Cases reported "Diabetes Mellitus"

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1/11. Type a syndrome of insulin resistance: anterior chamber anomalies of the eye and effects of insulin-like growth factor-I on the retina.

    BACKGROUND: The purpose of this work was to describe the anterior chamber and iris anomalies as well as to evaluate the effects of recombinant human insulin-like growth factor-I (rhIGF-I) on the retinal vessels in 2 diabetic patients with type A syndrome of insulin resistance, a rare condition associated with acanthosis nigricans. methods: Ophthalmologic examinations, including photographs and fluorescein angiograms, were performed before, and 2 and 4 weeks after starting subcutaneous rhIGF-I treatment, and 3 months after withdrawal of rhIGF-I treatment. RESULTS: Both patients had goniodysgenesis with mild elevation of the intraocular pressure. Before and after 2 weeks of treatment with rhIGF-I, the fundus and the fluorescein angiograms were mainly normal. After 4 weeks of rhIGF-I treatment both patients' retinas revealed leakage of fluorescein. Three (case 1) and 4 months (case 2) after withdrawal of rhIGF-I, the fundus of all four eyes were again without leakage. CONCLUSIONS: The anterior chamber anomalies found in these patients may be part of the type A syndrome of insulin resistance and could alert clinicians that these patients might not have the usual type of diabetes. Moreover, the data show that exogenous rhIGF-I administration in patients with type A syndrome of insulin resistance alters the permeability of the superficial layer of retinal capillaries which is comparable to the earliest angiographic changes in childhood diabetic retinopathy. Whether this is a direct effect of rhIGF-I, as suggested by experiments in an animal model, or an indirect effect due to the near-normalization of the glucose levels by rhIGF-I warrants further investigations. Finally, this work points to an important caveat regarding the therapeutic use of rhIGF-I in this patient population.
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2/11. diabetes mellitus and autonomic dysfunction after vacor rodenticide ingestion.

    A case of N-3 pyridylmethyl-N' 4 nitrophenyl urea (Vacor) rodenticide poisoning in a 52-year-old man is presented. Vacor is structurally related to alloxan and streptozotocin, agents that have been used extensively to produce diabetes mellitus in laboratory animals. Seven days after ingestion of Vacor, the patient presented in diabetic ketoacidosis complicated by postural hypotension and adynamic ileus. The patient recovered from ketoacidosis but has continued to require insulin. With infusion of arginine, glucagon rose from 185 to 650 pg./ml. and c-peptide from 0.5 to 3.4 ng./ml. Six weeks after onset of diabetes, no anti-islet-cell antibodies were detected. Muscle capillary basement membrane thickness on electron microscopy was found to be 1,918 /- 194 A. The absence of hyperglycemia after Vacor ingestion should not lead to complacency on the part of the attending physician. The patient must be observed closely for development of ketoacidosis and treated prophylactically with nicotinamide, the suggested antidote.
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3/11. diabetes mellitus following rodenticide ingestion in man.

    Ketotic, insulin-requiring diabetes mellitus and a severe peripheral neuropathy developed in a previously healthy 25-year-old man several days after he attempted suicide with rat poison containing N-3-pyridylmethyl N'-p-nitrophenyl urea. Study of islet-cell function ten months after ingestion showed a reduced disappearance rate of intravenous glucose and depressed c-peptide response to intravenous glucose when compared with a normal control but no impairment of glucagon release after intravenous arginine stimulation. Nerve conduction studies demonstrated severe sensory and mild motor neuropathy. Quadriceps capillary basement membrane thickness was in the diabetic range. Because at least 15 similar occurrences have been reported to the manufacturer, this agent appears to be diabetogenic in man, probably causing beta-cell destruction. niacinamide, which can prevent glucose intolerance in both streptozocin- and alloxan-treated animals and prevents death in rats given this rodenticide, may be a useful antidote.
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4/11. Isolation of a virus from the pancreas of a child with diabetic ketoacidosis.

    A healthy 10-year-old boy was admitted to the hospital in diabetic ketoacidosis within three days of onset of symptoms of a flu-like illness. He died seven days later and post-mortem examination showed lymphocytic infiltration of the islets of langerhans and necrosis of beta cells. Inoculation of mouse, monkey and human cell cultures with homogenates from the patient's pancreas led to isolation of a virus. Serologic studies revealed a rise in the titer of neutralizing antibody to this virus from less than 4 on the second hospital day to 32 on the day of death. Neutralization data showed that the virus was related to a diabetogenic variant derived from Coxsackievirus B4. Inoculation of mice with the human isolate produced hyperglycemia, inflammatory cells in the islets of langerhans and beta-cell necrosis. Staining of mouse pancreatic sections with fluorescein-labeled antiviral antibody revealed viral antigens in beta cells. Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.
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5/11. Severe persistent biphasic local (immediate and late) skin reactions to insulin.

    A patient with adult-onset insulin-requirging diabetes mellitus had persistent severe local reactions to all available insulins of animal origin. skin reactions were biphasic in nature with both immediate and late characteristics. An extensive immunologic investigation of this problem was undertaken, revealing evidence of reaginic antibody involvement in the reactions. Routine histologic studies suggested the possibility that Arthus-type mechanisms played a part, although this impression was not confirmed by immunofluorescent microscopy. A program of medical management provided some relief of symptoms.
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6/11. Pancreatic alpha cell tumors: case report and review of the literature.

