Risk factors of pancreatic graft loss and death of receptor after simultaneous pancreas/kidney transplantation.

Simultaneous pancreas/kidney transplants require a long graft survival and the recipient to present with more benefits than risks. We evaluated the risk factors of receptor's death and pancreatic graft loss on 2 occasions (3 and 12 months' postoperatively) in 292 transplants in whom 22 variables were evaluated. Variables were selected, 9 receivers, 8 donors, and 5 variables related to the surgical procedure. All independent variables were compared with the dependent variables of pancreatic graft losses and patient deaths. Those considered significant according to univariate analysis were analyzed by using multiple logistic regression techniques in an attempt to develop a mathematical model capable of predicting both pancreatic graft and patient losses. Lastly, based on the resulting models with all significant variables, scores were created to determine the risk of patient death and pancreatic graft loss. In the adjusted multivariate analysis, the significant variables were donor age, receiver's body mass index, initial pancreas implant, iliac venous drainage, and use of induction therapy related to pancreatic loss within 3 months after transplantation. Independent risk factors regarding the loss of patients within 12 months were body mass index and receptor induction therapy. The variables related to pancreatic graft loss within 3 months were donor age, receiver body mass index, initial use of pancreatic graft, iliac venous drainage, and induction therapy; these variables can be used for creating a risk score. The donor body mass index and the induction therapy were independently related to patient loss within 12 months after the transplant.

Época de colheita e qualidade fisiológica de sementes de coentro produzidas no norte de Minas Gerais / Harvest season and physiological quality of coriander seeds produced in the north of Minas Gerais

No presente trabalho, objetivou-se avaliar a época de colheita e a qualidade fisiológica de sementes de coentro produzidas no Norte de Minas Gerais. A primeira época de colheita das sementes foi realizada aos 15 dias após o florescimento pleno, quando aproximadamente 50 por cento das plantas apresentavam flores. As demais colheitas foram realizadas de 7 em 7 dias, até as sementes atingirem 14,0 por cento de umidade, fato que ocorreu na 6ª colheita. Imediatamente após cada colheita, as sementes foram avaliadas quanto ao teor de água, à germinação e ao vigor (testes de primeira contagem, emergência de plântulas e índice de velocidade de emergência). A maturidade fisiológica das sementes de coentro, cultivar Verdão, ocorre entre 42 a 44 dias após o florescimento, quando as sementes apresentam umidade em torno de 28,0 por cento, podendo a colheita ser realizada até 50 dias após o florescimento, quando as sementes apresentavam 14,0 por cento de umidade.

The present study aimed to evaluate the harvest season and physiological quality of coriander seeds produced in the North of Minas Gerais. The first season of harvest of the seeds was performed 15 days after full bloom, when approximately 50 percent of plants had flowers. The other crops were carried out 7 in 7 days, until the seeds reach 14,0 percent moisture, a fact that occurred in the 6th harvest. Immediately after each harvest, the seeds were evaluated for water content, germination and vigor tests (first count, seedling emergence and emergence speed index). The physiological maturity of coriander seeds, cultivate Verdão, occurs between 42 to 44 days after flowering, when the seeds had humidity around 28,0 percent at physiological maturity, the harvest may be held until 50 days after flowering, when seeds had 14,0 percent humidity.

Delayed kidney allograft function after simultaneous pancreas-kidney transplantation.

