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Patty_D.
on 11/20/05 8:09 am - Kershaw, SC
Obesity Surgery, 8, 67-72 Biliopancreatic Diversion Preserving the Stomach and Pylorus in the Treatment of Hypercholesterolemia and Diabetes Type II: Results in the First 10 cases Giuseppe Noya MD; Maria Laura Cossu MD; Massimiliano Coppola MD; GianCarlo Tonolo MD'; Maria Filippina Matte0 Ruggiu MD Cattedra di Chirurgia d'lkgenza e Clinica Chirurgica Metabolismo e Clinica Medica, Facolta' di Medicina Background: Besides weight loss Scopinaro's op- eration produces correction of hypercholesterolemia and noninsulin dependent diabetes mellitus in all patients who suffer from these conditions. These results encouraged us to perform biliopancreatic diversion (BPD) without gastric resection, thus pre- serving the functions of the stomach and pylorus in moderately overweight patients with hypercholester- olemia associated with diabetes type II and hyper- triglyceridemia. Methods: Between March 1996 and July 1997 we performed BPD without gastric resection on 10 moderately overweight patients [mean body mass index (BMI) = 33.2 kg/m2]. All patients had suffered from hypercholesterolemia and hypettriglyceridemia for more than 5 years. Ten patients suffered from diabetes type II; four of them had had insulin treatment or oral anti-diabetic agents; the other pa- tients all had hyperglycaemia in the fasted state and diabetes confirmed by preoperative oral glucose tolerance test (OGlT). Five patients suffered from hypertension. Results: In all patients, cholesterol and triglyceride levels returned to normal within the first postopera- tive month. Glycemia also stabilized at normal values in nine patients within the early weeks after surgery. One patient who took 70 U of insulin reduced his daily intake to 35 U 2 months postoperatively. In all patients blood pressure returned to normal. Weight loss was predictably slight (lo-15 kg). Conclusions: Our experience with the procedure found that this new method seems to be as effective in controlling lipidic metabolism and diabetes II as the original version of BPD. As expected, weight loss is only moderate, so that the modified BPD is not suitable for very obese patients. 0 1998 Rapid Science Ltd. Correspondence to: Giuseppe Noya, via Ft. Morandi 5, 07100 Sassari -Italy. Tel: (+39) 79 228224: fax: (+39) 79 228394. 0 1998 Rapid Science Ltd Angius MD'; Enrico Fais MD; Generale, and ICattedra di Malattie de1 e Chirurgia -Universita' di Sassari -Italy Key words: Biliopancreatic diversion, diabetes, hyper- tension, morbid obesity, serum lipids and cholesterol, surgery. Introduction The results of Scopinaro's surgical method for treating morbid obesity are well-known? As Dr. Scorpinaro points out the main weight loss is obtained in the first 12 months postoperation, due to the effect of gastric resection and consequent forced reduction in food intake. The reduction in body weight is maintained because the biliopan- creatic diversion (BPD) causes the selective malab- sorption of starches and fat in particular, resulting in a further slow weight loss that can be controlled by changes in the diet. Besides weight reduction, however, Scopinaro's operation produces a series of beneficial effects on other diseases directly associated with morbid obesity. Hypercholesterolemia and diabetes type II were corrected in all patients suffering from these conditions within 30-40 days of the operation. Hyperuricemia, hypertension and hypertriglycer- idemia also returned to normal in 90% of cases within 4-8 months. These results prompted us to perform BPD without gastric resection, preserving the stomach and pylorus (Figure 1) on moderately overweight patients suffering from hypercholesterolemia asso- ciated with diabetes and hypertriglyceridemia. Weight loss was predictably slight but easily controllable since the gastric function was totally Obesity Surgery, 8, 1998 67 Noya et al. Figure 1. Biliopancreatic diversion with pylorus-preser- ving technique (i.e. duodenal switch without restrictive gastric surgery). preserved, while at the same time, the selective malabsorption of fat and starches corrected hy- percholesterolemia, hypertriglyceridemia, diabetes and arterial hypertension. Materials and Methods Between March 1996 and July 1997 we performed BPD with preservation of the stomach and pylorus in 10 moderately overweight patients: five males and five females, mean age 52.1 years (range 40- 62 years); mean weight 85.2 kg (range 64-106 kg); mean BMI 33.20 kg/m2 (range 24.0-38.97 kg/m'). All the patients had had hypercholesterolemia and hypertriglyceridemia for over 5 years (choles- terolemia = 260-360; triglyceridemia > 160), and all had made various attempts to reduce cholester- ol by changes in their diet, with little success. Three patients had taken sinvastatin for years without much benefit. Ten patients suffered from diabetes mellitus, type II; two of them, both women, had had insulin treatment for several years, together with dietary regulation, while two others took oral anti-diabetic agents. One woman had taken anti-diabetic tablets and 20 U of insulin every evening for years and another took 70 U of insulin a day (12+23+35); two patients took two metformin tablets (one had been taking them for 4 years and the other for 6 years). The other patients all had hyperglycemia in the fasted state and diabetes confirmed by preoperative oral glucose tolerance test (OGTT). They were taking no medi- cation but followed a hypocaloric diet. Five pa- tients suffered from hypertension and had been taking medication for some years (Table 1). All the patients underwent BPD with preserva- tion of the stomach and pylorus and end-to-end or end-to-side duodenoileostomy (Figures 2 and 3) (with a biodegradable ring in three cases, manual in seven cases) and entero-enteroanastomosis 50 cm from the ileocecal valve, as in the original technique. Results The postoperative course of all patients was uneventful with canalization on the fourth day and nutrition resumed on day 10-12. Only in four patients was a transitory slow gastric emptying observed when nutrition was resumed with gas- tric stasis after eating and with subsequent spon- taneous remission after a few days of fasting. All patients were discharged by postoperative day 15. Endoscopy 1 month after the operation showed, in all cases, good functioning of the pylorus and normal motility with no gastric or ileal ulcers. No dietary restrictions were imposed on the patients after the operation but they were advised to have a varied and abundant diet, rich in fats, starches and particularly protein. Three patients have had a 12-month follow-up, four patients a 6 month follow-up and three patients a 2-3 month follow-up. The operation had an excellent effect on glyco-lipid metabolism and on the other parameters. Data are shown in Table 2. In all patients, cholesterol and triglyceride levels returned to normal within the first postoperative month and continued to be normal with no restrictions in the diet. Glycemia also stabilized at normal values in nine patients in the early weeks after surgery. The patient who took 70 U of insulin reduced daily intake to 35 U 2 months postopera- tively and gave up her moderately glycoprival 68 Obesity Surgey, 8, 1998 Modified BPD and Diabetes Type II Table 1. Preoperative data: weight, BMI, hypercholesterolemia, diabetes (and therapy), and hypertension Patient Sex Age (years) Weight (kg) Excess weight BMI (ks/m2) Cholesterol NIDDM Hypertension (kg) 1 M 48 98 27 33.56 290* 