    Twenty-eight cases of alpha cell tumors of the pancreatic islets have been reported. The clinical features include typical skin rash (termed migratory necrolytic erythema) and stomatitis with anemia, abnormal glucose tolerance, and weight loss. The time course of the disease is variable but the clinical syndrome may be present for up to 15 years (median five years) before discovery of the tumor. In 3 patients, cure was achieved by surgical resection, and in 17 patients in whom metastatic sites were evaluable, 16 involved the liver. Six patients have received chemotherapy: 4 with streptozotocin (STZ); 1 with dimethyl triazeno imidazole carboxamide (DTIC); and 2 with 5-fluorouracil. All 4 patients receiving STZ responded to therapy with objective regression of the tumor and in 3 the dermatitis syndrome receded as well. The selectivity of the STZ for beta cells observed in animals is contrasted with the specific antitumor activity of STZ for alpha as well as beta and delta cell tumors in man.
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7/11. clonidine and glucose intolerance.

    Changes in carbohydrate metabolism were observed in a diabetic, hypertensive patient managed with clonidine. After a slight increase in the clonidine dose, his blood sugar control deteriorated. However, when the clonidine was withdrawn, the glucose intolerance subsided. Because clonidine preferentially binds alpha 2-subtype receptors, we investigated animal pancreatic tissue by radioligand binding technique and found it to contain alpha-adrenergic receptors predominantly of the alpha 2-subtype. In consideration of the response from withdrawal of clonidine and the results of our radioligand studies, wer concluded the glucose intolerance seen in this patient was most likely due to the specific action of clonidine on alpha 2-pancreatic receptors.
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8/11. Cutaneous allergy to human (recombinant dna) insulin.

    p6 report two cases of cutaneous allergy to human (recombinant dna) insulin. Each patient had a history of systemic allergic reactions to porcine insulin and was at least as reactive to human as to porcine insulin by end-point cutaneous titration. Both patients' insulin allergy was managed with animal insulins and both have done well. Our experience with these two patients indicates that human insulin (rDNA) should not be expected to be efficacious in all patients with systemic allergy to insulin.
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9/11. Transient glucose intolerance in rats after a single injection of serum from a diabetic patient with an unusual insulin resistance.

    The single intravenous injection to rats of 1 ml of serum from an insulin resistant patient without an excessive titre of insulin antibodies (total extractable insulin levels: 0.8 U/l, serum insulin binding capacity: 1.58 U/l) and no demonstrable insulin receptor antibodies, produced fasting hyperglycemia in the animals on the fourth day following the injection (FPG: 212 /- 35 mg %). On the 7th day the FPG returned to normal but the IVGTT was still pathological. After 14 days there was complete normalisation of the IVGTT. glucose intolerance did not occur when rats were injected with 1 ml of the following control sera: the patient's serum following 6 months of treatment with cyclophosphamide when her insulin resistance was in remission, pooled sera from IDD's without insulin resistance, serum from an insulin resistant IDD with a high titre of insulin binding capacity (greater than 40 U/l) or with serum from a normal human subject. There were no alterations on light microscopy of the pancreatic islets of rats sacrificed on the 4th or 21st days. The above data suggest that our patient carried an uncharacterised substance which was capable of inducing glucose intolerance in rats. Hypothetically, it may be postulated that it was an immunoglobulin or some other protein acting via downregulation of insulin receptors or interfering with a post-receptor event mediating insulin action.
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10/11. transplantation of dispersed pancreatic islet tissue in humans: autografts and allografts.

    Islet transplantation is successful in animals and holds considerable promise as endocrine replacement therapy for patients with diabetes mellitus, but clinical application to diabetic patients has been difficult. We have shown the technical feasibility of human islet transplantation by autotransplantation of dispersed pancreatic islet tissue into the portal vein in three patients with chronic pancreatitis and incapacitating, intractable pain who underwent near-total (greater than 97%) pancreatectomy. In all three patients, the excised pancreas was dispersed by collagenase digestion, but no effort was made to purify the islets. Islet yield, as judged by tissue insulin content, ranged from 24 to 55%. The first patient, who never received insulin after the pancreatectomy and islet autotransplantation, had a normal oral glucose tolerance test by 3 wk and has remained normoglycemic for over 2 yr. In the second patient, viable islets were histologically identified in the liver parenchyma. The third patient was treated with hyperalimentation for 3 wk after the pancreatectomy and islet autotransplantation and, during this period, required insulin. After cessation of hyperalimentation and initiation of oral geedings, the patient was withdrawn from insulin. Although abnormalities of carbohydrate metabolism were present, the patient did not require insulin for more than 1 yr. Seven diabetic renal allograft recipients have received allografts of dispersed pancreatic islet tissue prepared in the same way. No patients were cured of diabetes, although transient evidence of islet function--increase in serum or urinary c-peptide levels or decrease in exogenous insulin requirements--occurred in some. Although rejection was probably responsible for most of the failures, transplantation of allogeneic human islet tissue as a free graft is metabolically inefficient. With the current state of immunosuppressive therapy, the primary role of islet transplantation may be in a situation where rejection cannot occur: as an autograft to obviate the occurrence of diabetes after extensive pancreatectomy for benign disease.
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