐鹏坤,智猛,韩煜.肩关节镜下双滑轮结合双排缝合技术治疗肩袖撕裂[J ].临床骨科杂志,2019,22(3):292-295.[11]㊀骆勇刚,陈俊,庄万强,等.肩关节镜下不同缝合固定修复技术治疗肩袖损伤的临床疗效[J ].局解手术学杂志,2021,30(6):535-540.[12]㊀郭伟康,黄健,刘松浪,等.肩关节镜下双滑轮结合缝线桥技术固定修复肩袖损伤的应用研究[J ].中华实用诊断与治疗杂志,2020,34(2):173-176.ʌ文章编号ɔ1006-6233(2023)09-1543-07改良悬雍垂腭咽成形术治疗OSAHS 伴认知功能障碍患者疗效及对呼吸功能脑电图和MMSE 评分的影响朱玉博,㊀程蕾蕾,㊀朱荣飞,㊀刘秋蕊,㊀徐艳红(四川省雅安市人民医院耳鼻咽喉头颈外科,㊀四川㊀雅安㊀625000)ʌ摘㊀要ɔ目的:观察改良悬雍垂腭咽成形术(H -UPPP )治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS )伴认知功能障碍患者疗效及对呼吸功能㊁脑电图和蒙特利尔认知评估量表(MMSE )评分的影响㊂方法:选取雅安市人民医院耳鼻喉头颈外科于2020年2月至2022年2月收治的中重度OSAHS 伴认知功能障碍患者124例为研究对象,采用简单随机法分为两组,单组62例㊂保守组采用行为治疗干预,观察组采用H -UPPP 联合行为治疗干预㊂比较两组多导睡眠参数㊁蒙特利尔认知评估量表(MO-CA )评分㊁睡眠评估量表(ESS )评分㊁LMT 延迟回忆(LMT DR )评分㊁Rey -Osterrieth 复杂图形测试(CFT )㊁逻辑记忆测试(LMT )㊁CFT 延迟回忆(CFT DR )评分㊁MMSE 评分及P300潜伏期的差异,统计两组6个月后脑电图异常率和总有效率㊂结果:保守组治疗6个月后呼吸暂停低通气指数(AHI )较前下降,LSpO 2较前升高(P <0.05)㊂观察组治疗6个月后AHI ㊁SaO 2<90%的时间占总监测时间百分比(TS90%)㊁(N1+N2)%较前下降,LSpO 2㊁N3%㊁快眼动睡眠期占总监测时间百分比(REM%)较前升高(P <0.05)㊂观察组AHI ㊁LSpO 2㊁TS90%㊁(N1+N2)%㊁N3%㊁REM%治疗前后差值高于保守组(P <0.05)㊂保守组治疗6个月后ESS 评分较前下降(P <0.05)㊂观察组治疗6个月后ESS 评分较前下降,MMSE 评分㊁MOCA 评分较前升高(P <0.05)㊂观察组治疗6个月后ESS 评分低于保守组(P <0.05)㊂保守组治疗6个月后CFT ㊁LMT 评分及其延迟回忆评分与治疗前比较,差异无统计学意义(P >0.05)㊂观察组治疗6个月后LMT 评分㊁LMT DR 评分较前升高,但CFT 评分㊁CFT DR 评分与治疗前比较,差异无统计学意义(P >0.05)㊂观察组MMSE 评分㊁MOCA 评分㊁ESS 评分治疗前后差值高于保守组(P <0.05)㊂保守组治疗6个月后P300潜伏期结果与治疗前比较,差异无统计学意义(P >0.05)㊂观察组治疗6个月后Fz ㊁Cz ㊁Pz ㊁C4点P300潜伏期较前下降,但C3点P300潜伏期与治疗前比较,差异无统计学意义(P >0.05)㊂观察组P300潜伏期治疗前后差值高于保守组(P <0.05)㊂观察组6个月后脑电图异常率为24.19%(15/62)明显低于保守组的50.00%(31/62),总有效率为88.71%(55/62)明显高于保守组的56.45%(35/62),有统计学差异(P <0.05)㊂结论:改良悬雍垂腭咽成形术治疗OSAHS 伴认知功能障碍可有效改善患者睡眠结构和脑电活动状态,有利于患者认知功能的恢复㊂ʌ关键词ɔ㊀改良悬雍垂腭咽成形术;㊀阻塞性睡眠呼吸暂停低通气综合征;㊀认知功能障碍;㊀睡眠结构;㊀脑电活动状态;㊀呼吸功能ʌ文献标识码ɔ㊀A㊀㊀㊀㊀㊀ʌdoi ɔ10.3969/j.issn.1006-6233.2023.09.024㊃3451㊃ʌ基金项目ɔ四川省医学科研课题,(编号:S20049)ʌ通讯作者ɔ徐艳红。

关于咖啡灌肠

关于咖啡灌肠灌肠法的历史表明这是一种长期采用的，有疗效的治疗方法：灌肠法一直以来是医院护理病人时所采用的最重要的疗法之一。

医院内采用灌肠法的科学文献记载为数不多，而护士们观察到的并发症情况也是寥寥无几。

医生和护士都知道，如果病人排便不正常，病人病情不可能获得实质性好转，因此灌肠法在病人优质护理方面是至关重要的。

每个病人护理记录上的都有一系列数据需要跟进。

这份病人管理表就是排便记录。

如果病人没有排便，就有肠梗阻的风险，而需接受治疗清洗结肠。

自古以来，结肠清洗疗法使用温水灌肠。

何要进行咖啡灌肠？咖啡灌肠可以为身体排毒。

配合食物排毒法或疗程，有助于更深入地治愈人体问题。

二十世纪四十年代和五十年代，马克斯·格森医学博士 (Dr. Max Gerson, MD) 是最早正式用咖啡灌现在，运用到癌症治疗上60多年后，在尼古拉斯·冈萨雷斯医学博士 (Dr. Nicolas Gonzalez, MD) 咖啡灌肠疗法通过刺激胆汁为肠排毒来治疗他的癌症病人的医生。