300 - 2 F 59 86 36 38.73 250* 132* - Tablets 3 20 UI 3 M 45 99 36 37.21 242* 169 + OGTT+ 4 M 58 88 28 34.37 261 120 + OGTT+ 5 M 59 106 41 38.97 351 128 - OGTT+ 6 F 50 88 26 32.35 292 130 + OGlT+ 7 M 45 64 3 24.71 221 160* - Tablets 2 8 F 62 64 9 24.71 200 120* + 70 UI 9 F 55 73 24 31.19 310 200* + Tablets 2 10 F 40 86 34 36.28 297 120 - OGTT+ *Patients on medical treatment (sinvastatin). Figure 2. Operative photograph showing the duodenoileostomy. Obesity Surgery, 8,1998 69 Nova et al. Figure 3. Stomach X-ray on day 7 showing the intact anastomosis and the normal gastro-ileal canalization. Table 2. Postoperative data; follow-up 2-l 8 months Patients Follow-up Weight Excess BMI Cholesterol NIDDM Hypertension OGTT IVGTT (months) (kg) weight (ks/m2) (kg) 1 18 80 9 27.39 170 -Normal Altered 2 16 72 22 32.43 150 -Normal Altered 3 11 78 15 29.43 176 -Normal Normal 4 6 70 10 27.34 168 -Normal Normal 5 4 78 13 28.67 174 - 6 3 80 18 29.41 160 - 7 3 60 -1 23.16 164 - 8 5 54 -1 20.46 172 35 UI 9 2 63 14 26.92 164 - 10 2 72 20 30.30 153 - diet; the other patient is taking no anti-diabetic measured both at home and in the hospital, had therapy and at 1 month after the operation her already returned to < 100 mg% l-2 months after OGTT was normal. the operation. In four patients (three at 1 year and one at 6 Patients with hypertension no longer required months after the operation) OGTT are normal and treatment and their blood pressure returned to in two of these patients the i.v. glucose tolerance normal. As regards the other parameters, excellent test was also within normal values. It-r the other results were achieved for sideremia, calcemia and, patients (folk\w-up at under 6 months) the gly-in particular, proteinemia (2 7 mg%) and albumi- cemia value in the fasting state and after meals, nemia (> 4%). A mean weight loss of lo-15 kg 70 Obesity Surgery, &I998 was observed in the first 3 months after the operation and weight remained stable 1 year later. Mean BMI in three patients was 30.50 kg/m2 after 1 year. Complications included one case of pulmonary embolism at postoperative day 20, caused by occlusion of a branch of the right pulmonary artery and which responded to thrombolytic treat- ment. In only one case was a second operation necessary to treat an obstruction due to stenosis of the duodenoileostomy made from a biodegradable ring (digital transpyloric dilatation). All patients took 300 mg ranitidine for 6 months after the operation in order to prevent anastomotic ulcers. Discussion Various methods of surgical management of non- insulin dependent diabetes mellitus and hyperch- olesterolemia in obese patients have been reported in recent years.2 These attempts became more frequent after it was found that some operations to treat morbid obesity had the important second- ary effect of correcting, to a greater or lesser extent, hypercholesterolemia and the hyperglyce- mia sometimes associated with it.3-10 It is clear from the literature that the operations to treat morbid obesity which also correct hy- percholesterolemia and hyperglycemia are mainly biliointestinal bypass procedures, in particular Scopinaro's BPDi and the distal gastric bypass. We agree with Scorpinaro that gastric resection plays an essential role in the initial and most marked weight loss, and cannot be replaced or modified in morbidly obese patients. Our short-term data suggest that a patient with serious hypercholesterolemia, with or without hyperglycemia, and with BMI not higher than 38-40 kg/m2, could undergo BPD with preserva- tion of the stomach and pylorus. The procedure that we performed was the same as Scopinaro's with regard to the length of intestine making up the alimentary loop and the common tract. It differed in that instead of resecting the stomach and making a gastroileostomy, we transected the duodenum and made a duodenoileostomy (Fig- ures 2 and 3).11,12 A cholecystectom, -rrqs done as a prophylactic measure. In two cases we also performed super selective vagotomy in order to prevent ileal anastomotic ulcers. Our 10 patients had a lo-15 kg reduction in body weight in the first month after the operation, Modified BPD and Diabetes Type II and 6-12 months later they are maintaining the reduced weight with an entirely unrestricted diet, and are taking no medication. Hypercholesterole- mia and hyperglycemia values went right down after the operation. It is possible, but needs testing, that a more or less moderate restriction in sugar intake would bring about a further loss in weight. Conclusions Our experience to date indicates that this new method seems as effective in controlling lipid metabolism and diabetes type II as the original BPD procedure. As expected, weight loss is only moderate so that the modified BPD is not recom- mended for morbid obesity. In these cases, Scopi- naro's method must be used unmodified despite the metabolic problems involved, until a better procedure is developed. A larger number of patients with the character- istics that we mention (BMI < 38, suffering from hypercholesterolemia and diabetes type II) under- going modified BPD with a longer follow-up (i.e. at least 5 years) will show whether our encoura- ging results are reproducible and will provide more reliable data on recovery of pancreatic func- tion. Studies presently being carried out indicate that it will be possible to characterize and select patients of normal weight who could benefit from the operation. One question to be carefully evaluated is whether a super selective vagotomy should ac- company this operation in order to prevent ileal anastomotic ulcers. References 1. Scopinaro N, Gianetta E, Adami GF et al. Biliopan- creatic diversion for obesity at eighteen years. Surgery 1996; 119: 261-8. 2. Buchwald H, Stoller D, Campos CT et al. Partial ileal bypass for Hypercolesterolemia. 20 to 26 year follow-up of the first 57 consecutive cases. Ann Surg 1990; 212: 318-31. 3. Pories WJ, Swanson MS, Mac Donald KG et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg 1995; 222: 339-52. 4. Smith SC, Edwards CB, Goodman GN. Changes in diabetic management after Roux-en-Y gastric by- pass. Obes Stlrg 1996; 6: 345-8. Obesity Surgery, 8, 1998 71 Noya et al. 5. Pories WJ. Why does the gastric by-pass control type 2 diabetes mellitus? Obes Surg 1992; 2: 303-13. 6. Castagneto M, De Daetano A, Mingrone G et al. Normalization of insulin sensitivity in the obese patient after stable weight reduction with biliopan- creatic diversion. Obes Surg 1994; 4: 161-8. 7. Jensen K, Mason EE, Scott DH. Changes in the postoperative hypoglycemic and anti-hypertensive medication requirements in morbidly obese diabetic patients after vertical banded gastroplasty. Obes Surg 1991; 1: 114 (abstract). 8. Sanderson J, Deitel M, Bojm MA. The handling of glucose and insulin response before and after weight loss with jejunoileal by-pass. JPEN 1983; 7: 274-6. 9. Deitel M, Sidhu I'S, Stone E. Effect of vertical banded gastroplasty on diabetes in the morbidly obese. Obes Surg 1991; 1: 113-4 (abstract). 10. Long S, Swanson MS, Pories WJ et al. Gastric bypass surgery prevents the development of overt NIDDM in patients with 'occult' NIDDM. Obes Surg 1996; 6: 307 (abstract). 11. Baltasar A, Escrivh C, Mire J et al The duodenal Switch in bariatric surgery. Obes Surg 1996; 6: 302 (abstract). 12. Vassallo C, Negri L, Della Valle A et al. PBD + transitory gastroplasty preserving duodenal bulb: 3 year's experience. ObesStlrg 1996; 6: 303 (abstract). (Received 6 October 1997; accepted 22 November 1997) 72 Obesity Surgey, 8, 1998
Patty_D.