BACKGROUND: Simultaneous pancreas-kidney transplantation (SPKT) is one of the treatments for insulin-dependent chronic renal failure patients. METHODS: One-year patient and kidney allograft survival rates of 150 patients undergoing SPKT were subjected to Cox regression and Kaplan-Meier analyses. Uni- and multivariate methods identified risk factors involved in allograft and patient survival. RESULTS: One-year patient and kidney allograft survival rates were 82% and 80%, respectively. Delayed graft function (DGF) (P = .001; hazard ratio [HR]5.41) and acute kidney rejection episodes (P = .016; HR 3.36) were related to 1 year patient survival as well as intra-abdominal infection (IAI) rates. (IAI). One-year kidney allograft survival was related to DGF (P = .013; odds ratio [OR] 3.39), acute rejection (P = .001; OR 4.74), and IAI (P = .003, OR 6.29). DGF was related to a time on dialysis >27 months (P = .046; OR 2.59), cold kidney ischemia time >14 hours (P = .027; OR 2.94), donor age >25 years (P = .03; OR 2.82), and donor serum sodium concentration >155 mEq/L (P < .0001; OR 1.09). Female kidney to male recipient in 17% of the cases did not increase the risk of DGF. We observed an important correlation between donor serum sodium and creatinine (P < .0001), which suggested undertreatment of diabetes insipidus secondary to brain death. CONCLUSIONS: DGF, acute rejection, and IAI were the main determinants of survival after SPKT. Improving the care of deceased donors may reduce DGF occurrence.

Intestinal obstruction due to internal hernia following pancreas transplantation.

BACKGROUND: Simultaneous pancreas-kidney transplantation has evolved as the best treatment for type 1 diabetic patients at end-stage renal disease. The surgical complication rate is high, which is an important barrier to the success of this procedure. The frequent complications that require relaparotomies include fistulas, graft thromboses, and intra-abdominal abscesses. Intestinal obstructions after pancreas transplantation due to internal herniation are not common. PURPOSE: The objective of this article was to review the literature about this problem and describe our personal experience in pancreas transplantation. METHODS: We examined the cases of small bowel obstruction secondary to an internal hernia after following 292 pancreas transplantations in our center from 2000 to 2009 as well as performed a Medline literature review. RESULTS: Only 2 articles described the diagnosis and treatment of internal hernias after pancreas transplantation. However, both contribution were from the same center reporting the same 3 cases, with surgical versus radiologic perspectives. We have described our 2 cases of young pancreas-kidney transplant patients who presented with acute intestinal obstruction due to internal hernia. CONCLUSION: Although internal hernias are rare, they are potentially fatal and difficult to diagnose when they occur after pancreas transplantation. Detection with early surgery demands a high degree of clinical vigilance.

Multivariate analysis of risk factors for early loss of pancreas grafts among simultaneous pancreas-kidney transplants.

UNLABELLED: To evaluate the risk factors for pancreas graft loss within 3 months postoperatively among 170 simultaneous pancreas-kidney transplantation (SPKT) we examined 38 variables. METHODS: Twenty-two variables were related to recipients; 12 to donors and 4 to the surgical procedure. In addition the latest follow-up dates as well as the transplant and/or death dates. Independent variables were examined with reference to the dependent pancreatic loss variable, excluding losses owing to deaths. Variables with statistical significance were analyzed to predict early graft loss. RESULTS: Univariate analyses determined the following significant variables: kidney cold ischemia time, older donors, non-white donors, death cause related to vascular disease, wound infection, and length of extended hospitalization. However, multivariate analysis showed that only donor age and kidney cold ischemia time were significant predictors for early pancreatic graft loss. CONCLUSION: Donor age and kidney cold ischemia time were independently related to pancreatic loss after SPKT within 3 months posttransplantation.

Extreme subcutaneous, intramuscular and inhaled insulin resistance treated by pancreas transplantation alone.

Diabetes mellitus with resistance to insulin administered subcutaneously or intramuscularly (DRIASM) is a rare syndrome and is usually treated with continuous intravenous insulin infusion. We present here two cases of DRIASM in 16 and 18 years female patients that were submitted to pancreas transplantation alone (PTA). Both were diagnosed with type 1 diabetes as young children and had labile glycemic control with recurrent episodes of diabetic ketoacidosis. They had prolonged periods of hospitalization and complications related to their central venous access. Exocrine and endocrine drainages were in the bladder and systemic, respectively. Both presented immediate graft function. In patient 1, enteric conversion was necessary due to reflux pancreatitis. Patient 2 developed mild postoperative hyperglycemia in spite of having normal pancreas allograft biopsy and that was attributed to her immunosuppressive regimen. Patient 1 died 9 months after PTA from septic shock related to pneumonia. In 8 months of follow-up, Patient 2 presented optimal glycemic control without the use of antidiabetic agents. In conclusion, PTA may be an alternative treatment for DRIASM patients.