和美国癌症研究所的共同努力下，咖啡灌肠排毒疗法终于成为一门严肃的科研课题。

的流量和增强肝脏的酶促反应，提高肝脏与胆囊的解毒功能，祛除毒谷胱甘肽S-转移酶是 (GST) 是一种重要的解毒酶。

咖啡中的棕榈酸酯把 GST 的生成提高了700倍。

这种强大无比的自由基淬灭酶有助于更加有效地此外，咖啡含有植物碱基茶碱素，消除癌变副产物。

增强肝脏对人体的解毒功能，可以舒张血管，提高肠壁间的血液透析加快肠道供血可以提高肌肉张力，改善消化功能，还可以增强排泄功能。

此外，鉴于我们所有血咖啡灌肠排毒疗法的保健功能，随着格森 (Gerson) 应用到癌症患者治疗上而广为人知，在整个格森疗法如何治愈疾病”(How the Gerson Therapy Heals)，1990年流每三分钟流过肝脏一次，这种12-15分钟的咖啡滞留型灌肠剂增强血液到肝脏的流动，形成透析，产生具有独特效用的解毒功能。

葛森疗法讲解课件

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详细描述
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学习放松技巧，如深呼吸、渐进性肌肉放松等，缓解紧张和焦虑。
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培养积极的心态，保持乐观、向上的情绪状态。
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学习有效的沟通技巧，建立良好的人际关系，增强社会支持系统。
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寻求专业心理咨询和治疗，解决心理问题和障碍。
相比具有更高的安全性。
然而，葛森疗法通常需要患者进行长期的调整和生活方式的改变，对于一些急性疾病或严重病症可能不是首选治疗方法。
传统医学和葛森疗法并非相互排斥，在某些情况下可以结合使用，以达到更好的治疗效果。
PART 02
葛森疗法的基本原则
整体健康观念
整体健康观念是葛森疗法的基础，它强调人体的整体性，认为身体的各个系统、器官之间相互关联、相互影响。治疗时应从整体角度出发，全面考虑身体状况，以达到最佳的治疗效果。
深入研究机制
进一步揭示葛森疗法的机制和原理，为未来的发展奠定基础。
对患者和社会的意义
提高生活质量
通过减轻疾病症状和提高治疗效果，帮助患者改善生活质量。
降低医疗成本
葛森疗法可能为患者提供更经济、更有效的治疗选择，降低医疗成本。
推动医学进步
葛森疗法的发展有助于推动医学的进步和创新，为人类健康事业做出贡献。
案例二
一位患有慢性疲劳的患者，在使用葛森疗法后，疲劳感减轻，身体状况明显好转。
患者反馈和建议
患者反馈
大多数患者对葛森疗法的效果表示满意，认为生活质量得到了提高，身体状况得到了改善。
患者建议
希望葛森疗法能够得到更广泛的推广和应用，让更多的人受益。同时，也希望在治疗过程中能够更加注重患者的个体差异，提高治疗的针对性和效果。

一种帮助李开复恢复健康的自然疗法——葛森疗法

一种帮助李开复恢复健康的自然疗法——葛森疗法一种帮助李开复恢复健康的自然疗法——葛森疗法一种帮助李开复恢复健康的自然疗法——葛森疗法【特别推荐】宋美龄运用数十年的长寿抗老祕诀；影响星野仁彦、济阳高穗、新谷弘实等日本名医；诺贝尔和平奖得主史怀哲、英国王储查尔斯王子诚心推荐。

有机园生物科技公司总经理于建华社区大学讲师&生机饮食专家王明勇无毒的家及吉胃福适创办人王康裕埔里信望爱圆缘园创办人&现任财团法人爱德园文教基金会董事长李秋凉健康促进股份有限公司总经理＆中国一级健康管理师吴世楠棉花田创办人翁湘淳高雄医学大学兼任助理教授&畅销书作家陈立川全球华人防癌长链倡导人梅襄阳许医师自然诊所负责人许达夫绿色小镇有机事业创办人＆海力捷两岸绿色平台宣导人詹益清欧阳英乐活生机网网主欧阳英强力推荐●精采试阅可以吃和禁止吃的食物葛森疗法就是如此注重细节，才能够在某些极为晚期的疾病案例，或是原本被认为无药可医的疾病中发挥疗效。

在加州的波尼塔市合作建立了葛森研究所之后，夏绿蒂．葛森广为宣传这套对抗疾病的饮食方案中，究竟有哪些该吃和不该吃的东西。

可以大量食用的食物任何种类的水果均可接受，大多数是新鲜水果，加上部分以不同方式准备的水果；新鲜现榨的蔬菜汁；水果色拉；水果冷汤；香蕉泥、磨碎的生苹果、苹但苜蓿芽除外，因为苜蓿芽禁止食用。