on 11/20/05 8:12 am - Kershaw, SC
Restoration of Euglycemia and Normal Acute Insulin Response to Glucose in Obese Subjects With Type 2 Diabetes Following Bariatric Surgery Eftihia V. Polyzogopoulou,1 Fotios Kalfarentzos,2 Apostolos G. Vagenakis,1 and Theodore K. Alexandrides1 Insulin resistance and loss of glucose-stimulated acute insulin response (AIR) are the two major and earliest defects in the course of type 2 diabetes. We investigated whether weight loss after bariatric surgery in patients with morbid obesity and type 2 diabetes could restore euglycemia and normal AIR to an intravenous glucose tolerance test (IVGTT). We studied 25 morbidly obese patients--12 with type 2 diabetes, 5 with impaired glucose tolerance, and 8 with normal glucose tolerance (NGT)--before and after a biliopancreatic diversion (BPD) with Roux-en-Y gastric bypass (RYGBP). Twelve individuals with normal BMI served as control subjects. Twelve months after surgery, in the diabetes group, BMI decreased from 53.2 2.0 to 29.2 1.7 kg/m2, fasting glucose decreased from 9.5 0.83 to 4.5 0.13 mmol/l, and fasting insulin decreased from 168.4 25.9 to 37.7 4.4 pmol/l (mean SE; P < 0.001). AIR, the mean of insulin concentration at 2, 3, and 5 min over basal in the IVGTT, increased by 770 and 935% at 3 and 12 months after surgery, respectively (from 24.0 22.7 to 209 43.4 and 248 33.1 pmol/l, respectively; P < 0,001). Conversely, in the NGT group, the AIR decreased by 40.5% (from 660 60 to 393 93 pmol/l; P 0.027) 12 months after surgery. BPD with RYGBP performed in morbidly obese patients with type 2 diabetes leads to significant weight loss, euglycemia, and normal insulin sensitivity; but most importantly, it restores a normal -cell AIR to glucose and a normal relationship of AIR to insulin sensitivity. This is the first study to demonstrate that the lost glucose-induced AIR in patients with type 2 diabetes of mild or moderate severity is a reversible abnormality. Diabetes 52:1098-1103, 2003 From the 1Department of Internal Medicine, Division of Endocrinology, University of Patras Medical School, Patras, Greece; and the 2Nutrition Support and Morbid Obesity Clinic, Department of Surgery, University of Patras Medical School, Patras, Greece. Address correspondence and reprint requests to Theodore K. Alexandrides, Associate Professor of Medicine, Department of Internal Medicine, University Hospital of Patras, Rion, 26500, Greece. E-mail: [email protected]. Received for publication 17 October 2002 and accepted in revised form 11 February 2003. AIR, acute insulin response; BPD, biliopancreatic diversion; FFM, fat-free mass; IGT, impaired glucose tolerance; IVGTT, intravenous glucose tolerance test; NGT, normal glucose tolerance; OGTT, oral glucose tolerance test; QUICKI, Quantitative Insulin Sensitivity Check Index; RYGBP, Roux-en-Y gastric bypass. © 2003 by the American Diabetes Association. Epidemiological studies have shown that obesity is a significant risk factor for type 2 diabetes and that 41% of morbidly obese patients have abnormal glycemic control (1). Insulin resistance is more pronounced in obese subjects with type 2 diabetes (2,3). It has been shown that progression from normal to impaired glucose tolerance and diabetes is associated with a reduction in insulin sensitivity and a progressive decrease of the acute insulin response (AIR) to glucose, which is lost at the onset of diabetes (4,5). Moderate weight loss following a hypocaloric diet can improve insulin action and secretion, but the effect is rather weak (6). Metabolic control has been shown to improve the defect of early insulin response only minimally or partially (3,7,8). Individuals with morbid obesity and type 2 diabetes benefit from weight loss, as this allows better glycemic control and modifies the coexisting risk factors for coronary heart disease, namely hypertension, dyslipidemia, insulin resistance, sleep apnea, and other comorbidities that constitute the metabolic syndrome (9-15). Although weight loss can be achieved by low-calorie diet, exercise, behavior modification, and medical treatment, late weight gain has been an almost universal problem. Conversely Roux-en-Y gastric bypass (RYGBP) maintains a weight loss of 33% of body weight for 10 years, a result associated with normalization of glucose levels in patients with impaired glucose tolerance (IGT) and type 2 diabetes, in the vast majority of the cases (1,9-16). It also normalizes insulin action and secretion in normal glucose tolerant subjects with morbid obesity (17,18). To our knowledge, there are no other antidiabetic therapies that can produce such effective and long-term glycemic control. The purpose of the present study was to investigate whether weight loss after gastric bypass can correct the AIR to glucose in morbidly obese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS Subjects. Twenty-five patients with morbid obesity were included in the study: 12 with type 2 diabetes, 5 with IGT, and 8 with normal glucose tolerance (NGT) who underwent a biliopancreatic diversion (BPD) with RYGBP. All consecutive patients with diabetes and IGT who agreed to participate were included in the study. The patients with NGT were selected to match the other two groups with regard to BMI, age, and sex. Two of the diabetic patients were on oral hypoglycemic agents that were discontinued 1 month before evaluation, and the other patients had hyperglycemia in the fasting state. The DIABETES, VOL. 52, MAY 2003 E.V. POLYZOGOPOULOU AND ASSOCIATES TABLE 1 Characteristics of the control subjects and the patients in the diabetes group Diabetes group Control subjects Preoperative 3 months 6 months 12 months n 12 11 11 11 11 M/F 3/9 2/9 Age (years) 36.8 3.0 40.1 2.5 Weight (kg) 64.5 3.0 143.3 9.5 112.5 7.0 94.9 6.4 77.8 4.5 BMI (kg/m2) 22.3 0.5 53.2 2.0 41.7 1.4 35.3 1.6 29.2 1.7 FFM (kg) 75.3 2.9 65.5 5.0 61.9 5.5 55.1 4.7 Fat mass (kg) 60.9 2.9 45.6 3.0 33.1 2.5 22.6 3.4 Fasting glucose (mmol/l) 4.7 0.11 (4.2-5.3) 9.5 0.83 (6.9-15.5) 5.1 0.17 (4.2-5.9) 4.7 0.13 (4.1-5.3) 4.5 0.13 (3.9-5.1) Fasting insulin (pmol/l) 44.4 6.0 168.4 25.9 55.3 9.1 33.5 6.1 37.7 4.4 QUICKI 0.365 0.007 0.278 0.007 0.357 0.015 0.396 0.019 0.378 0.011 1st phase insulin (pmol/l) 332.4 39.6 24.0 22.7 208.8 43.4 261.8 40.4 248.5 33.1 2nd phase insulin (pmol/l) 207.0 18.6 410.9 57.1 235.9 43.2 172.2 30.2 127.6 22.5 Data are means SE (range) unless otherwise indicated. duration of diabetes ranged from 3 to 5 years. Six of the 12 diabetic patients, 4 of the 5 IGT patients, and 2 of the 8 NGT patients had first-degree relatives with a history of diabetes. The diagnosis of diabetes, IGT, or NGT was established by a 75-g oral glucose tolerance test (OGTT), according to the criteria of the American Diabetes Association (19), 1 month after the initial evaluation. Twelve subjects with normal OGTT and BMI, matched to the diabetes group for age and sex, served as normal control subjects. All subjects were asked to consume a diet ri*****arbohydrates for 3 days before testing. The patients were in good health and gave informed consent before surgery. The basic characteristics of the patients are summarized in Tables 1 and 2. Only 11 of the 12 patients in the diabetes group are shown in Table 1; because one of the patients had fasting insulin levels 13.5 standard deviations above the mean of the group, her data were not included in the statistical analysis and are discussed separately. Surgery. BPD with RYGBP was constructed with a gastric pouch 15 5 ml, a biliopancreatic limb 150-200 cm, a common limb 100 cm, and an alimentary limb composed of the remainder of the small intestine (16). Cholecystectomy and appendectomy were performed in all patients. Postoperatively during the first month, the patients consumed a liquid diet of 600-800 kcal/day composed of 50% carbohydrates, 30% protein, and the remainder lipids. For the next 2 months, they consumed a regular diet of similar composition containing 1,000 -1,200 kcal/day and increasing gradually to 1,500 -2,000 kcal/day during the 1st year. AIR to glucose. Intravenous glucose tolerance tests (IVGTTs) were carried out preoperatively and 3, 6, and 12 months postoperatively. At 8:00 -9:00 A.M, after a 12-h overnight fast, blood samples were collected at 10 min, immediately before the infusion of 35 g glucose (35% wt/vol, over 2 min), and 2, 3, 5, 10, 20, and 30 min after the end of glucose infusion. The first phase of insulin or acute insulin response was calculated as the difference ()ofthe mean insulin concentration at 2, 3, and 5 min minus the mean insulin concentration at -10 and 0 min of the test. Insulin sensitivity. The Quantitative Insulin Sensitivity Check Index (QUICKI) was used to assess insulin sensitivity according to the formula 1/(log [fasting insulin] log [fasting glucose]). This method of insulin sensitivity estimation is considered reliable and correlates very well with the hyperinsulinemic isoglycemic glucose clamp, especially in the obese population (r 0.89) (20 -22). Body composition. The percentages of body fat (fat mass) and fat-free mass (FFM) were determined by bioelectrical impedance (TANITA Body Composition Analyzer, Tokyo, Japan). Assays. Serum glucose was assayed by the glucose oxidase method within 1 h of sample collection, using an automatic analyzer (Olympus, AU640, Medicon). Serum samples were stored at 40°****il they were assayed for insulin by a micro particle enzyme immunoassay (Abbott IMX System, Dainabot, Tokyo, Japan). This assay is specific for insulin and does not recognize proinsulin. Intra-and interassay coefficients of variation were 3.1 and 3.8%, respectively, and the sensitivity of the method was 6.0 pmol/l. Statistical analysis. Student's t test was used for parametric and Mann- Whitney U test for nonparametric evaluation of differences between groups. Paired t test was used for evaluation of differences between time points within the same group during the follow-up. Statistical significance was set at P 0.05. RESULTS Preoperatively. The three groups with morbid obesity had similar BMI, which was higher than that of the control group (P 0.01). Fat mass and FFM were also similar among the three surgical groups (Tables 1 and 2). The diabetes group had a higher waist-to-hip ratio than the NGT group, but it did not reach statistical significance (0.962 0.029 vs. 0.880 0.028, P 0.07). The diabetes and IGT groups had higher fasting serum glucose (P 0.01) and higher fasting plasma insulin concentrations (P 0.05) than the NGT and control groups (Tables 1 and 2). The NGT group had higher fasting insulin (P 0.05) but similar fasting glucose to that of control subjects. Insulin sensitivity, as expressed by the QUICKI, was reduced in the three surgical groups compared with control subjects (P 0.005), but the NGT group was less insulin resistant than the diabetes and IGT groups (P 0.001) (Tables 1 and 2). AIR was absent in 8 of the 11 subjects in the diabetes group and substantially reduced in the other 3 subjects (Table 1, Fig. 1A). The IGT group had a reduced response (P 0.001) (Table 2, Fig. 2). When AIR was plotted against insulin sensitivity in either group and was compared with the control group (Fig. 3), it was noted that AIR was very diminished for the degree of insulin resistance in the IGT group and virtually absent in the diabetes group. In contrast, the NGT group had two times greater AIR than control subjects (P 0.001) (Table 2, Fig. 2), but this response was appropriate for their insulin resistance (Fig. 3). The second phase of insulin secretion, calculated as the mean of the total insulin concentration at 10, 20, and 30 min or as the area under the curve, was greatly increased (200%) in all surgical groups compared with control subjects (P 0.05, Tables 1 and 2). Postoperatively. Four and two of the eight patients in the NGT group missed their 3-month and 6-month appointments, respectively. All patients were studied 12 months postoperatively. Body weight decreased significantly in all patients. All surgical groups showed