Mycophenolate mofetil versus enteric-coated mycophenolate sodium after simultaneous pancreas-kidney transplantation.

INTRODUCTION: Adverse gastrointestinal events are frequent after mycophenolate use. The objectives of the present study were to report the incidence of acute noninfectious diarrhea, to determine the risk factors, and to compare the severity of reactions between mycophenolate mofetil (MMF) and enteric-coated mycophenolate sodium (EC-MPS) after simultaneous pancreas kidney transplantation (SPKT). METHODS: We included 165 SPKT patients from December 2000 to May 2007. Uni- and multivariate analyses were performed, using acute noninfectious diarrhea as the dependent variable. P < .05 was considered significant. RESULTS: Mean age and duration of dialysis and of diabetes were 34.9 +/- 8.2 years, 27.3 +/- 18.3 months, and 21.9 +/- 16.2 years, respectively. Sixty-three percent used MMF, 36.4% used EC-MPS, and 0.6% used azathioprine. Multivariate analysis showed that the duration of diabetes (P = .049, confidence interval [CI] 1.0- 1.13) and MMF use (P = .013, 95% CI 0.2-0.82) were the main determinants of acute diarrhea after SPKT. MMF dose reduction (79.2% vs 62.3%, P = .024) and severity of diarrhea associated with orthostatic hypotension were more pronounced among MMF than EC-MPS patients (42.4% vs 15.1%, P = .001). There was no difference between MMF and EC-MPS after dose reduction in relation to the occurrence of acute kidney rejection (30.8% vs 26.7%, P = .53). CONCLUSIONS: Acute noninfectious diarrhea after SPKT was related to the duration of diabetes and to prescription of MMF. Preferential use of EC-MPS was associated with a lower necessity of dose reduction and less severe episodes of acute diarrhea compared with MMF, although dose reduction was equally associated with acute episodes of kidney rejection.

Asynchronous kidney allograft loss after simultaneous pancreas-kidney transplantation: impact on pancreas allograft outcome at a single center.

OBJECTIVE: We analyzed the clinical evolution of pancreas allografts in simultaneous pancreas-kidney transplantation (SPKT) cases after asynchronous kidney allograft loss and kidney retransplantation at a single non-United States center. PATIENTS AND METHODS: We performed a retrospective analysis of 168 SPKT from December 2000 to June 2007. RESULTS: The 5-year kidney allograft survival rate was 71%. Excluding cases of death with a functioning graft after SPKT (n = 35; 74.4%), 12 kidney allografts were lost due to acute rejection (n = 7; 15%) or chronic allograft nephropathy (n = 5; 10.6%). Delayed graft function contributed to kidney allograft loss. Five of 12 patients underwent kidney retransplantation. Sixty percent of pancreas allografts were lost after this procedure, which was attributed to either the diabetogenic effects of the immunosuppressive regimen or to the perioperative stress. Oral glucose tolerance tests performed before kidney retransplantation identified patients with good pancreas allograft function versus those with intolerance on glucose tests who received reduced glucocorticoid doses. CONCLUSIONS: In SPKT, pancreas allograft function was seriously affected by kidney retransplantation. Oral glucose tolerance tests performed before kidney retransplantation were helpful to assess beta-cell function and suggest prescription of lower steroid doses to decrease the pancreas allograft dysfunction.

Donor liver dysfunction: application of a new scoring system to identify the marginal donor.