※禁止的食品如果可能的话，我们会简略说明为什麽葛森饮食疗法不允许下列这个禁止类别中列出的各种食物。

所有经过制造（加工）的食物，例如装瓶、装罐、冷冻、腌制、精制、加盐、烟燻或硫化（除非特别提到可以允许）都在禁止之列。

所有类型的乳制品，例如乳品和乳品加工产品（包括羊奶）都禁止食用。

这些禁止项目包括起司、奶油、冰泣淋、冰牛奶、牛油和白脱牛奶，除非是为了蛋白质而特别允许。

乳制品一般来说脂肪含量极高，起司可能有65%的脂肪，而且含有大量的钠。

市售的白脱牛奶经过「发酵」（以剩馀牛奶生产，经过调味，增加浓稠度），含有脂肪和钠。

葛森疗法讲解

Chamomile 洋甘菊
Ø扮演著排毒角色
Cleansing Reaction
咖啡灌肠如何实施
Coffee Breaks 灌肠专用咖啡
灌腸袋和灌腸用的硅胶管子
ky水溶性的潤滑液
內外痔專用
灌腸時請注意三度是否正确
右側躺,左腳拱起
三度: 1.高度 2.溫度 3.速度
How to do Coffee Enema?
Palmitic Acid 棕榈酸 Water 水
GST 6.5X
Source: /wiki/Glutathione_S-transferase ,Jakoby, W.B., The glutathione S-transferases: a group of multifunctional detoxification proteins. Adv. Enzymol. Relat. Areas Mol. Biol. 46: 383-383 (1978). [PMID: 345769] /pubmed/6339228, Ketterer B, Coles B, Meyer DJ., The role of glutathione in detoxication. Environ Health Perspect. 1983 Mar;49:59-69.
中国健康人群仅占总人口15％亚健康人群比例达70％，另有15％的人处于疾病状
全世界亚健康人群比例统计
造成亚健康的原因
饮食因素（25%）：饮食不合理
当机体摄入热量过多或营养贫乏时，都可导致机体失调。过量吸烟、酗酒、缺少运动以及大气污染、水污染、食品污染、长期接触药品、
有毒物品，也可出现这种状态。
葛森专家-丹尼儿老师特别推荐-纽崔莱营养补充食品

延长哀伤障碍的诊断评估与治疗研究进展

一些病例研究表明，5-羟色胺再摄取抑制剂的抗抑郁药可
DSM-5 并未直接采纳 PGD 这一术语及其诊断标准，但在附录中
能有助于治疗 PGD[24]；而另一项随机对照试验发现，三环类抗抑
新增了持续性复杂丧亲障碍（PCBD）的诊断。
郁药对于减轻哀伤不起作用，即使它对丧亲者主要的抑郁症状
对于这种疾病的不同名称和提出的症状标准是否一致，研
估和治疗等方面的研究成果，以期帮助心理卫生工
作者更准确地评估和诊断新冠肺炎疫情后潜在的哀
伤患者，并选择合适的疗法进行干预。
近 20 年来，大量研究致力于论证 PGD 独立于其
他精神障碍，
并尝试为其制定诊断标准。
Horowitz 等 [11] 对 70 例丧亲者进行了追踪研究，
并于 1997 年提出了复杂性哀伤（CG）诊断标准：共有
知。在荷兰的 1 项对丧亲者的研究中，54 例 PGD 患者被随机分
PCBD）。近年来，
PGD
一种由挚爱的亲人去世引发的病理性哀伤反应。
《国
这一术语开始流行起来，研究者们认为“ 延长的
际疾病分类（第 11 版）》
（International Classification of
（prolonged）”一词更能准确反映这类异常哀伤反应
Disorders，ICD-11）将其定义为：在丧亲至少 6 个月
与健康研究中心
关键词
武汉 430074
延长哀伤障碍；
诊断评估；治疗方法；
综述
中图分类号 R741；R741.05；R749 文献标识码 A
DOI 10.16780/ki.sjssgncj.20210852
2.武汉市精神卫

格森疗法

格森疗法以下有关Gerson格森疗法的信息是基於以下参考文献：∙ Charlotte Gerson 和 Morton Walker撰写的 2001年由Kensington 出版公司出版的THE GERSON THERAPY 一书。

ISBN1-57566-628-6∙ Max Gerson 1958年第一版，1999年Gerson研究所再次印刷的A CANCER THERAPY一书，总结了50例用饮食疗法治愈的进展期的肿瘤病人， ISBN 0-88268-203-2∙ GERSON THERAPY HANDBOOK手册总结了50位病例，修订至第5版, 是A CANCER THERAPY同系列书。

∙录像带 THE GERSON THERAPY AT HOME,可以在Gerson研究所购得。

************************************************************* *********格森疗法摘要Gerson疗法对於肿瘤病人是一种真正的营养治疗，同时对其他新陈代谢性疾病也有效。

Gerson疗法有三项同等重要的步骤需要同步进行。

∙第一是用咖啡灌肠清除毒素。

∙第二是Gerson饮食提供必要(包括酶)的营养素：每日13杯新鲜蔬菜水果汁。

事实上 Gerson疗法是一种自然酶疗法，与一般传统的酶疗法仅限於数种有限酶类相比，Gerson疗法从自然食物中获得数千种酶类。

第三是补充缺乏的营养素，特别是钾、碘和甲状腺激素。

其他次要的补充剂包括烟酸(niacin)、胰液素(pancreatin)、亚麻油(flaxseed oil)、蓖麻油(castor oil)、辅酶Q10(coenzyme Q10) 、德国生产的酶产物Wobe-Mugos、苦杏仁精(amygdalin)、天然肝脏(crude liver)或维生素B12注射和许多胃肠里提取的酶产物。

治疗的目的是使体内病变的细胞恢复正常，其结果是恢复健康的机体和所有新陈代谢问题的消失，例如癌症、高血压、糖尿病、关节炎和其他现代病。

丧亲者哀伤辅导及其干预模式的研究进展

丧亲者哀伤辅导及其干预模式的研究进展盛艳蕾1，2，胡露红1*，何丽2，王倩云11.华中科技大学同济医学院附属同济医院，湖北 430030；2.华中科技大学同济医学院护理学院Research progress on grief counseling and intervention models for bereaved family members SHENG　Yanlei，HU Luhong, HE　Li, WANG　QianyunTongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei 430030 China Corresponding Author HU Luhong, E⁃mail: *******************Keywords hospice care； the bereaved； grief counseling； complicated grief； intervention；review摘要对安宁疗护服务中丧亲者的哀伤状态、哀伤评估和干预方式进行综述，并提出在安宁疗护实践中哀伤辅导所需的关键结构和过程，为临床探索哀伤干预模式奠定理论基础。

关键词安宁疗护；丧亲者；哀伤辅导；复杂哀伤障碍；干预；综述doi:10.12102/j.issn.1009-6493.2024.05.014哀伤是所爱之人死亡时人们产生的一种情绪反应。

随着时间的推移，大多数人会适应没有逝者的生活，逐渐恢复正常；对有些人来说，悲伤过程漫长而痛苦，最终发展成复杂哀伤障碍（complicated grief，CG）[1]。