similar decreases in BMI (24 kg/m2 for the diabetes, 21.5 for the IGT, and 18.2 for the NGT group) at the end of the 1st year (Tables 1 and 2). The decline of BMI was greater during the first 3 DIABETES, VOL. 52, MAY 2003 TABLE 2Characteristics of the patients in the IGT and NGT groups IGT group NGT group Preoperative 3 months 6 months 12 months Preoperative 3 months 6 months 12 months n 55558468 M/F 0/5 0/8 Age (years) 37.8 4.3 34.1 3.3 Weight (kg) 125.7 10.5 96.6 9.1 83.5 9.3 74.4 7.8 124.9 6.2 100.7 5.2 88.4 5.0 77.9 4.8 BMI (kg/m2) 52.2 3.7 39.8 4.6 34.4 4.8 30.7 3.4 46.6 1.8 36.7 1.7 33.0 1.9 28.4 1.7 FFM (kg) 65.2 4.5 61.1 3.9 55.8 3.5 54.5 2.3 65.1 2.5 57.8 1.9 54.8 1.6 55.6 1.5 Fat mass (kg) 60.6 7.0 35.3 7.3 27.7 8.0 19.8 6.5 59.3 4.0 43.0 3.6 33.6 3.7 22.3 3.7 Fasting glucose (mmol/l) 6.1 0.19 (5.6-6.6) 4.2 0.29 (3.1-4.7) 4.4 0.23 (3.7-4.9) 4.5 0.30 (3.8-5.6) 4.9 0.12 (4.3-5.4) 4.3 0.16 (3.9-4.7) 3.9 0.12 (3.5-4.3) 4.1 0.08 (3.8-4.5) Fasting insulin (pmol/l) 172.2 17.4 48.0 18.6 40.2 13.8 49.2 14.4 79.1 13.6 45.7 3.6 33.9 7.7 34.6 4.4 QUICKI 0.286 0.005 0.378 0.018 0.416 0.034 0.377 0.028 0.33 0.007 0.360 0.007 0.396 0.015 0.385 0.009 1st phase insulin (pmol/l) 276.0 51.6 246.6 55.2 392.4 147.0 372.6 87.0 659.6 60.2 356.4 23.3 428.8 126.9 393.1 92.8 2nd phase insulin (pmol/l) 532.2 120.6 272.4 87.0 246.6 102.6 243.6 78.6 429.3 86.0 206.4 36.6 237.9 89.9 167.7 40.9 Data are means SE (range) unless otherwise indicated. months following surgery and continued to decline thereafter at a slower rate for the rest of the 1st year. All surgical groups also showed a significant and similar decrease in fat mass and FFM postoperatively (Tables 1 and 2), and there were no cases of hypoalbuminemia or other signs of malnutrition. The postoperative decrease in fat mass was proportional to the preoperative fat mass (r 0.91, P 0.006) in the diabetes group, but not in the other two groups. All patients in the diabetes group had normal fasting glucose 3 months after the operation. Fasting plasma insulin concentration declined significantly in all groups during the early postoperative period and became normal 3 months after surgery (Tables 1 and 2). Insulin sensitivity improved quickly and became normal in all surgical groups after the 3rd postoperative month (Tables 1 and 2). AIR was restored the 3rd postoperative month in all patients in the diabetes group and continued to improve further during the rest of the 1st year (Fig. 1B-D and Fig. 2). The IGT group also showed an improvement of AIR postoperatively (Fig. 2). In both groups, the relationship of AIR to insulin sensitivity that was displaced down and far to the left relative to the control group showed a dramatic shift and became normal (Fig. 3). Conversely, the exaggerated AIR in the NGT group decreased to normal levels in parallel with insulin resistance by the third postoperative month. AIR was similar in all groups 12 months after surgery (Fig. 2, Table 2). Increased second-phase insulin secretion declined gradually to control levels during the postoperative period in all groups and below control levels in the diabetes group (P 0.01) (Tables 1 and 2). One diabetic patient with preoperative BMI 46 kg/m2, fat mass 56.1 kg, and fasting glucose 8.7-9.0 mmol/l had a fasting insulin concentration of 1,332 pmol/l, 13.5 SD above the mean of the diabetes group. Therefore, this patient was not included in the statistical analysis of the data, although inclusion of the patient did not modify the results. Three months after the operation, BMI was 36.3 kg/m2, fat mass was 42.1 kg, fasting glucose was 4.2 mmol/l, fasting insulin was 88.2 pmol/l, and the absent AIR was above normal (670 pmol/l). DISCUSSION The BPD with RYGBP procedure was successful in all patients, and weight reduction was impressive, although the patients were still obese 1 year after the operation, with an average BMI 30 kg/m2. There was a complete remission of diabetes in all cases and reappearance of a normal acute insulin response by the 3rd postoperative month. Insulin sensitivity also became normal within the same period, although the patients were still morbidly obese. The abnormal relationship of AIR to insulin sensitivity became normal. Finally, the greatly increased and prolonged second phase of insulin secretion returned to normal. Our results confirm the findings of previous studies showing the control of diabetes in morbidly obese patients following BPD with RYGBP (9,11-14). This beneficial effect was evident from the early postoperative period, despite the presence of morbid obesity. Other studies had similar results concerning weight loss and improvement in insulin sensitivity in morbidly obese patients with normal RESTORATION OF AIR IN TYPE 2 DIABETES DIABETES, VOL. 52, MAY 2003 E.V. POLYZOGOPOULOU AND ASSOCIATES glucose tolerance after bariatric surgery (17,23). In our patients, euglycemia was restored in parallel with the normalization of insulin sensitivity, the reappearance of a normal AIR to glucose, and the restoration of a normal relationship of AIR to insulin sensitivity. Previous studies have shown that tight metabolic control restores minimally or partially the defect in the first phase of insulin response (7,8). Hughes et al. (24) have reported that in obese patients with type 2 diabetes subjected to Roux-en-Y gastrojejunostomy, the defect in insulin secretion did not improve with weight reduction, although insulin sensitivity did. The possible explanations for these discrepancies between our study and the findings of Hughes et al. (24) are the rather moderate weight loss in their study due to the different surgical procedure, the failure to restore euglycemia and normal insulin sensitivity, and finally, the more severe degree and longer duration of diabetes in their patients. The preoperative findings in our study are consistent FIG. 2. Acute insulin response during IVGTT. The difference ()inthe mean insulin concentration at 2, 3, and 5 min over basal (mean SE) is plotted. C, control