Livers from marginal donors are increasingly used for transplantation due to the shortage of donor organs. The definition of a marginal donor remains unclear; prediction of organ function is a challenge. In the literature the use of steatotic livers has been associated with poor liver function or even primary dysfunction of the allograft. Tekin et al created a scoring system that classifies a donor as marginal or nonmarginal, using a mathematical model based on donor age and steatosis degree. The aims of this study were to apply the Tekin method to identify marginal and nonmarginal donors and evaluate the influence of the cold ischemia time (CIT) on allograft evolution. We retrospectively reviewed deceased donor liver transplantations performed from October 1995 to March 2006, namely, 177 adult liver transplantations in 163 patients. Fifty-five were excluded due to retransplantation (14) or insufficient data (41). Donor age and macrovesicular steatosis were evaluated according to the mathematical formula proposed by Tekin et al, classifying the donors as marginal versus nonmarginal. The authors also analyzed the CIT, 3-month mortality, and development of primary nonfunction or primary dysfunction. The median donor age was 38.9 years (range, 6-71). The postreperfusion biopsy specimen showed moderate to intense steatosis (>30%) in 14.75% of specimens, with no steatosis or mild steatosis in 85.25%. Sixty-one grafts (50%) developed primary graft dysfunction (PGD): 10 grafts, with primary nonfunction (PNF); and 51 with initial poor function (IPF). Using the criteria provided by Tekin et al, we obtained 41 marginal and 81 nonmarginal allografts. The marginal group showed 61.9% PGD, compared with 59.2% of PGD by the nonmarginal group. The CIT was greater than 12 hours in 5 marginal group transplants and 4 PGD cases (80%). Of the nonmarginal allografts, the CIT was greater than 12 hours in 29.6%, with 75% PGD. The 3-month graft survival rate was 80% in the marginal group with ischemia time more than 12 hours: 86.1% of the same group when CIT was less than 12 hours, and 82.7% in the nonmarginal group. In contrast, when we analyzed the occurrence of allograft dysfunction, the 3-month mortality rate was 34% among, grafts with dysfunction, whereas, in those without initial dysfunction, it was 4.1%. In conclusion, the score suggested by Tekin et al that classifies the donors as ideal (nonmarginal) or marginal was not able to predict initial primary dysfunction.

Pancreas retransplantation: outcomes of 20 cases.

The objective of this paper was to evaluate our initial experience with pancreas retransplantation. From January 26, 1996 to February 2005, 285 pancreas transplantations were performed, including 20 (7%) retransplants. The causes of primary graft loss were graft thrombosis in 11 (55%, 7 venous and 4 arterial); 4 (20%) chronic rejections; 2 (10%) ischemia/reperfusion injury; 1 severe graft pancreatitis; 1 primary nonfunction; and 1 sepsis. Venous drainage was placed in the iliac vessels in 14 (70%), vena cava in 5 (25%), and portal drainage in 1. The exocrine drainage was vesical in 16 (80%) and enteric in 4 (20%). In 14 cases (70%), the primary graft was removed before and in 6 (30%) at the time of retransplantation. Immunosuppression was based on antilymphocyte induction, tacrolimus, mycophenolate mofetil, and steroids in all patients. One-year patient and graft survivals were 95% and 85%. In conclusion, pancreas retransplants were feasible with results comparable to a primary pancreas transplantation.

Effects of metformin on the glycemic control, lipid profile, and arterial blood pressure of type 2 diabetic patients with metabolic syndrome already on insulin.

Fifty-seven type 2 diabetic patients with metabolic syndrome and on insulin were assessed by a paired analysis before and 6 months after addition of metformin as combination therapy to evaluate the impact of the association on glycemic control, blood pressure, and lipid profile. This was a historical cohort study in which the files of type 2 diabetic patients with metabolic syndrome on insulin were reviewed. The body mass index (BMI), waist circumference, lipid profile, A1C level, fasting blood glucose level, daily dose of NPH insulin, systolic blood pressure, and diastolic blood pressure were assessed in each patient before the start of metformin and 6 months after the initiation of combination therapy. Glycemic control significantly improved (P < 0.001) after the addition of metformin (1404.4 +/- 565.5 mg/day), with 14% of the 57 patients reaching A1C levels up to 7%, and 53% reaching values up to 8%. There was a statistically significant reduction (P < 0.05) of total cholesterol (229.0 +/- 29.5 to 214.2 +/- 25.0 mg/dL), BMI (30.7 +/- 5.4 to 29.0 +/- 4.0 kg/m2), waist circumference (124.6 +/- 11.7 to 117.3 +/- 9.3 cm), and daily necessity of insulin. The reduction of total cholesterol occurred independently of the reductions of A1C (9.65 +/- 1.03 to 8.18 +/- 1.01%) and BMI and the reduction of BMI and WC did not interfere with the improvement of A1C. In conclusion, our study showed the efficacy of the administration of metformin and insulin simultaneously without negative effects. No changes were detected in HDL-cholesterol or blood pressure.