复杂哀伤障碍又称延长哀伤障碍（prolonged grief disorder，PGD），是一种病理反应，指人们在经历丧亲后哀伤情绪至少持续6个月，并出现分离痛苦与认知、情绪、行为等一系列失调反应[2]，美国精神病协会将复杂哀伤障碍作为一种精神障碍纳入精神障碍与诊断手册（DSM⁃5）[3]。

漫谈预防医学

漫談預防醫學現代科技與疾病之預防(97-12-30 and 98-01-06)謝明昆老師疾病預防觀念已日漸普及﹕1.健康、養生食品充斥市面2.注重家庭疾病史3.對周遭環境中有害物質的警覺性提高4.身體之定期檢查5.及早發現及早治療預防醫學包括:1.健康之促進心理、生理、生活、社會因素2.疾病的預防生活、教育、健康檢查健康檢查1.傳統健康檢查: 心肺系統、胃腸肝膽系統、腎臟泌尿系統、血液循環系統、內分液系統2.數位影像健康檢查: 超音波、電腦斷層掃描、磁振造影檢查3.基因健康檢查(篩選):a.【聯合報／藍青／台大醫院復健部兼任主治醫師】基因檢驗別當健康檢查--基因是「成之於天」，生活型態是「操之在我」，只要保持健康的生活型態，自然可以延年益壽。

b.遺傳性疾病c.癌症相關的基因d.人類基因體計畫(Human genome project, HGP)超音波檢查:超音波掃描儀利用聲波頻率造出影像，其探頭內的晶片具有壓電效應，可把機械能（音波）與電能相互轉換。

電腦斷層掃描（computed tomography, CT）:結合Ｘ光攝影和電腦組成二度空間影像，能看到人體一層層的斷面影像，以避免在同一位置可能有多個器官交互重疊而擋住了醫師所要觀察的目標。

磁振造影檢查（magnetic resonance imaging, MRI）:利用磁場原理，把人體置於強大且均勻的靜磁場中，再利用特定的射頻無線電波脈衝，激發人體組織內的氫原子核。

由於人體內的許多分子都含有氫原子核，這些氫原子核本身又具有磁場特性，如同一個小小的磁鐵。

若使儀器改變體內氫原子核的旋轉排列方向，原子核就會釋放吸收的能量，能量激發後放出電磁波信號，再經由電腦分析組合成影像，這就是一般所看到的MRI 影像。

人類基因體計畫(Human genome project, HGP)1.計劃是從西元1990年10月正式開始，原本預計在DNA結構發現五十周年，也就是西元2003年完成，但在西元2000即提早完成。

反复促通疗法

特定神经通路的形成和强化有两个原则
1.无错误学习——反复向目标的神经通路进行兴奋传导
2.兴奋传导——提高突触的传递效率和强化组织性结合
参考文献：Exercise Therapy for Recovery from HemiplegiaTheory and Practice of Repetitive Facilitative Exercise，5p，2022Tanji J. Motor-related areas and motor programming, brain and neuralnet. In Amari S, Sakata H, editors. Asakura Publishing Co., Ltd; 1994. p. 203–217. (in Japanese).Kawahira K. Effects of intensive exercise to facilitate the functional recovery of the hemiplegic lower limb and effects of an anabolic steroid and muscle strengthening exercise in patients with hemiplegia (current Technology in Rehabilitation for patients with stroke). Rehabil Med. 2002;39:86–90. (in Japanese).
神经肌肉促通法只重视抑制这些阳性症状邻近损伤部位的未受损伤的大脑皮质和非损伤侧大脑半球之间无法形成新的上、下位中枢神经系统的神经通路(神经束)
优先考虑挛缩抑制的思维方式使运动努力而获得的运动模式难以反复进行重建、强化连接大脑皮质和脊髓前角细胞的神经通路，形成大脑皮质的程序及小脑的内部机制都无法顺利进行只注重挛缩抑制的治疗方法因其治疗效果不佳对瘫痪恢复帮助不大