subjects; DM, diabetes mellitus group; Pre, preoperative. FIG. 1. Insulin response after intravenous glucose infusion (IVGTT) in normal control subjects (E) and patients with type 2 diabetes, before gastric bypass (A) and 3 months (B), 6 months (C), and 12 months (D) after gastric bypass. with the changes that occur during the transition from NGT to type 2 diabetes. The NGT group, although insulin resistant, maintained NGT by increasing the AIR proportionally to the degree of insulin resistance, and this is the feature that differentiates this group from the other two (25-28). In contrast, the IGT group had a decreased AIR for the degree of insulin resistance (Fig. 3). This is in agreement with previous studies (4,25-30). Impaired AIR normalized quickly after surgery in parallel with insulin sensitivity, although BMI was still high. It is reasonable to assume that the improvement in the first phase of insulin secretion followed the normalization of insulin sensitivity. Finally, the diabetes group was the most insulin resistant, but AIR was absent. Because our diabetic patients had diabetes of rather mild to moderate severity, they maintained increased fasting insulin concentration and increased and prolonged second-phase insulin secretion, but they had lost the AIR to glucose. It has been shown that AIR to glucose is lost when fasting glucose concentration exceeds 115 mg/dl (4). It is also known that the -cell at this stage of type 2 diabetes can respond to other secretagogues, such as glucagon or amino acids, and that the defect is specific to the glucose-induced AIR (3,26). The relationship of AIR to insulin sensitivity was significantly altered in the IGT and diabetes groups relative to that in control subjects (Fig. 3), as previous studies have shown (27,28,30,31). This altered relationship became normal postoperatively, suggesting that this type of operation, namely BPD with RYGBP, not only normalized insulin sensitivity early after surgery, when the patients were still very obese, but also restored a normal AIR appropriate to the degree of insulin sensitivity. To our knowledge, no other therapeutic intervention has had such an effect so far. Insulin resistance is inherited and is present many years before the onset of type 2 diabetes (3). Obesity, usually present in patients with type 2 diabetes, further increases DIABETES, VOL. 52, MAY 2003 RESTORATION OF AIR IN TYPE 2 DIABETES FIG. 3. Relationship between insulin sensitivity and acute insulin response in patients with morbid obesity and diabetes mellitus (DM), IGT, or NGT before and 12 months after BPD with RYGBP (mean  SE), as compared with normal control subjects (curve). Pre, preoperative. insulin resistance, which deteriorates with age, but diabetes develops only when the -cell fails to compensate for the increased insulin demands (27,28). It has been shown that amelioration of insulin resistance after treatment with troglitazone can delay or prevent the onset of type 2 diabetes in Hispanic women at high risk for the development of type 2 diabetes (30). Protection from diabetes, in the same study, was closely related to the degree of reduction in endogenous insulin requirements and the preservation of -cell compensation for insulin resistance. In prospective studies it has been shown that normal glucose tolerant subjects with insulin resistance do not develop diabetes if they can increase insulin secretion, in particular the AIR, as insulin resistance deteriorates with time. Alternatively, the subjects who develop IGT and later diabetes exhibit an inappropriate progressive decrease in the AIR to glucose in the presence of increasing insulin resistance (27,28). A reduced AIR for the degree of insulin resistance has been shown in subjects at high risk for the development of type 2 diabetes, such as first-degree relatives of patients with type 2 diabetes, older subjects, women with a history of gestational diabetes or polycystic ovary syndrome (25-31). Insulin secretion, when expressed as an index normalized for insulin sensitivity, is a very useful trait for identifying genetic predisposition to type 2 diabetes (32). We observed that BPD with RYGBP normalized the altered relationship of AIR to insulin sensitivity that characterizes this category of subjects, and this change was probably crucial for the restoration of NGT in our patients. The detailed mechanisms that lead to normalization of glucose tolerance and insulin secretion in our study are not entirely clear, however. BPD with RYGBP reduces the total caloric intake and particularly carbohydrate consumption in part due to dumping syndrome (33), leading to weight loss and reduction in insulin resistance. It also induces lipid malabsorption, reduces the elevated free fatty acids in the circulation, and therefore reduces their adverse effects on insulin action and secretion (34,35). Changes in ghrelin, glucagon-like peptide-1, enterogluca gon, and gastric inhibitory polypeptide secretion after BPD with RYGBP have also been shown to occur and may contribute to the same results (36 -39). Changes in fat distribution after surgery, e.g., preferential loss of intra- abdominal and intramyocellular fat, have a major impact on insulin sensitivity (23). BPD with RYGBP increases IGF-I levels and lowers leptin and pancreatic polypeptide levels in morbidly obese patients with or without type 2 diabetes, as reviewed elsewhere (40). The restoration of normal insulin sensitivity in our morbidly obese patients 3 months after the operation alleviated the high burden imposed upon the -cell and possibly played a central role in the restoration of the AIR, but it is also possible that changes in the enteropancreatic axis played a significant role. In conclusion, our findings support the concept that the diminished AIR for the degree of insulin resistance is important for the development of IGT and diabetes. The lack of glucose intolerance in the severely obese and insulin-resistant NGT group that maintained an appropriately exaggerated AIR points