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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Illness and stress are common occurrences. For the person with type 1 diabetes, these events can be triggers for counterregulation and [table: see text] subsequent metabolic deterioration if there is no attention to diabetes management tasks. Sick-day management requires increased monitoring of blood glucose and assessment for ketosis. Although urine testing for ketones has been the standard approach to sick-day management, new technology for self-monitoring of blood 3HB levels is now available. According to the American Diabetes Association, blood measurement of 3HB "may offer a useful alternative to urine ketone testing." This new technology may provide an opportunity to improve the management of uncontrolled diabetes and sick days in an attempt to reduce the human and economic burden of DKA.
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PMID:Sick-day management in type 1 diabetes. 1114 58

DKA and HHS represent two extremes in the spectrum of decompensated diabetes mellitus. Their pathogenesis is related to absolute or relative deficiency in insulin levels and elevations in insulin counterregulatory hormones that lead to altered metabolism of carbohydrate, protein, and fat and varying degrees of osmotic diuresis and dehydration, ketosis, and acidosis. In DKA, insulin deficiency and ketoacidosis are the prominent features of the clinical presentation, and insulin therapy is the cornerstone of therapy. In HHS, hyperglycemia, osmotic diuresis, and dehydration are the prominent features, and fluid replacement is the cornerstone of therapy. As many as one-third of patients may have mixed features of both DKA and HHS. Because the three-pronged approach to therapy for either DKA or HHS consists of fluid administration, intravenous insulin infusion, and electrolyte replacement, mixed cases are managed using the same approach. The therapeutic regimen is tailored according to the prominent clinical features present. In adult patients with mixed features, fluids may be administered more rapidly than they would be in younger patients, or in patients with DKA alone, because the risk for fatal cerebral edema in adults is low and the consequences of undertreatment include vascular occlusion and increased mortality. In younger patients with mixed features, rapid correction of metabolic abnormalities and, consequently, of hyperosmolarity by administration of hypotonic fluids and insulin should be avoided to decrease the risk for precipitating cerebral edema. In addition, if ketoacidosis has been a prominent feature in a mixed case, the patient may have type 1 diabetes with no residual pancreatic islet beta cell secretion and may subsequently need ongoing, life-long insulin therapy after resolution of the acute episode of decompensated diabetes. ICU admission is indicated in the management of DKA, HHS, and mixed cases in the presence of cardiovascular instability, inability to protect the airway, obtundation, the presence of acute abdominal signs or symptoms suggestive of acute gastric dilatation, or if there is not adequate capacity on the floor unit to administer the intravenous insulin infusion and to provide the frequent and necessary monitoring that must accompany its use.
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PMID:Management of decompensated diabetes. Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. 1121 36

Glycemia varies widely in patients with diabetic ketoacidosis (DKA), with plasma glucose concentrations between 10 to 50 mmol/L commonly encountered. The mechanism of this glycemic variability is uncertain. Our study examined the differential effects of fasting and dehydration on hyperglycemia induced by withdrawal of insulin in type 1 diabetes. To evaluate the respective roles of dehydration and fasting in the pathogenesis of DKA, 25 subjects with type 1 diabetes were studied during 5 hours of insulin withdrawal before (control) and after either 32 hours of fasting (n = 10) or dehydration of 4.1% +/- 2.0% of baseline body weight (n = 15). Samples were obtained every 30 minutes during insulin withdrawal for substrate and counterregulatory hormone levels and rates of glucose production and disposal. Fasting resulted in reduced plasma glucose concentrations compared with the control study, while dehydration resulted in increased plasma glucose concentrations compared with the control study (P < .001). Glucose production and disposal were decreased during the fasting study and increased during the dehydration study compared with the control study. Glucagon concentrations and rates of development of ketosis and metabolic acidosis were increased during both fasting and dehydration compared with control. These data suggest that fasting and dehydration have differential effects on glycemia during insulin deficiency, with dehydration favoring the development of hyperglycemia and fasting resulting in reduced glucose concentrations. This finding is probably attributable to the differing effect of these conditions on endogenous glucose production, as well as to differences in substrate availability and counterregulatory hormone concentrations. The severity of pre-existing fasting and dehydration likely explains much of the variability in plasma glucose concentrations observed in DKA.
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PMID:Differential effects of fasting and dehydration in the pathogenesis of diabetic ketoacidosis. 1122 25