Gerson Therapy

BY VANCE FERRELLPilgrims BooksThe Gerson Therapy for Those Dying of CancerSEVENTY YEARS WERE SPENT IMPROVING A CANCER TREATMENT– HERE IT ISTHIS BOOK WAS PREPARED FOR CANCER PATIENTSWHOSE DOCTORS HAVE TOLD THEM THEY ARE GOING TO DIEFOR ADDITIONAL COPIES: One copy - $4.00, plus $2.50 p&h / Two copies - $3.75 each, plus $3.00 p&hIn Tennessee, add 9.25% tax on totalPB–282The Gerson TherapyFor Those Dying of Cancer by Vance FerrellPublished by Pilgrims BooksBeersheba Springs, TN 37305 USA Printed in the United States of America Cover and Text Copyright © 1999by Pilgrims Books“The physician . . hesitates to take risks for his patients by applying a not-recognized treatment . . I was in a more fa-vorable position. Ninety to ninety-five percent of my patients were far advanced (terminal) cases without any risk to take;either all recognized treatments had failed or the patients were inoperable from the beginning.”—Max Gerson, A Cancer Therapy, p. xiv“I should like to tell you what we do to prove that this treat-ment really does work on cancer. Number one, the results. I think I can claim [stated in 1956] that I have, even in these far advanced cases, 50% results.”—Max Gerson, A Cancer Therapy, p. 411This book is only written for those whom the physicians have given up on. It can provide you with information you need as you consult with a Gerson-trained physician at the Gerson Institute.Caution: Consult with your physician and do not,without his guidance, attempt self-help therapy. The author and publisher are not responsible for any attempt to do so. This information is provided as an educational tool concerning certain aspects of cancer.3The Physiology of Coffee 4Preface 6The Story of Max Gerson 81 - INTRODUCTIONThe reasoning behind this therapy Four Special Problems 12Solving the Four Problems 13Better in Seven Ways 13Five Dangers 14Why Did Gerson Succeed? 14Gerson Explains His Method 142 THE BASIC THERAPYWhat is included in the program How to Begin 17Do this First 17Special Needs 18FORBIDDEN FOODSForbidden Foods 18Forbidden Non-food Substances 19 FOODSFoods to Use 20More on Foods to Use 20Foods to Eat Each Day 21Sample Menu 21Sodium-Potassium Ratios 21 Medications - 1 22Foods Temporarily Forbidden 23 FOOD PREPARATIONPurchase of Food 23Kitchen Equipment to Use 24Kitchen Equipment Not to Use 24 Juices 24Preparation of Carrot and Apple Juice 24 Chart: Using the Norwalk Juicer 25 Preparation of Citrus Juices 26 Preparation of Green Leaf Juice 26 Preparation of Cooked Vegetables 26 Preparation of Special Soup(Hippocrates’ Soup) 26Preparation of Peppermint Tea 27 Medications - 2 27 DETOXIFICATIONPhysiology of Coffee Enemas 28Preparing the Enema Mixture 29 Taking the Enema 29Taking Castor Oil by Mouth 30Taking Castor Oil By Enema 30 DEALING WITH PAINPain Triad 30Castor Oil Pack for Pain 30 Hydrotherapy for Pain 31Heat above the Abdomen for Upset Intes-tinal Tract 31Chamomile Tea Enema for Upset Intesti-nal Tract 31Potassium Added to Enema Water 31 Flare-ups and Reactions 31Clay Poultice 32OTHER POINTSGreen Leaf Tea Enema 32Massage 32The Will to Live and Push Through 32 Instructions for Giving Injections 32 Why Do Some Cancer Patients Do Better after Surgery? 35How to Prevent Cancer 353 - SCHEDULES AND SUPPLIESPutting it all together SCHEDULESCharts: Two Schedules 34Initial House Preparation 35Sample Enema Schedule 35Daily Schedule 35SUPPLIESKitchen Supplies 36Three Months’ Supply 37Gerson Supply Sources 38Locating Organic Food 40Supply Order Form 39Lab Tests 40Improving Your Water Supply 40 Gerson Therapy Recipies 414 - NON-CANCER DISORDERSMilder measures for non-malignancy The Gerson Therapy in the Treatment of Non-Cancerous Disorders 41Contents4Summary of the Gerson Therapy The Physiology of CoffeeJust what does coffee do in the human body?It is a remarkable fact that, according to the manner in which it is taken, it has two entirely different effects.If a diluted mixture of coffee is taken in an enema, it opens up the bile ducts so toxic sub-stances can be emptied out of the liver. For about 54 years, Dr. Max Gerson used coffee enemas to do this—and found no other side effects. Instead, he found that diluted coffee enemas would save lives, when nothing else would.“Where do we begin? The most important first step is the detoxification. So let us go into that.First we gave some different enemas. I found out that the best enema is the coffee enema as it was first used by Prof. O.A. Meyer in Goettingen. This idea occurred to him when, together with Prof.Heubner, he gave caffeine solution into the rectum of animals. He observed that the bile ducts were opened and more bile could flow . .“These patients who absorb the big tumor masses [from the tumor into the blood stream into the liver] are awakened with an alarm clock every night because they are otherwise poisoned by the absorption of these masses. If I give them only one or two or three enemas, they die of poisoning. I did not have the right as a physician to cause the body to absorb all the cancer masses and then not to detoxify enough. With two or three enemas they were not detoxified enough! They went into a coma hepaticum (liver coma).“Autopsies showed that the liver was poisoned. I learned from these disasters that you can’t give these patients too much detoxification . . When I didn’t give these patients the night enemas, they were drowsy and almost semi-conscious in the morning. The nurses confirmed this and told me that it takes a couple of enemas till they are free of this toxic state again. I cannot stress the detoxifi-cation enough. Even so with all these enemas, this was not enough! I had to also give them castor oil by mouth and by enema every other day, at least for the first week or so.“After these two weeks you wouldn’t recognize these patients any more! They had arrived on a stretcher, and now they walked around! They had appetite. They gained weight and the tumors went down.”—Max Gerson, A Cancer Therapy, pp. 407-408.In strong contrast, if a cup of coffee is swal-lowed, it has entirely different effects—and all of those effects are extremely negative:“A cup of coffee taken by mouth has an entirely different effect . . It heightens the reflex response, lowers the blood pressure, increases heart rate, per-spiration, causes insomnia and heart palpita-tion.”—Max Gerson, A Cancer Therapy, p. 191.Checking a standard 1,450-page textbook (pp. 374-377 of Mosby’s Pharmacology in Nursing) which deals with the subject, the effects of drinking coffee or other caffeine products are well-known.“More frequent side effects include increased nervousness or jittery feelings and irritation of GI tract resulting in nausea. More frequent adverse reactions in neonates abdominal swelling or dis-tension, vomiting, body tremors, tachycardia, jit-ters, or nervousness.”