Effects of metformin on the glycemic control, lipid profile, and arterial blood pressure of type 2 diabetic patients with metabolic syndrome already on insulin

Fifty-seven type 2 diabetic patients with metabolic syndrome and on insulin were assessed by a paired analysis before and 6 months after addition of metformin as combination therapy to evaluate the impact of the association on glycemic control, blood pressure, and lipid profile. This was a historical cohort study in which the files of type 2 diabetic patients with metabolic syndrome on insulin were reviewed. The body mass index (BMI), waist circumference, lipid profile, A1C level, fasting blood glucose level, daily dose of NPH insulin, systolic blood pressure, and diastolic blood pressure were assessed in each patient before the start of metformin and 6 months after the initiation of combination therapy. Glycemic control significantly improved (P < 0.001) after the addition of metformin (1404.4 ± 565.5 mg/day), with 14 percent of the 57 patients reaching A1C levels up to 7 percent, and 53 percent reaching values up to 8 percent. There was a statistically significant reduction (P < 0.05) of total cholesterol (229.0 ± 29.5 to 214.2 ± 25.0 mg/dL), BMI (30.7 ± 5.4 to 29.0 ± 4.0 kg/m²), waist circumference (124.6 ± 11.7 to 117.3 ± 9.3 cm), and daily necessity of insulin. The reduction of total cholesterol occurred independently of the reductions of A1C (9.65 ± 1.03 to 8.18 ± 1.01 percent) and BMI and the reduction of BMI and WC did not interfere with the improvement of A1C. In conclusion, our study showed the efficacy of the administration of metformin and insulin simultaneously without negative effects. No changes were detected in HDL-cholesterol or blood pressure.

Simultaneous pancreas-kidney transplantation: infectious complications and microbiological aspects.

OBJECTIVE: The purpose of this study was to describe the clinical and microbiological characteristics of the infectious complications among simultaneous pancreas-kidney transplantations (SPKT). MATERIALS AND METHODS: Among the first 45 SPKT the mean age was 34 years (range, 21 to 49) and the mean duration of follow-up 13 months (range, 2 to 27 months). RESULTS: Twenty-three patients (51%) presented at least one to three episodes (1.7 mean) of infectious complications that needed hospitalization. The etiology of the infections included 71% bacterial (44% gram-negative rods and 27% gram-positive cocci), 16% viral (12% from CMV and 4% from Herpes sp) and 13% fungal (8% by Candida sp and 4% by others fungus). Wound and urinary infections were most frequent, occurring in 22% and 28% of the patients, respectively. All patients who were submitted to vesical drainage developed infections in contrast a rate of only 44% among patients undergoing enteric drainage. CONCLUSION: Infectious complications are the main cause of morbidity and mortality following simultaneous pancreas-kidney transplantation, especially with vesical drainage. The use of enteric drainage combined with administration of broad spectrum prophylactic antibiotics is recommended.

Risk factors for the development of posttransplantation diabetes mellitus in simultaneous pancreas and kidney recipients.

