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1/13. Brachial plexopathy in diabetic ketoacidosis.

    We report the clinical and electrodiagnostic findings of a 39-year-old patient who presented with severe, bilateral and asymmetrical, axon-loss brachial plexopathies occurring in the midst of diabetic ketoacidosis. This patient's unusual presentation is not consistent with the rare diabetic polyradiculopathy of the upper extremities usually occurring in association with diabetic amyotrophy.
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2/13. Clinical features of a young Japanese woman having marked obesity and abrupt onset of diabetes mellitus with ketoacidosis.

    The subject was a 26-year-old Japanese woman of 148 cm height, 96.2 kg of body weight (BW) (body mass index (BMI) of 43.8 kg/m(2)). She was referred to our hospital on May 1, 2000 for the evaluation of marked hyperglycemia with clinical symptom of general malaise, polydipsia, and ketonuria (3 ). She did not smoke, or drink alcohol. But, she tended to eat lots of sweet food every day before the onset of this symptom. Her father was diagnosed type 2 diabetes mellitus. Her fasting plasma glucose and HbA(1c), and serum c-peptide were 398 mg/dl, 7.8% and less than 0.05 ng/ml [normal range: 0.94-2.8], respectively. She tested negative for anti-glutamic acid decarboxylase (GAD) antibodies and islet-cell antibodies. c-peptide level in her urine was as low as 3.4 microg/day. We immediately started insulin treatment under the diagnosis of abrupt onset of diabetes mellitus with diabetic ketoacidosis on the day of her admission, and the insulin treatment was continued after her being discharged. She showed continuous BW reduction until her BW reached approximately 60 kg, followed by her BW being plateau. During the period, intra-abdominal visceral fat (VF) and subcutaneous fat (SF) volume assessed by helical computerized tomography (CT) showed a substantial reduction [3.9-0.5 l for VF, 19-3.2 l for SF volume]. Pre-heparin plasma lipoprotein lipase (LPL) mass showed a considerably lower value when she had continuous BW reduction than did it when her BW reduction discontinued. These findings suggest that in this subject, continuous BW reduction after the abrupt onset of diabetes is closely associated with intra-abdominal fat mass reduction, which may be related to decreased production of LPL.
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3/13. 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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4/13. death caused by hyperglycemic hyperosmolar state at the onset of type 2 diabetes.

    Seven obese African American youth were considered to have died from diabetic ketoacidosis (DKA) due to type 1 diabetes, despite meeting the criteria for hyperglycemic hyperosmolar state and not for DKA. All had previously unrecognized type 2 diabetes, and death may have been prevented with earlier diagnosis or treatment.
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5/13. memory of insulin pumps and their record as a source of information about insulin therapy in children and adolescents with type 1 diabetes.

    BACKGROUND: This study was designed to provide information regarding basal and bolus insulin dosage in children and adolescents using continuous subcutaneous insulin infusion (CSII) and to evaluate the safety and efficacy of the CSII method in youths. patients AND methods: Data from 100 patients (1.6-18 years old) were collected during scheduled visits in an outpatient clinic. The mean duration of diabetes was 4.57 years (range 0.6-16 years), and mean duration of CSII therapy was 1.75 years (range 0.5-3.0 years). Each child had his or her insulin doses reviewed using the Medtronic MiniMed (Northridge, CA) Pumps&Meters software program. At each visit glycosylated hemoglobin (HbA1c) values and growth parameters (weight and height) were assessed, and episodes of severe hypoglycemia and ketoacidosis were recorded. RESULTS: The mean HbA1c value in our study group was 7.63 /- 0.09% (range, 5.15-12.5%). Statistically significant better metabolic control was found in children under 10 years of age, in children with lower body mass index (r = 0.33), in patients with a lower contribution of basal insulin to the total daily dose (r = 0.35; P < 0.05), and in boys. Ten percent of participants skipped mealtime boluses, which correlated with their glycemic control; in those children HbA1c was 8.67 /- 0.57% (r = 0.34; P < 0.05). The mean total daily insulin was 0.79 /- 0.02 U/kg/day (range, 0.3-2.0 U/kg/day). Basal insulin constituted on average 35.6 /- 1.1% (5-70%) of the daily insulin dose. We found a statistically significant higher contribution of basal insulin dose in patients who missed mealtime boluses (r = 0.42; P < 0.05) and a significantly lower contribution in pre-pubertal children and in boys (P < 0.05). Around 7% of patients made mistakes in programming the basal insulin. CONCLUSIONS: CSII may be safely and efficiently used in children with type 1 diabetes in different age groups. This method of treatment requires regular visits to an outpatient clinic, proper education, and frequent revisions of the pump's memory.
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6/13. The use of continuous subcutaneous octreotide infusion in brittle type 1 diabetic patients.