—Mosby’s Pharmacology in Nursing, p. 375.It is an intriguing fact that not one of these terrible side effects occurs when a coffee enema is given! Max Gerson said that “a cup of coffee taken by mouth has an entirely different effect.” That was his observation from about 1925, onward to his death in 1959.A diluted coffee enema has one, different, and powerful effect: the strong dilation of the bile ducts. This never occurs when coffee is drunk by mouth.It is clear that drinking coffee by mouth and taking a diluted mixture of it, temporarily into the lower bowel, have totally different effects.Why is this?Here are four reasons why:First, God made the stomach and small in-testines to be the normal means of absorbing substances from the food. This includes carbohy-drates, amino acids, fats, and other nutrients.Apparently, the lower bowel was not designed to absorb substances as well. It does not have the lacteals, found in the small intestine, which absorb nutrients into the blood stream.Second, coffee drunk by mouth, passes through the entire gastro-intestinal system. In contrast, a diluted coffee enema only enters the lower part of the large bowel.Max Gerson’s consistent practice (continued5today by the Gerson Institute and all patients) is never to give high colonics, but only low enemas. The fluid enters and is retained only in the lower bowel.Third, coffee, when drunk, remains in the body for up to 5-6 hours, until it is entirely ab-sorbed by the lacteals and has passed into the blood stream, thence to be carried throughout the body and into every organ, wreaking havoc on the entire system.But, in accordance with consistent Gerson di-rectives, a diluted coffee enema only remains in the lower bowel 12 to 15 minutes—and then it is ex-pelled.Fourth, in order to produce so many differ-ent effects, coffee taken by mouth would have to enter the bloodstream,Y et it is quite obvious that a diluted coffee en-ema does not enter the bloodstream—for if it did, it would produce the very same effects,—which it does not. Instead it produces a single, entirely different effect: the powerful opening of the bile ducts, so poisons stored in the liver can be released.What is the mechanism by which this occurs?Max Gerson has stated that the diluted coffee in the enema, instead of actually traveling to the liver in the bloodstream, may only send a signal to it.The present author suggests that it would have to be the latter. If the coffee entered the blood stream and was carried to the liver,—that same coffee would also travel throughout the body and produce all those negative effects which coffee taken by mouth does (heart palpitations, body tremors, etc.).But since a coffee enema produces none of these bad effects, it must be that coffee only sends a sig-nal, via the nerves, to the liver.Thus we are confronted by the fact that cof-fee enemas apparently are not harmful to the system. This conclusion may be incorrect. But that is where the observable facts lead us.However, let us take this matter one step fur-ther:I know any number of people who would never drink a cup of coffee, yet who are quick to take an antibiotic when they are sick. Yet drinking a cup of coffee is far less dangerous!I have never drunk coffee nor taken a coffee enema, yet it is clear to me that we are here dealing with saving human lives.If taking diluted coffee enemas will help save the life of a cancer patient who is dying, then I for one will not be the one to tell him he should not take them.And I do not believe I am wrong in making this decision.The Physiology of CoffeeAre there other problematic substances used in the Gerson Therapy?There are several other Gerson “medications”which are not needed by those who are healthy, but which are given to help the sick recover health.The Gerson therapy is focused on but two ob-jectives: filling the body with nutrients and ex-pelling toxic substances from the body. In the process of doing these two things, the cancer is totally eliminated. Everything is done to achieve these two goals.1 - Liver extract is given because of the continu-ally lowered quality of fresh fruits and vegetables. Gerson began using such a product in 1950, be-cause he found that lab reports revealed that, by the late 1940s, fresh fruits and vegetables no longer had as much nutrients as they had in the early 1930s!If you think you can obtain enough nourishment from fruit and vegetables, then skip the liver.2 - Pancreatin tablets are given. These help to reduce digestive problems during the heavy detoxi-fication process.But if you do not need it, do not take it.3 - In addition to iodine (Lugol’s solution), thy-roid is also given. The purpose of this is to ensure that enough iodine is obtained by the cells. (It is the potassium and iodine which starve the sodium out of the cancer cell, killing it.)If you think you are likely to obtain enough io-dine from the Lugol’s, then do not use the thyroid.4 - Castor oil is given to help flush the poisons out of the intestinal tract, which have been poured into it from the liver through the bile ducts. The effect of castor bean oil is similar to the laxative herbs, except that it is more efficient.Y ou would be very wise not to skip it.In all these matters, you are the boss. But know that Gerson worked out a formula which produces terrific results—but primarily in those who care-fully remain on the full program for 18 to 24 months.6Summary of the Gerson TherapyThis book is written for all those on the other side of hope, for the weary, and for those who despair of holding on to life—yet want to cling to it.There is hope in this book. There is a way out of the dark tunnel, back into the land of the living.But it will take dedication and work.If you are not living in the shadow of death, then this book is not for you. Pass it on to someone who will value it.Dr. Albert Schweitzer, the missionary physician to Africa, wrote this about his friend of many years, Dr. Max Gerson:“ . . I see in Gerson one of the most eminent medical geniuses in the history of medicine. He pos-sessed something elemental. Out of deepest thought about the nature of disease and the process of heal-ing, he came to walk along new paths with great success. Unfortunately, he could not engage in sci-entific research or teach; and he was greatly im-peded by adverse political conditions. In ordinary times he would have been able to expound his ideas for many years as professor at one of the impor-tant German universities; would have taught pu-pils who could carry on his research and teach-ings; would have found recognition and encourage-ment . . All this was denied him.“His was the hard lot of searching and working as an uprooted immigrant, to be challenged and to stand as a fighter. We who knew and understood him admired him for working his way out of dis-couragement again and again, and for undertak-ing to conquer the obstacles.”—Dr. Albert Schweitzer, quoted in Journal of the Gerson In-stitute, Fall 1981, p. 14.The following two statements will provide re-searchers with a better idea of the success rate of the Gerson therapy—and the difficulties:“By application of these principles, the Gerson therapy is able to achieve almost routine recovery—90% or better—from early to intermediate cancer.When cancer becomes incurable by orthodox meth-ods (i.e., involves the liver or pancreas or is metas-tasized inside the body), about 50% recoveries can be achieved by the Gerson method.“Norman Fritz gives laetrile as an example of other good nontoxic therapies. It has a good short-term response—relief from pain, remission of ma-lignancy, improvement in appetite and sense of well-being or increase in strength—in 70% or 80% of cancer cases. The long-term recovery rate, however, is about 15% or less. In most cases degeneration progresses to where the laetrile is no longer suffi-cient. In some cases other nontoxic therapies may be constructively combined with the Gerson therapy.