We describe a patient with type I diabetes, clinical findings consistent with velocardiofacial syndrome, and a chromosome 22q11.2 deletion. A nine-year-old boy presented with a history of polyuria, polydipsia, weight loss, hyperglycemia, ketosis, serum insulin antibodies, and a low C-peptide level. He had distinctive facial features, learning disabilities, short stature, and a history of glottic web and clubfoot. Although a normal karyotype was obtained, fluorescence in situ hybridization (FISH) revealed a submicroscopic deletion in the DiGeorge/velocardiofacial syndrome critical region at 22q11.2. His maternal half-brother also carried a chromosome 22q11.2 deletion. His mother has similar facial features and hypoparathyroidism. Autoimmune problems associated with chromosome 22q11.2 deletions have been reported. We suggest that the defects in immune regulation due to T-cell deficiency in chromosome 22q11.2 deletion syndrome may predispose to autoimmune disorders, including type I diabetes mellitus.
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PMID:Type I diabetes mellitus in a patient with chromosome 22q11.2 deletion syndrome. 1134 31

A 66-year-old Japanese woman presenting with recent onset of type 1 diabetes mellitus and cerebellar ataxia was admitted to our hospital. Physical examination on admission revealed coordinate disturbance due to cerebellar ataxia, and the laboratory examination showed marked hyperglycemia with ketosis and impaired insulin secretion. Anti-glutamic acid decarboxylase (GAD) antibodies in high titer were detected in patient's serum. Immunoblotting showed the patient's serum reacted with a 65 kDa protein in tissue extracts from rat pancreas and cerebellum, and immunohistochemical study produced positive immunostaining in the pancreatic islets of Langerhans, the axons of Purkinje cells and the nerve terminals in the granular layers of cerebellum of the rat. This is the first case presenting with concomitant type 1 diabetes and cerebellar ataxi associated with high titers of circulating anti-GAD antibodies which may play a critical role in the development of the diseases.
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PMID:A patient with type 1 diabetes mellitus and cerebellar ataxia associated with high titer of circulating anti-glutamic acid decarboxylase antibodies. 1145 77

The aim of this study was to analyse the immunological and clinical characteristics of a group of patients at the onset of type 1 diabetes and to determine if these findings are age related. For this purpose, 68 newly diagnosed type 1 diabetes mellitus patients referred to our hospital between 1997 and 1999 were studied; 42 were adults (mean age 24+/-3.5 years) and 26 children (mean age 6.1+/-4 years). Autoantibody markers islet cell antibodies, glutamic acid decarboxylase antibodies (GADA) and tyrosine phosphatase antibodies (IA-2A), pancreatic reserve (glucagon test) and HbA1c were determined. Some clinical characteristics, such as mode of presentation and insulin requirements, were also analysed. Type 1 diabetes mellitus was found to be autoimmune in 83.8% of the patients and idiopathic in 16.2%, without significant differences between adults and children. In the whole autoimmune group, GADA was more prevalent in adults and IA-2A more frequent in children. On the other hand, adults showing autoimmune markers developed ketosis more frequently and needed higher insulin doses at diagnosis, while children did not exhibit clinically significant differences associated with the presence or absence of antibodies. In conclusion, in children the presence of autoimmune markers is not related to the mode of presentation or characteristics of type 1 diabetes. In adults, however, the autoimmune group presents with more-severe clinical disease than antibody negative patients. Age at onset seems to be an important parameter in the natural history of type 1 diabetes and must be taken into account in epidemiological or intervention studies.
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PMID:Influence of age on clinical and immunological characteristics of newly diagnosed type 1 diabetic patients. 1148 74

