Cases reported "Insulin Resistance"

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1/29. Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia.

    West, R. J., Lloyd, J. K., and Turner, W. M. L. (1975). archives of disease in Childhood, 50, 703. Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia. A syndrome comprising unusual facies, dry skin, acanthosis nigricans, thickened nails, hirsutism, dental precocity and dysplasia, abdominal protuberance, and phallic enlargement is described in 2 sibs. Both have developed diabetic ketoacidosis with insulin resistance. The elder child, a girl, had recurrent septic episodes and died at the age of 7-8 years. At necropsy the pineal gland was hyperplastic, weighing 900 mg. Investigation of the younger sib over a 4-year period has shown decreasing glucose tolerance, and he was frankly diabetic with ketoacidosis by the age of 6-8 years. serum insulin concentrations have always been grossly raised. Though the mechanism for insulin resistance has not been definitely established, a functional abnormality of the hypothalamus or pituitary is postulated to explain the many endocrine features of the syndrome.
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2/29. Evaluation of insulin resistant diabetes mellitus in alstrom syndrome: a long-term prospective follow-up of three siblings.

    alstrom syndrome is a rare cause of diabetes mellitus. We studied two generations of a Turkish family in whom four members were affected by alstrom syndrome. The natural course of the syndrome in three sisters was followed for 13 yr. The three sisters had short stature and truncal obesity, and developed complete blindness due to retinitis pigmentosa at 10, 5 and 13 yr of age. Two had sensorineural hearing loss and mild mental retardation, while the other developed diabetic ketoacidosis (DKA) at 14 yr and was treated with insulin from onset of diabetes. In the second case, diagnosis of diabetes was made by an OGTT at age 20 yr, and controlled with diet alone for 11 yr, then with a sulphonylurea for 2.5 yr, then with insulin. The third case developed acute hyperglycaemia at 20 yr, and required insulin from onset. Moreover, transitional features of impaired carbohydrate and fat metabolism (severe hyperinsulinaemia and insulin resistance progressing to islet beta cell failure, and hypertriglyceridaemia with fatty liver) were demonstrated, in accord with the literature. Previously unreported findings characteristic of nephro-uropathy with early-onset hypertension were also detected, and included in all cases proteinuria, glomerulopathy, and abnormal locations of the kidneys, narrowed uretero-renal junctions and dilated ureters.
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3/29. Type 2 diabetes presenting as diabetic ketoacidosis in adolescence.

    We report two black adolescent subjects who presented with diabetic ketoacidosis, but who lacked autoimmune markers and demonstrated clinical and biochemical characteristics more typical of Type 2 diabetes, including obesity, acanthosis nigricans, positive family history for Type 2 diabetes, and Type 2 diabetic dyslipidaemia. Subsequent to acute presentation, insulin was discontinued in both subjects and excellent glycaemic control was achieved with metformin therapy alone. Four months following acute presentation, both had adequate c-peptide responses to intravenous glucagon. Type 2 diabetes can present as diabetic ketoacidosis in obese adolescent subjects.
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4/29. Transient extreme insulin resistance in shock during diabetic ketoacidosis.

    Transient extreme insulin resistance was encountered during an episode of diabetic ketoacidosis (DKA) in an insulin-treated diabetic patient. On admission, the plasma glucose level was 1241 mg dl-1 and arterial blood pH 6.895 with HCO3- 4.7 mEql-1. An intravenous bolus injection of 20 units, followed by continuous infusion of 20 units h-1 of short-acting regular human insulin, was instituted. Ischemic myocardial changes were noted on the initial electrocardiogram, therefore fluid replacement was limited to 1,000 ml of 0.9% saline solution in the first hour. As the plasma glucose level declined by only 203 mg dl-1 (41 mg dl-1 h-1) in the first 5 h, the insulin dose was doubled every 2 h. At hour 4, the patient developed circulatory shock which required vasopressor support and respiratory assistance. A plasma glucose level of 300 mg dl-1 was not achieved until the total dosage of insulin amounted to 91,580 units at hour 25. insulin resistance was not observed from that point on. The patient had neither insulin antibodies nor anti-insulin receptor antibodies in serologic testing. The insulin binding characteristics of the patient's erythrocytes were similar to those from healthy controls both with and without experimental acidosis and with a high level of beta-hydroxybutyrate. Among multiple potential factors, the severe shock associated with DKA has been considered as a primary cause of the transient severe insulin resistance in this case.
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5/29. insulin resistance complicating pregnancy in a human immunodeficiency virus-infected patient treated with protease inhibitors and corticosteroids.

    BACKGROUND: Protease inhibitor therapy in human immunodeficiency virus (HIV)-infected adults has been associated with onset or aggravation of glucose intolerance. We report a case of a pregnant HIV-infected woman receiving highly active antiretroviral therapy who developed acute onset of severe insulin resistance during treatment for preterm labor. CASE: A 26-year-old multigravida with HIV infection treated with highly active antiretroviral therapy presented in preterm labor. During treatment, including corticosteroids for fetal lung maturity, severe hyperglycemia and ketonemia suggestive of diabetic ketoacidosis were detected. Aggressive intravenous fluid and insulin therapy was necessary to correct hyperglycemia. CONCLUSION: We found that HIV-positive pregnant women receiving highly active antiretroviral therapy may be at increased risk for development of glucose intolerance. The use of medications that impair glucose tolerance, for example, corticosteroids, may have a synergistic effect in aggravating insulin resistance. Additional screening for glucose intolerance later in the third trimester should be considered in these patients.
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6/29. Subcutaneous insulin resistance successfully circumvented on long term by peritoneal insulin delivery from an implantable pump in four diabetic patients.