We sought to determine the risk factors involved in the development of posttransplantation diabetes mellitus (PTDM) following simultaneous pancreas and kidney transplantation. Correlations were sought between tacrolimus (FK-506) levels/dose 2-hour capillary glucose (CG) and glycosylated hemoglobin (HbA(1c)), cyclosporine (CSA) levels/dose with HbA1c, 2-hour CG with prednisone dose and body mass index (BMI) and PTDM. Four patients (9.3%) developed PTDM. Three treated with FK-506 had altered 2-hour CG at 3 months after transplantation; 1 prescribed CSA displayed diabetes diagnosed after 1 year. There was no statistically significant difference among HbA(1c) values and FK-506 (P =.18) or CSA (P =.81) doses or FK-506 (P =.53) and CSA (P =.54) levels. In contrast, there was a statistically significant relationship between elevated 2-hour CG (> or =200 mg/dL) and daily prednisone dose (9.7 mg vs. 16.2 mg; P =.003). There was no correlation between 2-hour CG and FK-506 dose (P =.084) or FK-506 levels (P =.075). The greater BMI correlated with an increased risk of PTDM (21.25 +/- 3.13 kg/m(2) vs 24.67 +/- 2.38 kg/m(2); P =.034). Two-hour CG may be a useful tool to screen the diabetogenic effects of corticosteroids. A BMI increase should be discouraged due to the risk of PTDM.

Non-obese adult onset diabetes with oral hypoglycemic agent failure: islet cell autoantibodies or reversible beta cell refractoriness?

Pancreatic ß cell function and insulin sensitivity, analyzed by the homeostasis model assessment, before and after 24 weeks of insulin therapy were studied and correlated with the presence of autoantibodies against ß cells (islet cell and anti-glutamic acid decarboxylase antibodies), in a group of 18 Brazilian lean adult non-insulin-dependent diabetes mellitus (NIDDM) patients with oral hypoglycemic agent failure (OHAF). Median fasting plasma glucose before and after insulin treatment was 19.1 and 8.5 mmol/l, respectively (P < 0.001); median HbA1c was 11.7 percent before vs 7.2 percent after insulin treatment (P < 0.001). Forty-four percent of the patients were positive (Ab+) to at least one autoantibody. Fasting C-peptide levels were lower in Ab+ than Ab- patients, both before (Ab+: 0.16 ± 0.09 vs Ab-: 0.41 ± 0.35 nmol/l, P < 0.003) and after insulin treatment (Ab+: 0.22 ± 0.13 vs Ab-: 0.44 ± 0.24 nmol/l, P < 0.03). Improvement of Hß was seen in Ab- (median before: 7.3 vs after insulin therapy: 33.4 percent, P = 0.003) but not in Ab+ patients (median before: 6.6 vs after insulin therapy: 20.9 percent). These results show that the OHAF observed in the 18 NIDDM patients studied was due mainly to two major causes: autoantibodies and ß cell desensitization. Autoantibodies against ß cells could account for 44 percent of OHAF, but Ab- patients may still present ß cell function recovery, mainly after a period of ß cell rest with insulin therapy. However, the effects of ß cell function recovery on the restoration of the response to oral hypoglycemic agents need to be determined

Non-obese adult onset diabetes with oral hypoglycemic agent failure: islet cell autoantibodies or reversible beta cell refractoriness?

Pancreatic beta cell function and insulin sensitivity, analyzed by the homeostasis model assessment, before and after 24 weeks of insulin therapy were studied and correlated with the presence of autoantibodies against beta cells (islet cell and anti-glutamic acid decarboxylase antibodies), in a group of 18 Brazilian lean adult non-insulin-dependent diabetes mellitus (NIDDM) patients with oral hypoglycemic agent failure (OHAF). Median fasting plasma glucose before and after insulin treatment was 19.1 and 8.5 mmol/l, respectively (P < 0.001); median HbA1c was 11.7% before vs 7.2% after insulin treatment (P < 0.001). Forty-four percent of the patients were positive (Ab+) to at least one autoantibody. Fasting C-peptide levels were lower in Ab+ than Ab- patients, both before (Ab+: 0.16+/-0.09 vs Ab-: 0.41+/-0.35 nmol/l, P < 0.003) and after insulin treatment (Ab+: 0.22+/-0.13 vs Ab-: 0.44+/-0.24 nmol/l, P < 0.03). Improvement of H was seen in Ab- (median before: 7.3 vs after insulin therapy: 33.4%, P = 0.003) but not in Ab+ patients (median before: 6.6 vs after insulin therapy: 20.9%). These results show that the OHAF observed in the 18 NIDDM patients studied was due mainly to two major causes: autoantibodies and beta cell desensitization. Autoantibodies against beta cells could account for 44% of OHAF, but Ab- patients may still present beta cell function recovery, mainly after a period of beta cell rest with insulin therapy. However, the effects of beta cell function recovery on the restoration of the response to oral hypoglycemic agents need to be determined.