in the same direction. Furthermore, our results show that the loss of glucose- induced AIR in obese patients with type 2 diabetes of mild or moderate severity is not permanent but reversible. Finally, the altered relationship of AIR to insulin sensitivity that characterizes subjects with diabetes or IGT or subjects at high risk for the development of type 2 diabetes becomes normal and suggests that this type of surgical operation can be of value in these groups of patients, even in the presence of milder degrees of obesity. ACKNOWLEDGMENTS This work was supported by Grant no. 2421 "K. Karatheodoris" from the Research Council of the University of Patras, Patras, Greece. We thank Dr. Maria Makri and Dr. Marina Michalaki for their valued help in hormonal analysis. REFERENCES 1. Buffington CK, Cowan GS Jr: Gastric bypass in the treatment of diabetes, hypertension and lipid/lipoprotein abnormalities of the morbidly obese. In Update: Surgery for the Morbidly Obese Patient. Deitel M, Cowan GS Jr, Eds. Toronto, FD-Communications, 2000, p. 435-449 2. Kahn BB, Flier JS: Obesity and insulin resistance. J Clin Invest 106:473- 481, 2000 3. De Fronzo RA: Pathogenesis of type 2 diabetes: metabolic and molecular implications for identifying diabetes genes. Diabetes Rev 5:177-269, 1997 4. Brunzell JD, Robertson RP, Lerner RL, Hazzard WR, Ensinck JW, Bierman EL, Porte D Jr: Relationship between fasting plasma glucose levels and insulin secretion during intravenous glucose tolerance tests. J Clin Endocrinol Metab 42:222-229, 1976 5. Weir GC, Bonner-Weir S: Insulin secretion in non-insulin-dependent diabetes mellitus. In Diabetes Mellitus. 2nd ed. Le Roith D, Taylor SI, Olefsky JM, Eds. Philadelphia, Lippincott, Williams and Wilkins, 2000, p. 595- 603 6. Weyer C, Hanson K, Bogardus C, Pratley RE: Long term changes in insulin action and insulin secretion associated with gain, loss, regain and maintenance of body weight. Diabetologia 43:36-46, 2000 7. Garvey WT, Olefsky JM, Hamman RF, Kolterman OG: The effect of insulin treatment on insulin secretion and insulin action in type II diabetes mellitus. Diabetes 34:222-234, 1985 8. Vague P, Moulin JP: The defective glucose sensitivity of the -cell in insulin dependent diabetes: improvement after twenty hours of normoglycaemia. Metabolism 31:139-142, 1982 9. Cowan GS Jr, Buffington CK: Significant changes in blood pressure, glucose and lipids with gastric bypass surgery. World J Surg 22:987-992, 1998 DIABETES, VOL. 52, MAY 2003 E.V. POLYZOGOPOULOU AND ASSOCIATES 10. Smith SC, Edwards CB, Goodman GN: Changes in diabetic management after Roux-en-Y gastric bypass. Obes Surg 6:345-348, 1996 11. Mac Donald Jr KG, Long SD, Swanson MS, Brown BM, Morris P, Dohm GL, Pories WJ: The gastric bypass operation reduces the progression and mortality of non-insulin-dependent diabetes mellitus. J Gastrointest Surg 1:213-220, 1997 12. Pories WJ, Swanson MS, Mac Donald Jr KG, Long SB, Morris P, Brown BM, Bakarat HA, deRamon RA, Israel G, Dolezal JM, Dohm GL: Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg 222:339-352, 1995 13. Pories WJ, Mac Donald Jr KG, Flickinger EG, Dohm GL, Sinha MK, Barakat HA, May HJ, Khazanie P, Swanson MS, Morgan E, Leggett-Frazier N, Long SD, Brown BM, O'Brien K, Caro JF: Is type II diabetes mellitus (NIDDM) a surgical disease? Ann Surg 215:633- 643, 1992 14. Long SD, O' Brien K, Mac Donald Jr KG, Leggett-Frazier N, Swanson MS, Pories WJ, Caro JF: Weight loss in severely obese subjects prevents the progression of impaired glucose tolerance to type II diabetes: a longitudinal international study. Diabetes Care 17:372-375, 1994 15. Sjostrom CD, Lissner L, Wedel H, Sjostrom L: Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study. Obes Res 7:477- 84, 1999 16. Kalfarentzos F, Dimakopoulos A, Kehagias I, Loukidi A, Mead N: Vertical banded gastroplasty versus standard or distal Roux-en-Y gastric bypass based on specific selection criteria in the morbidly obese: preliminary results. Obes Surg 9:433- 42, 1999 17. Lextiexhe MR, Scheen AJ, Gerard PL, Desaive C, Lefebvre PJ: Postgastroplasty recovery of ideal body weight normalizes glucose and insulin metabolism in obese women. J Clin Endocrinol Metab 80:364 -369, 1995 18. Scheen AJ, Paquot N, Letiexhe MR, Paolisso G, Castillo MJ, Lefebvre PJ: Glucose metabolism in obese subjects: lessons from OGTT, IVGTT and clamp studies. Int J Obes 19 (Suppl. 3):S14 -S20, 1995 19. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 20:1183-1197, 1997 20. Katz A, Nambi SS, Mather K, Baron AD, Follmann AD, Sullivan G, Quon MJ: Quantitative Insulin Sensitivity Check Index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab 85:2402- 2410, 2000 21. Mather KJ, Hunt Evay A, Steinberg HO, Paradisi G, Hook G, Katz A, Quon MJ, Baron AD: Repeatability characteristics of simple indices of insulin resistance: implications for research applications. J Clin Endocrinol Metab 86:5457-5464, 2001 22. Quon MJ: QUICKI is a useful and accurate index of insulin sensitivity. J Clin Endocrinol Metab 87:949 -950, 2002 23. Greco AV, Mingrone G, Giancaterini A, Manco M, Morroni M, Cinti S, Granzotto M, Vettor R, Camastra S, Ferrannini E: Insulin resistance in morbid obesity: reversal with intramyocellular fat depletion. Diabetes 51:144 -151, 2002 24. Hughes TA, Gwynne JT, Switzer BR, Herbst C, White G: Effects of caloric restriction and weight loss on glycemic control, insulin release and resistance, and atherosclerotic risk in obese patients with type 2 diabetes mellitus. Am J Med 77:7-17, 1984 25. Kahn SE: The importance of the -cell in the pathogenesis of type 2 diabetes mellitus. Am J Med 108 (Suppl. 6A):2S-8S, 2000 26. Weir GC: -Cell adaptation and decompensation during the progression of diabetes. Diabetes 50 (Suppl. 