Cases reported "Diabetes Mellitus, Type 1"

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1/11. Antibody-mediated insulin resistance treated by cessation of insulin administration.

    A 45-year-old Japanese man was referred to our hospital because of hyperglycemia despite the administration of as much as 120 U/day of human insulin. He had no history of injecting animal insulin. Free insulin was below 5 microU/ml, but a high titer of total insulin (about 3,000 microU/ml) was observed, suggesting the presence of antibodies against human insulin. Scatchard analysis showed an increased insulin binding capacity in the plasma characterized by a higher affinity for insulin. He was successfully treated by cessation of insulin administration. A Scatchard analysis series showed that a reduction in the insulin binding capacity of antibodies paralleled the improvement in glycemic control.
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2/11. Unexplained deaths of type 1 diabetic patients.

    The suggestion of an increase in the number of sudden deaths of young people with Type 1 diabetes in the UK has been investigated. It was suggested that such deaths were due to hypoglycaemia and related to the increasing use of human insulin. In total we were notified of 50 deaths of people with Type 1 diabetes under age 50 years in the UK in 1989 which our informants (relatives, physicians, and pathologists) considered sudden and unexpected. An autopsy had been done in all cases and we supplemented this with detailed clinical information from relatives and case records. Of the 50 cases we excluded five with a definite cause of death, 11 suicides or self-poisonings, six cases of ketoacidosis, and four in which there was insufficient information about the circumstances of death to drawn any conclusions. Of the other 24 cases, two patients had been found with irreversible hypoglycaemic brain damage and died after a period of artificial ventilation. The most puzzling group were 22, aged 12-43 years, most of whom had gone to bed in apparently good health and been found dead in the morning. Nineteen of the 22 were sleeping alone at the time of death and 20 were found lying in an undisturbed bed. Most had uncomplicated diabetes and in none were anatomical lesions found at autopsy. There are major difficulties in diagnosing hypoglycaemia post-mortem, but the timing of death and other circumstantial evidence suggests that hypoglycaemia or a hypoglycaemia-associated event was responsible. All patients were taking human insulin at the time of death but most had been changed from animal insulin between 6 months and 2 years earlier and there was nothing to implicate the species of insulin as a factor in these deaths.
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3/11. 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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4/11. Insulin allergy in clinical practice.

    Insulin allergy, either localized or systemic, is a clinical problem that may be encountered by nurse practitioners. Studies have shown that 10 to 37 percent of patients started on animal-source insulin developed an allergic reaction to the agent. With the advent of purified animal-source insulins and of human insulin, this number has decreased, but the problem is unlikely to be completely eradicated. This article presents information about the diagnosis, treatment and management of patients presenting with localized or systemic insulin allergy. A brief discussion of the antigenicity of insulin and the basic immune processes operating in insulin allergy will be included. It is hoped that by acquainting nurse practitioners with the manifestations of insulin allergy and the treatment involved, earlier recognition and intervention will occur. This will help remove an extra burden from a patient who is already trying to adjust to the necessity of daily insulin injections.
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5/11. Conventional and human insulin: complications of insulin therapy in children.

    The management of complications of insulin therapy, such as lipoatrophy, allergic reactions, insulin resistance, and insulin edema, is outlined. Human and animal insulin preparations currently available in the united states are discussed, highlighting the comparative costs and indications for use.
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6/11. Treatment of a diabetic vegetarian with human insulin (recombinant dna): a case report.

    A patient with insulin-dependent diabetes mellitus is described. He refused treatment with conventional (animal-derived) insulin since it would have compromised his principles as a vegetarian. Therapy was successfully instituted with human insulin (recombinant dna).
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7/11. pancreas in recent onset insulin-dependent diabetes mellitus. Changes in HLA, adhesion molecules and autoantigens, restricted T cell receptor V beta usage, and cytokine profile.