Latent autoimmune diabetes of the adult (LADA) in a Brazilian Indian.

CONTEXT: Latent autoimmune diabetes of the adult (LADA) as originally described represents perhaps as many as 10 - 20% of adult-onset patients with diabetes. DESIGN: case report. CASE REPORT: A 38-year-old Brazilian Xavante-Jê Indian with Latent Autoimmune Diabetes of the Adult (LADA) is described, coming from the Sangradouro community in Poxoréu, Mato Grosso. The onset of diabetes after reaching 25 years of age, the evolution to insulin deficiency after a period of insulin-independence and the presence of auto-antibodies to glutamic acid decarboxylase (GAD) characteristic of LADA were present. This patient may represent the first case of LADA in a Brazilian with full Indian heritage. Further studies are necessary to verify the prevalence of this new type of diabetes in this population that does not have Caucasoid admixture and has a particular environmental background.

Cetoacidose diabética desencadeada por resistência imunológica à insulina / Diabetic ketoacidosis induced by immunologic insulin resistance

A cetoacidose diabética (CAD) é a emergência endocrinológica mais freqüente e de boa evoluçäo, na maior parte dos casos. Os autores apresentam evoluçäo atípica de três casos de CAD precipitada por resistência imunológica à insulina (RII). RELATO DE CASO. Três pacientes: H.M.L. (46 anos, diabetes mellitus (DM) tipo II, há 6 anos), D.R.J (39 anos, DM, secundário à pancreatopatia, há 11 anos) e D.L.S. (54 sanos, DM tipo II, há 9 anos) foram admitidos na Unidade de primeiro Atendimento do Hospital Säo Paulo em CAD: H.M.L. (glicemia: 716mg/dL, pH: 6,8), D.R.J. (glicemia: 684mg/dL, pH 6,.9) e D.L.S. (glicemia: 384mg/dL, pH: 7,2), todos apresentavam cetonúria. As necessidades de insulina para o controle metabólico foram: H.M.L.: 1.369UI, D.R.J.: 1.496UI, D.I.S. 1.369UI em, respectivamente: 212, 206 e 72 horas. Os anticorpos antiinsulina (AI) foram dosados por RE e ELISA: H.M.L.: 7.186nU/ml, 3,6IE; D.R.J.: 7,879nU/mL, 3,24IE; D.I.S: 8.377nU/mL, 2,88IE. O seguimento ambulatorial revelou queda progressiva dos níveis de AI:H.M.L.: 3.393nU/mL, 1,39, após dez meses da CAD; d.r.j.: 4,673Nu/Ml, 2,34 E d.i.s.: 1,510nU/mL, ambos após 18 meses da CAD. A queda nos níveis de anticorpos foi significativa nos três pacientes e foi acompanhada de melhor controle metabólico. Discussäo. A ausência de fator desencadeante, o elevado tempo, as altas doses de insulina empregadas para a compensaçäo metabólica levaram os autores à suspeita diagnóstica de RII. O diagnóstico foi confirmado pelos altos níveis séricos dos AI. O controle metabólico nestes pacientes foi obtido somente após a introduçäo de insulina na humanizada. CONCLUSAO. A resistência imunológica à insulina pode ser uma das causas de CAD sem fator precipitante aparente e má resposta às medidas terapêuticas habituais