1):S154 -S159, 2001 27. Kahn SE: The importance of -cell failure in the development and progression of type 2 diabetes. J Clin Endocrinol Metab 86:4047-4058, 2001 28. Weyer C, Bogardus C, Mott DM, Pratley RE: The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest 104:787-794, 1999 29. Reaven GM, Hollenbeck CB, Chen YDI: Relationship between glucose tolerance, insulin secretion and insulin action in non-obese individuals with varying degrees of glucose tolerance. Diabetologia 32:52-55, 1989 30. BuchananTA, Xiang AH, Peters RK, Kjos SL, Marroquin A, Goico J, Ochoa C, Tan S, Berkowitz K, Hodis HN, Azen SP: Preservation of pancreatic -cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk Hispanic women. Diabetes 51:2796-2803, 2002 31. Pratley RE, Weyer C: The role of impaired early insulin secretion in the pathogenesis of type II diabetes mellitus. Diabetologia 44:929-945, 2001 32. Elbein SC, Hasstend SJ, Wegner K, Kahn SE: Heritability of pancreatic -cell function among nondiabetic members of Caucasian familiar type 2 diabetic kindreds. J Clin Endocrinol Metab 84:1398 -1403, 1999 33. Marceau P, Hould FS, Lebel S, Marceau S, Biron S: Malabsorptive obesity surgery. Surg Clin North Am 81:1113-1127, 2001 34. Poitout V: Lipid partitioning in the pancreatic -cell: physiologic and pathophysiologic implications. Curr Opin Endocrinol Diabetes 9:152-159, 2002 35. Mingrone G, DeGaetano A, Greco AV, Capristo E, Benedetti G, Castagneto M, Gasbarrini G: Reversibility of insulin resistance in obese diabetic patients: role of plasma lipids. Diabetologia 40:599 - 605, 1997 36. *******s DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, Purnel JQ: Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med 346:1623-30, 2002 37. Mason EE: Ileal transposition and enteroglucagon/GLP-1 in obesity (and diabetic?) surgery. Obes Surg 9:223-228, 1999 38. Naslund E, Backman L, Holst JJ, Theodorsson E, Hellstrom PM: Importance of small bowel peptides for the improved glucose metabolism 20 years after jejunoileal bypass for obesity. Obes Surg 8:253-260, 1998 39. Kieffer TJ, Habener JF: The glucagon-like peptides. Endocr Rev 20:876- 913, 1999 40. Rubino F, Gagner M: Potential of surgery for curing type 2 diabetes mellitus. Ann Surg 236:554 -559, 2002 DIABETES, VOL. 52, MAY 2003
barbie12
on 11/20/05 9:11 am - OH
Please stop harrazing our board with all this crap. We dont give a rats a-- . Please go to mexico and drink some water
choeffel
on 11/20/05 9:24 am - cincinnati, OH
Did you understand that Ann Dee? Maybe she will type that again. She has a CURE for diabetes. Interesting aren't they? YOU PUT THAT WELL,LOL
barbie12
on 11/20/05 10:46 am - OH
They dont get it. We dont care. God they must have a boring board to come to our board and start trouble. Very lonely group. They need to meet up in MEXICO FOR SOME DRINKS. and continue their education BARB
barbie12
on 11/20/05 10:46 am - OH
They dont get it. We dont care. God they must have a boring board to come to our board and start trouble. Very lonely group. They need to meet up in MEXICO FOR SOME DRINKS. and continue their education BARB
Diane B
on 11/20/05 10:09 am - Oregon, OH
OMG Barb- you are tooooo funny. This is the first laugh I've had in this entire idiotic fiasco. Talk about beating a dead horse! Anyway, thanks for the much needed chuckle.
Kevin McB
on 11/20/05 5:41 am - Columbus, OH
Maybe they should call this the Ohio RNY board..... I'm from Ohio, and even though I stick mostly to the DS board, I really feel that the DS is a comparible if not argueably better surgery..... not better because I say its better, but for the clinical reasons that say it does a better job at combating obesity, and diabetes. I've said this before, and I feel that many, but certainly not all RNYers fall into this category, but I have a few friends from work that have had the RNY. They are all happy with their decision to have the RNY. The biggest problem that I have with them is they knew nothing about the DS, and one of them didn't even know that what he had was an RNY!!! Now that is just a lack of knowledge. It's like choosing a surgeon without finding out first if he has a reputation for leaving people dead, or if he has done more than five operations since graduating from medical school. I hope everyone has the surgery that they want, but how could anyone say they didn't want a DS if they never researched the DS in the first place. This is of course not ALL RNYers, but I will say this for the DSers that I have been able to interact with on this site, They are all well informed about both surgeries, many of them went from first choosing to have an RNY, to going with the DS. I was one of these people. Seeing more information allowed me to make an informed decision. We get alot of heat on the DS side of the mountain, and some of that is of our own making in how we respond to others, but the truth of it is that the DS is maligned in a totally unfair way by many of our brothers and sisters here in the WLS community. Dr. C's biggest problem is as I said previously, he doesnt perform the DS, and has made "HIS" standard (not THE standard) for having it so high that few would ever qualify for it. this of course is JMHO. kevin
choeffel
on 11/20/05 5:58 am - cincinnati, OH
Personally Kevin, Dr. C doesn't have a problem. He knows exactly what he is doing and what he wants to do. I think you all need to stay on the DS board. I researched everything and I am very happy. I'm thinking everyone here is happy with RNY so let it be. Dr. C is a wonderful doctor with extremely high standards and work ethics. All of you just let us alone. Are you all just trying to get us to be sorry for what we did? We are happy aren't you? I don't get how this all started.Let it go, Cindy
LeaAnn
on 11/20/05 6:13 am - Huntsville, AL
YOU let it go. You're the one starting new threads complaining about us "second guessing" a doctor that called a woman "nuts." And effectively, he called all of you "nuts" as well if you had an RNY instead of a lapband if you weren't over 50 BMI. THAT'S how this all started. We're here because one of our own came to the DS board HURT that she'd been called NUTS! But obviously, you didn't see that happen, so what do you know? LeaAnn
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