    Insulin-dependent diabetes mellitus (IDDM), in which only the pancreatic beta cells are destroyed by the autoimmune response, is the paradigm of organ-specific autoimmunity. As a result of a combination of factors, the number of immunohistologic/cellular/molecular studies of pancreas in IDDM is very limited. We report here studies conducted in the pancreata of two IDDM patients: one newly diagnosed (case 1) and one long standing (case 2). In case 1, we demonstrated the presence of morphologically normal viable beta cells without evidence of viral infection. In both cases the expression of the autoantigens defined by islet cell Abs and by glutamic acid decarboxylase was markedly reduced in the islet cells whereas expression of hsp60, another putative autoantigen, was normal. Over-expression of HLA class I was detected in 58% of the islets in pancreatic sections and in cultured beta cells in case 1 and also in 30% of islets in case 2 but it was not restricted to any insular cell type. In case 1, there was "inappropriate" HLA class II expression in islets cells but it was a rare finding and not beta cell specific. The analysis of the correlation between class I overexpression, residual insulin, and insulitis suggests that the first event is the increase of HLA class I expression. Of adhesion molecules, ICAM-1, VLA, VCAM, and LFA-3 were normal and only ICAM-1 was moderately overexpressed in and around the islets of case 1 insulitis, as was detected by immunofluorescence which showed that 18% of the islets of case 1 had CD8 lymphocytes as the predominant population. reverse transcription-PCR demonstrated moderate V beta skewing and the profile of cytokines expected in CTLs: IL-2, IL-4, IL-10, and IFN-gamma negative, perforin positive. In addition, IFN-alpha, IFN-beta, and IL-6 transcripts were detected in the case 1 pancreas, consistent with the existence of a silent viral infection. overall, the results indicated that, differently from spontaneous animal models of diabetes, in the pancreas of IDDM patients there are no elements of the inductive phase of the autoimmune response.
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8/11. Diabetic death bed: post-mortem determination of hypoglycaemia.

    The post-mortem biochemical determination of hypoglycaemia in the practice of forensic medicine is notoriously imprecise and attracts perennial criticisms, particularly from those who may be alien to the peculiarities of medical jurisprudence. There has been re-emphasis recently on the neuropathological pathoclisis ascribed to prolonged hypoglycaemia. Unfortunately, the value perceived is limited by pathognomonic unreliability owing to agonal multifactorial influences and rapidly fatal nocturnal hypoglycaemia. The predicament is oppressive to a consideration of preponderant evidence and an unpopular diagnosis of peri-mortem hypoglycaemia, unless audacious, may be precluded simply because the proof is difficult. This is likely to contribute to diagnostic under-estimation of enigmatic diabetic deaths. A suspected case of lethal nocturnal hypoglycaemia in a young diabetic on 'animal' insulin is presented to restore some perspective to the clinico-pathological deference for an endangered post-mortem diagnosis of hypoglycaemia inferred from minimal evidence.
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9/11. Metabolic cataracts in newly diagnosed diabetes.

    The morphologically distinct diabetic or 'metabolic' cataract is rare in newly diagnosed insulin dependent diabetes. The cases described are of five adolescents (three girls, two boys) with newly diagnosed insulin dependent diabetes who developed metabolic cataracts close to the time of diagnosis (0-16 months). They all had a prolonged duration of symptoms before diagnosis (4-24 months) and high glycated haemoglobin levels at diagnosis (15-21%). The pathogenesis of diabetic cataract is not well understood in humans. An attempt is made to link clinical observations with evidence from experimental animal models to understand the mechanism of cataract formation, with particular reference to the aldose reductase pathway. It is recommended that the lens and retina are examined at the onset of diabetes in all children, especially those who have a prolonged duration of symptoms before diagnosis and who report persistent blurred vision.
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10/11. The diabetic cataract: an unusual presentation in a young subject: case report.

    This case report concerns a 14-year-old female patient, whose insulin-dependent diabetes mellitus was displayed by one infrequent complication, the cataract. This is an unusual manifestation in a 14-year-old patient; indeed, there are many findings in experimental animals demonstrating the development of this complication by maintaining blood glucose levels above 12 mM. After surgical therapy, complete vision was recovered, but we think that an earlier diagnosis and therapy of metabolic derangement of diabetes may have avoided this complication.
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