“The other big advantage of the Gerson therapy is that it usually heals the body of all the degenera-tive diseases rather than just healing cancer. Many cancer patients are suffering from other degenera-tive conditions also—arthritis, heart conditions, diabetes, etc.”—Cancer News Journal, 1983 Up-date.Of the many, many cases which could be de-scribed, here was one among several where the patient had do everything by himself:“Fifteen years ago, at age 70, Earl Taylor of Cairo, Illinois, was sent home to die by his doctor. Earl had prostate cancer which was spreading exten-sively as a large mass in the groin, in spite of the harmones his doctor had been giving him. His doc-tor told him to get his affairs in order, as there was nothing that could be done to save him.“Earl had read about Dr. Gerson and the Gerson Therapy in Prevention magazine. He contacted Dr.Gerson’s daughter in New York. She sent him Dr.Gerson’s book, A Cancer Therapy — results of 50 cases. Earl had completed the sixth grade as a boy and spent all of his life working in a junk yard. He called Dr. Gerson’s daughter again and told her that he couldn’t understand the book. She suggested that he just follow the treatment outlined on page 235 in the book (page 236 in the latest edition, now gives an hourly schedule).“Earl said it was the hardest thing he ever did in his life. His wife had died years before, so he was all alone. (The institute tells people they should have help with the therapy, to have the best chance of winning.)“Earl was in pain, and the easiest thing to do was to stay in bed; but, he thought, ‘If I do that, I’llPreface7just die.’ So he forced himself out of bed, to grind and press the hourly raw juices and to do the rest of the therapy . Soon the pain was gone. In a month his doctor could no longer feel any of the large mass.“In a few months he felt well enough to go each day to help his friend, Gwinn Dunbar, who was dying of cancer spread through both lungs. Both patients recovered on the Gerson therapy and are still alive 15 years after being hopeless.”—Journal of the Gerson Institute and the Gerson Therapy,Fall, 1981, 5.Here is a second comment on Earl, which clari-fies his case still more:“Earl Taylor , 85, metastasized prostate cancer.Prostate cancer diagnosed by biopsy , 1963. Treated with female hormones. In 1966, mass spreading to groin, much pain, told to go home and get hisPrefaceaffairs in order. At age 70, started Gerson therapy .In one month, mass no longer palpable by physi-cian. In 1980, accident caused rib fracture. Bone scan showed no sign of cancer . Remains in good condition, still working part time at 85.”—Op. cit.,4.Birger Jansson, Ph.D., of the University of Texas, found that patients with a higher sodium to potassium ratio in their diets were the ones most likely to have cancer. Stephen Thompson, Ph.D., at the University of California, San Diego, found that in-creasing the sodium content of the diet—would ac-celerate the rate at which metastasis of colon cancer in animals occurred.“Cancer is now the only major killing disease in the industrialized world whose rates are sharply rising. Just by way of quantitative contrast, mortality from AIDS, another eminently preventable dis-ease, although highly alarming if not catastrophic, is relatively low.About 30,000 cases, more than half already fatal, have been re-ported since 1981 when the disease was first detected; additionally,it is estimated that 2-3 times as many Americans suffer from ad-vanced symptoms of the AIDS-related complex which oftenprogresses to frank AIDS. Rapidly increasing numbers of cases,totaling some 270,000 are projected by 1991. In contrast, there have been major reductions in deaths from cardiovascular disease, still the number one killer in the U.S., probably because of a recent de-cline in smoking and attention to diet and exercise.“With over 900,000 new cases and 450,000 U.S. deaths last year,cancer has now reached epidemic proportions, with an incidence of one in three and a mortality of one in four. Analysis of overall cancer rates, standardized for age, sex and ethnicity, has demonstrated steady increases since the 1930s, with more recent sharp annual increases in incidence rates by some 2% and in mortality rates by some 1%.“Can c er is an age-old and ubiquitous group of diseases. Its rec-ognized causes and influences are multifactorial and include natu-ral environmental carcinogens (such as aflatoxins and sunlight),lifestyle factors, genetic susceptibility, and more recently industrial chemicals. Apart from modern lifestyle factors, particularly smok-ing, increasing cancer rates reflect exposure to industrial chemicals and runaway modern technologies.”—Samuel Epstein, M.D., profes-sor of occupational and environmental medicine, University of Illi-nois Medical Center of Chicago, quoted in 1987 Congressional Record, 133(135):E3452-3453.8Summary of the Gerson TherapyMax Gerson, M.D., was born in Germany on Oc-tober 18, 1881. For his graduation tests, at the age of 19, Max wrote a totally new approach to a math-ematics problem. His teacher could not figure it out, so sent it to the University of Berlin. They wrote back, that it was the work of a brilliant mathemati-cian and that Gerson should be directed into higher mathematical studies. But Gerson had other plans. He wanted to become a medical doctor. Max wanted to help people.Graduating from the University of Freiburg in 1907 as a physician, he received advanced training under five of the leading medical experts in Germany.Shortly after completing medical school, Ger-son began experiencing severe migraine headaches. He was only 25, yet he would have to lie in a dark-ened room for two or three days in pain.The doctors had no answer. One told him, “Y ou will feel better when you are 55.” But that was not much of a solution.Then Max read about a woman in Italy who had changed her diet, and her migraines lessened. This gave him an idea, so he began tinkering with his diet. In his case, he had excellent feedback: If he made a beneficial change, the migraines reduced in intensity and frequency; if he made a mistake, one would be-gin within 20 minutes.First, he tried a milk diet, but that was useless. Then he went off all milk, and that helped a little.Then he tried eating apples only—raw, cooked, baked—and that was a great help. Slowly he added other things, till eventually he had totally eliminated his migraines.So he told his migraine patients about his diet. He called it his “migraine diet.” When they returned, they would tell him theirs was gone too. But one said it had also eliminated his lupus (lupus vulgaris, or tuberculosis of the skin). Gerson knew the man could not have had lupus since it is incurable, but the pa-tient showed him his medical records. The year was 1922.It was obvious to Gerson that the medical theory, that there is but one medicine for each disease, was incorrect. As he later stated it, the great truth was this: “Nourish the body and it will do the healing.”So Max treated some other lupus patients, and their problem vanished also. But patients came back with the news that their other problems had disap-peared as well. The careful dietary program he de-vised was successful in treating asthma and other al-lergies; diseases of the intestinal tract, liver, and pan-creas; tuberculosis; arthritis; heart disease, skin con-ditions, and on and on! Some of his most striking successes were in liver and gallbladder diseases.In Germany at that time, trains often had pri-vate