    Extreme subcutaneous insulin resistance is a rare syndrome characterized by a severe resistance to subcutaneous (S/C) insulin together with persistence of normal or near normal intravenous (IV) insulin sensitivity. Its pathophysiology is unknown, although increased insulin degrading activity has been reported in the S/C adipose tissue fraction in some cases. Until now, proposed treatments have been disappointing. We report 4 cases who were successfully treated by intraperitoneal (IP) route. methods: The diagnosis of subcutaneous insulin resistance was based upon following combined conditions: resistance to hypoglycaemic action of subcutaneous insulin but normal or near normal sensitivity to IV or IP insulin. RESULTS: 4 patients among those followed by EVADIAC group met these criteria: 3 with type 1 diabetes (C peptide=0), the last one with unexplained non insulin-deficient diabetes (no anti-GAD antibodies, C peptide=5 ng/ml). All of them had been treated with subcutaneous insulin therapy without success despite huge doses (up to 4000 IU/day in two patients). The 3 type 1 diabetic patients presented with a history of repeated ketoacidosis episodes. A treatment of insulin mixed with aprotinin had been proposed to 2 patients without success. The IV insulin sensitivity was proved to be normal in two patients by euglycaemic clamp data. A skin biopsy was performed in 1 patient. An accumulation of insulin in the derma was revealed with no increase of degradation products of insulin. In these 4 patients, a dramatic improvement of diabetes control was obtained by IP insulin delivery from an implantable pump (HbA1c decrease by at least 3%). CONCLUSION: Although pathophysiology of the subcutaneous insulin resistance syndrome remains unexplained, our data show that intra-peritoneal insulin therapy from an implantable pump allows diabetes control in patients affected by this uncommon but severely disabling condition.
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7/29. Glycemic control with continuous subcutaneous insulin infusion with use of U-500 insulin in a pregnant patient.

    OBJECTIVE: To demonstrate the benefits and to advocate the safety and efficacy of using an insulin pump with U-500 insulin in comparison with U-100 insulin for a pregnant patient with diabetes requiring massive doses of insulin. methods: We present a detailed case report about the use of continuous subcutaneous insulin infusion with U-500 insulin during pregnancy. Dose calculation is reviewed, and the benefits of insulin pump therapy in patients with diabetes are discussed. RESULTS: A 34-year-old white woman, with a history of type 2 diabetes for 7 years, was seen at 17 weeks of gestation because of episodes of hyperglycemia and hypoglycemia accompanied by a very high insulin requirement. At the time of initial assessment, the patient was hospitalized with diabetic ketoacidosis and was being treated with 400 U/day of intravenously administered insulin. She responded well to intravenous therapy, but when switched to a regimen of NPH and regular insulin, she continued to have high blood glucose levels (despite 4 to 5 insulin injections a day, with a total daily dose up to 400 to 450 U). Use of an insulin pump was instituted, which presented another challenge because of the limited reservoir capacity and the need to change sites at least once or twice a day. We decided to initiate U-500 insulin therapy with a total basal rate of 40 U/day. Her meal carbohydrate insulin ratio and correction bolus were calculated on a U-100 scale. Then each estimated dose for meal coverage, depending on her carbohydrate intake, as well as the appropriate corrections were totaled and divided by 5 to convert to U-500. Throughout the rest of her pregnancy, the patient was able to maintain tight glycemic control, with no further hospitalizations for stabilization of hyperglycemia or hypoglycemia. CONCLUSION: To our knowledge, this is the first report of successful management of difficult to control diabetes by means of an insulin pump with use of U-500 insulin in a pregnant patient who required massive doses of insulin.
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8/29. diabetic ketoacidosis and insulin resistance with subcutaneous terbutaline infusion: a case report.

    diabetic ketoacidosis may occur in women treated with intravenous beta-sympathomimetic agents for tocolysis. We describe diabetic ketoacidosis and transient severe insulin resistance in a woman with diabetes who was treated with subcutaneous terbutaline infusion. Subcutaneous terbutaline infusion may precipitate transient insulin resistance and diabetic ketoacidosis in women with diabetes.
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9/29. diabetic ketoacidosis and pregnancy.

    This paper describes the clinical course of a young diabetic primigravida who presented to her physician with vomiting and abdominal pain. Despite the conventional doses of intravenous fluid and insulin that were used to treat her suspected diabetic ketoacidosis, she remained severely acidotic and developed increasing abdominal pain. Two hundred twenty units of regular insulin over a 5-hour period were required to reverse the lipolysis, acidemia, and abdominal pain, which characterized her severe episode of diabetic ketoacidosis. This discussion emphasizes the importance of insulin in the reversal of the hyperglycemia and acidosis that accompany a diabetic crisis. The roles of bicarbonate, phosphorous, magnesium, insulin, potassium, and fluids are discussed along with conditions such as pregnancy, infection, pancreatitis, and abdominal pain, which can complicate the management of diabetic ketoacidosis.
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10/29. Subcutaneous insulin resistance syndrome. Effects of long-term aprotinin therapy.

    The case of a young Type 1 diabetic patient with subcutaneous insulin resistance, causing recurrent ketoacidosis, is reported. Intramuscular and intravenous insulin administration remained effective. After failure of CSII, continuous intramuscular insulin infusion was used during 10 months followed by a combination of insulin and a protease inhibitor aprotinin, with good results. After 18 months' aprotinin therapy, subcutaneous insulin resistance disappeared. The subcutaneous insulin resistance syndrome and the role of aprotinin are discussed.
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