We report a 43-year-old man who presented diabetic ketoacidosis 1 year after receiving kidney transplantation. He was a recipient of renal transplantation treated with metyl-prednisolone and tacrolimus regimen. The serum level of tacrolimus was 12.4 ng/ml, and he showed hyperphagia before a month of admission. A week before admission, he was aware of polydipsia, polyuria, and general fatigue. He visited our hospital and was found to have severe hyperglycemia (925 mg/dl), significant ketosis and mild metabolic acidosis (pH 7.341), although he had not been diagnosed as diabetes mellitus. He administrated in our hospital, and was treated with insulin for 5 weeks. He was not obese (BMI = 18.2 kg/m(2)) and had no family history of type 2 diabetes. He was finally treated with diet therapy alone. The 24 h urine C-peptide secretion on the third hospital day was low (8.4 microg per day). However, no autoantibodies against pancreatic islets were positive, and his insulin secretion was recovered at discharge suggesting that he was not type 1 diabetes. Although, tacrolimus has been reported to cause or worsen diabetes mellitus, the present case suggests that it could cause severe decrease in insulin secretion which leading to diabetic ketoacidosis in lean subject without previous history of diabetes mellitus.
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PMID:Sudden onset of diabetes with ketoacidosis in a patient treated with FK506/tacrolimus. 1187 16

Diabetes is an evolving disease, with changing patterns seen in both type 1 and type 2 diabetes. A wide (over 400-fold) variation exists in worldwide incidence rates of type 1 diabetes, with the highest occurring in Finland (over 45 per 100,000 under the age of 15 years) and the lowest in parts of China. In many countries (e.g. in Europe, the Middle East, Australia) the incidence of autoimmune-mediated type 1 diabetes in children <15 years of age has risen by 2-5% per annum. Type 2 diabetes is also increasing rapidly globally and is occurring at a younger age, including in adolescence and childhood. In the USA, approximately one third of newly diagnosed in the adolescent age group is type 2, with up to 20% presenting with ketosis and ketoacidosis. The management of type 2 diabetes is especially difficult in the adolescent age group. Obesity is the single most obvious risk factor for type 2 diabetes. Lifestyle modification programmes starting in childhood are urgently needed and society needs to change its attitudes to childhood nutrition, play and exercise.
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PMID:Childhood diabetes: a global perspective. 1197 14

Diabetes mellitus in humans is a heterogeneous disorder classified clinically into two main types. The diagnosis of type 1 versus type 2 diabetes is made phenotypically using criteria such as age at onset, abruptness of hyperglycemic symptoms, presence of ketosis, degree of obesity and the perceived need for insulin replacement. The pathogeneses of type 1 and type 2 diabetes are believed to be different. Type 1 diabetes is an autoimmune disease mediated by cellular effector mechanisms; whereas classic type 2 diabetes is not autoimmune but results from insulin resistance and a nonautoimmune insulin secretory defect. Most type 1 diabetes patients are diagnosed in childhood or young adulthood before the age of 35 years. However, there is clearly a subgroup of patients clinically diagnosed with type 2 diabetes who are greater than 35 years of age and have evidence of autoimmunity. The disease of these autoantibody-positive type 2 diabetics is often termed latent autoimmune diabetes in adults (LADA), slowly progressive type 1 diabetes, latent type 1 diabetes, and type 1.5 diabetes. This group of patients comprises approximately 10-15% of Caucasian type 2 diabetes patients. Type 1.5 diabetes patients tend to present with islet cell autoantibodies, islet-reactive T cells, higher HbA(1c) levels, lower C peptide, and a propensity toward insulin dependency compared to autoantibody-negative classic type 2 diabetes subjects.
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PMID:Beta cell rest and recovery--does it bring patients with latent autoimmune diabetes in adults to euglycemia? 1202 Oct 87

Malnitrition-modulated diabetes mellitus ((MMDM) was previously known as protein-deficient diabetes mellitus (PDDM). Its clinical picture is similar to that of type 1 diabetes, but it develops over a background of chronic malnutrition from childhood. In spite of severe hyperglycemia, ketonuria never occurs. MMDM patients are extremely lean and require high doses of insulin-over 2.0 U/kg/day for good glycemic control. Even when optimally controlled, these patients maintain their leanness. Infections of the skin and soft tissues and pulmonary tuberculosis are often seen, whereas micro- and macrovascular complications are rare, even after long-term follow-up. Ultrasonographic evaluation of the abdomen clearly differentiates MMDM from fibrocalculous pancreatic diabetes. Absence of ketonuria and ketosis despite very severe hyperglycemia in emaciated young subjects is the most significant marker of MMDM.
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PMID:Clinicoepidemiological and biochemical profile of malnutrition-modulated diabetes mellitus. 1202 Oct 92


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