compartments, each one seating six. One day, as a train was about to pull out from the station, a man entered one of the compartments. The only other person there was a distinguished-appearing gentleman who said nothing. As the train got un-derway, the man started chattering to no one in par-ticular. The gentleman tried to ignore him.Soon the man jovially got on the subject of health, and the gentleman wished he could get to his destina-tion a little quicker.Then, opening his shirt slightly, the man said, “And you know, I had this lupus, right here on my chest. And this doctor, he cured it. Now it’s gone!”At this, the gentleman jumped up, lunged at the man, reached for his shirt and said, “Let me see that!”The gentleman was Ferdinand Sauerbruch, M.D., one of Europe’s leading skin and tuberculosis doc-tors. He well-knew that lupus cannot be cured!Obtaining Gerson’s name and address from the man, Sauerbruch contacted Gerson as soon as he reached his office. A friendship was started, and Sauerbruch, impressed with his humility and sincer-ity, arranged a test using Gerson’s remarkable diet on 450 “incurable” lupus patients.But after a week or so, it was obviously a failure. Sauerbruch did not think it would come to this; he had hoped against hope. So he penned a letter to his friend Gerson and, then, slowly walked back across the hospital grounds after posting the note.He was on his way to cancel the test; but, on the way, met a woman carrying two large trays full of meat, gravy, sugary foods, and all the trimmings. Asking her what she was doing, she replied airily: “Oh, the people over in this building are starving, so we’re sneaking food in to make them happy. They have a crazy doc-tor!”Sauerbruch quickly set guards to keep the diet the way Gerson had prescribed it, and then wrote a second letter informing Gerson the test was still in progress.Result: 446 of 450 incurable patients (99%) re-covered. Lupus had been shown to be curable by dietThe Story of Max Gerson9therapy.But Gerson still had not tried his therapy oncancer patients. Even in Germany, physicians were careful about trying out new cancer remedies. Whena couple of cancer victims came to him, he turned them down. But one day, a lady called him to her home, but would not tell him what was wrong with her. Arriving, she told him she had cancer and pled for him to help her. She was in bed, weakened, and in terrible condition. He told her he could not do so. “Please, she said, just write out your dietary for-mula, and I will sign a paper not holding you re-sponsible for what happens.” Gerson did so and left. It was obvious she was too weak to even follow the directions.All alone, the sick woman struggled to follow the program—and recovered totally from cancer.Learning of this, Gerson began treating other can-cer patients. The year was 1928. Of his first 12 cases, 7 responded favorably, remaining symptom free for seven and a half years.(Some of these facts we know because of testi-mony presented by him and others at the July 1-3, 1946, senate hearings, conducted by Claude Pepper of Florida.)Gerson also treated Dr. Albert Schweitzer, his wife, and daughter for various health problems. Gerson saved Mrs. Helene Schweitzer from hopeless lung tu-berculosis in 1931; and, several years later, he healed their daughter of a rare, serious “incurable” erupting skin condition that defied diagnosis.Dr. Schweitzer himself came to Gerson at the age of 75, depressed and weary with advanced diabetes. In five weeks, Dr. Schweitzer had cut his insulin dos-age in half, and in ten was completely off of it. Healed, and with new energy, he returned to Africa where he worked past the age of 90. In response, the world-famed Schweitzer declared, “I see in him one of the most eminent medical geniuses in the history of medi-cine.”Schweitzer afterward required that his physi-cians in Lambarene, Africa, study Gerson’s book, Therapy of Lung Tuberculosis, before they started to treat the patients in his hospital.Gerson was remarkable. Geniuses tend to focus their thoughts, whereas most people scatter theirs. Because of this trait, Gerson could not ride a bicycle. He would be so deep in thought that he would smash it. After having destroyed four of them, his family for-bade more of that. For the same reason, he could not drive a car. His mind was continually at work, devis-ing ways to help his patients.One day while walking in the woods in the Harz Mountains near Bielefeld (before moving to Kassel), Max met a man who raised foxes. The rancher told him that he ran a very successful fox farm. He would buy sick, tubercular foxes for almost no cost, and later sell them. He said his foxes had the finest coats and their pelts brought the highest prices. Gerson asked him how he could do this. Mentioning that it was a secret which must not be shared with the other fox farmers, he said there was a doctor, somewhere in Germany, named Max Gerson who had a nutri-tional cure for disease. The farmer bought sick foxes which had lung tuberculosis, healed them with Gerson’s diet of organic vegetables and fruits, and then sold them at a good profit because they produced such high-quality fox furs. Both men were happy when Gerson introduced himself.At the age of 51, Gerson was asked to presenthis findings, by appointment, at a meeting of the German Medical Association. At last he would havean opportunity for the world to learn of his work to save people. On April 1, 1933, as he sat in the rail-road car, on his way to Berlin, the train stopped at a station and Hitler’s SS troups entered.When a young, inexperienced SS officer asked Gerson where he was going, Gerson, not knowing there was any danger, enthusiastically showed him X-rays and told him about his work. Impressed, the young man replied that he hoped Gerson would suc-ceed, forgot to ask the question, and passed on to the next man just behind Gerson. For the first time, Gerson heard the question the troops were asking each passenger on the train: “Are you a Jew?”Immediately, Max sensed the terrible danger. All the passengers except Gerson were asked that ques-tion, and Max saw one young man, a Jew, led out-side, where he was gunned down as Gerson watched through the window. He had just seen the first large-scale action to collect 6,000,000 Jews for extermina-tion in the Nazi concentration camps.As the train continued on, Max completely changed his plans. Instead of getting off at Berlin, he contin-ued on the train to Vienna, Austria. From there, he contacted his wife and told her to immediately come with their three girls, which she did. He also contacted all their brothers, sisters, and relatives, and offered to send money for them to leave. But they laughed at his concerns. They had their homes, their businesses, and there was nothing to fear from Hitler.Max Gerson, his wife, and their relatives were Jews. All of those relatives (15, plus children) later perished. From Vienna, Gerson later went to Paris.In 1936, he emigrated to America, and went to school to learn English. In January 1938 he received his medical license and began practicing in New Y ork City. By this time, Gerson could enlarge or shrink surface cancers at will. He knew exactly what was needed to help his patients. The only question gener-ally was whether they were in earnest enough to fully follow his program when they went home.His first contact with medicine in America wasThe Story of Max Gerson。