    Two Type 1 diabetic patients with brittle diabetes were successfully treated using continuous SC octreotide (Sandostatin) infusion (200 micrograms 24-h-1) for 6 months and 12 months. When the analogue was discontinued, rapid deterioration in glucose control and ketonuria recurred in one patient and diabetic ketoacidosis in the other. These were corrected after reinstitution of the analogue.
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7/13. Severe metabolic acidosis induced in a patient during fasting by KCl administration.

    The purpose of this study was to determine the cause of an acute metabolic acidosis of the normal anion gap type which developed during a 3 day period when 64 mmol of KCl was administered daily to an obese but otherwise healthy subject fasted for 2 weeks (called the index case). She had typical ketoacidosis of fasting for the first 13 days of fasting; since the plasma [K] was 3.6 mmol/l, she was given 64 mmol of KCl daily for 3 days. On day 3 of KCl treatment, the plasma [HCO3] was 13 mmol/l with no change in the plasma anion gap or 3-hydroxybutyrate concentration; the plasma [K] had risen to 4.3 mmol/l. The cause of the acidosis was a reduction of urine ammonium excretion by 42 mmol/day without a parallel fall in the rate of 3-hydroxybutyrate excretion. Since renal ammonium production can be inhibited by K administration, 5 other obese subjects were studied in a similar fashion to gain insight into the problem. They had a similar reduction in the daily rate of ammonium excretion (41 mmol) after KCl; however, their daily 3-hydroxybutyrate excretions declined by a similar amount (47 mmol) and thus metabolic acidosis did not develop.
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8/13. insulin resistance: definition and treatment.

    Two cases of insulin resistance are described, and recent developments in the pathogenesis and treatment of insulin resistance are reviewed. Both immune and nonimmune types of insulin resistance have been described. Immune resistance is related to the presence of circulating antibodies directed against exogenous insulin or the insulin receptor sites. Nonimmune resistance is associated with obesity, ketoacidosis, infection, or endocrinopathies. Treatment of insulin-resistant diabetics can include proper diet and weight control; use of insulin in large quantities; selection of less antigenic forms of insulin, such as pork, fish, or sulfated insulin; oral hypoglycemics such as tolbutamide; and immunosuppressive therapy with corticosteroids. The production of human insulin by recombinant dna technology promises benefits to patients with high levels of antibodies directed against insulin from animal sources. True insulin resistance is a rare phenomenon, which must be documented adequately before vigorous treatment is considered.
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9/13. Glucocorticoid-induced ketoacidosis in gestational diabetes: sequela of the acute treatment of preterm labor. A case report.

    pregnancy induces complex changes in energy metabolism, manifested clinically by insulin resistance, low fasting blood glucose levels, and proneness to ketosis. It is quite unusual for pregnant women who do not have type I diabetes to progress from ketosis to frank ketoacidosis, although this phenomenon is common in larger mammals. In the case described here, glucocorticoid administration in the setting of a prolonged fast triggered a metabolic cascade leading to ketoacidosis in a pregnant woman without type 1 diabetes. Other details of this illustrative case serve to synthesize several disparate observations regarding the pathogenesis of pregnancy ketoacidosis. physicians should be aware of the potential for rapidly developing ketoacidosis with atypical biochemical and clinical features in pregnant women who are treated with high doses of glucocorticoids.
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10/13. Characteristics of youth-onset noninsulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus at diagnosis.

    OBJECTIVE: To describe the characteristics of youth-onset noninsulin-dependent diabetes mellitus (NIDDM) at diagnosis and compare them with youths with insulin-dependent diabetes mellitus (IDDM) when matched for age, sex, and geographic region of residence. STUDY DESIGN: medical records of youths referred for evaluation of diabetes to a pediatric tertiary care center from 1988 to 1995 were reviewed to identify youths diagnosed with NIDDM. patients selected for study met National Diabetes Data Group criteria for type of diabetes. RESULTS: Fifty patients with NIDDM were reviewed and compared with similar IDDM patients. The NIDDM female:male ratio was 1.6:1 and 74% were African-American. Only 18% of the IDDM patients were African-American. The mean body mass index /- standard error at diagnosis of NIDDM patients was 35 /- 1.1 kg/m in contrast to IDDM, 20 /- .8 kg/m. Ninety-six percent of NIDDM and 24% of IDDM youths had a body mass index >/=85th percentile. More then 30% of NIDDM youths presented with hypertension. diabetic ketoacidosis was present in >25% of NIDDM patients. acanthosis nigricans was documented in 86% of NIDDM and 0% of IDDM patients. CONCLUSIONS: In arkansas, youths with NIDDM are characterized by significant obesity in contrast to youths with IDDM. Physical characteristics such as obesity, acanthosis nigricans, and hypertension on examination of any youth with new-onset diabetes should raise suspicion of NIDDM.
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