1/34. Diabetes as a result of atypical anti-psychotic drugs--a report of three cases.AIMS: Atypical anti-psychotic drugs (APDs) are widely used in psychotic disorders refractory to conventional neuroleptic agents. RESULTS: Three cases of new-onset diabetes are reported in Caucasian men who were on clozapine (one) or olanzapine (two) for 3-6 months. They had a distinct presentation: weight loss, ketosis (one ketoacidosis), severe hyperglycaemia requiring insulin therapy, and relative insulin deficiency as reflected by glucagon stimulatory tests. In all cases, insulin was stopped within 1 month after the APD was discontinued. CONCLUSIONS: Novel APDs not only induce diabetes as a result of weight gain in predisposed patients, but can also lead to a reversible state of insulin deficiency, and sometimes ketoacidosis.- - - - - - - - - - ranking = 1keywords = deficiency (Clic here for more details about this article) |
2/34. diabetes mellitus associated with recombinant human growth hormone for hiv wasting syndrome.Recombinant human growth hormone (rhGH) is an important treatment option for patients with human immunodeficiency virus (HIV) wasting syndrome. Side effects of rhGH are minimal when administered at physiologic and moderately high dosages, as seen in growth hormone deficiency and Turner's syndrome, respectively. The dosage of rhGH is significantly higher to treat wasting syndrome and still is being studied to determine its long-term efficacy and safety. Individuals with HIV infection are at increased risk for adverse effects due to polypharmacy, immune system alterations, and treatment with newer agents that lack long-term safety data. In addition, rhGH's potential for side effects becomes greater when given at high dosages for wasting syndrome. Clinically significant hyperglycemia developed in an HIV-positive man who started rhGH for wasting syndrome 38 days before the diagnosis of diabetes mellitus.- - - - - - - - - - ranking = 1keywords = deficiency (Clic here for more details about this article) |
3/34. Marked atherosclerosis in a patient with familiar lecithin: cholesterol acyltransferase deficiency associated with end-stage renal disease and diabetes mellitus.Familial lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare genetic disorder of the lipid metabolism caused by the absence of LCAT activity in plasma. It is not generally accompanied by atherosclerosis in spite of low high-density lipoprotein cholesterol levels nor by diabetes mellitus. However, reports of long-term follow-up or autopsy findings are rare, and the true incidence of atherosclerosis in LCAT deficiency is not clear. We report on the long-term observation of a patient with familial LCAT deficiency who developed renal failure, diabetes mellitus, and marked atherosclerosis. The patient died of sepsis from foot ulcers 7 years after starting hemodialysis and 13 years after the diagnosis. Marked atherosclerosis characterized by medial calcification in small arteries was observed at autopsy. The genesis of the atherosclerosis seemed to be on the basis of a combination of factors.- - - - - - - - - - ranking = 3.5keywords = deficiency (Clic here for more details about this article) |
4/34. Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency.Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Metabolic balance studies revealed, in addition to diabets, the presence of isolated aldosterone deficiency of the hyporeninemic type. Intravenous glucose infusions (0.5 g/kg body weight) produced significant hyperkalemia but desoxycortisone acetate (DOCA) therapy (10 mg/day) prevented the glucose-induced hyperkalemia. In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. These studies illustrate the risk of raising blood glucose levels in patients with combined aldosterone and insulin deficiency and the tendency towards hyperkalemia in diabetic patients under certain clinical conditions.- - - - - - - - - - ranking = 3keywords = deficiency (Clic here for more details about this article) |
5/34. Maternal uniparental disomy for chromosome 14 with diabetes mellitus.A 20-year-old Japanese man was admitted to our hospital because of thirst and weight loss. His fasting plasma glucose, glycated hemoglobin, and urinary c-peptide were 262 mg/dl, 13.6%, and 44.8 microg/day, respectively, and the autoimmune antibodies related to type 1 diabetes were negative. Chromosome analysis of his peripheral blood lymphocytes showed a mos45,XY,der(14;14)(q10;ql0)[129]/ 46,XY, 14, der(14;14)(q10;q10)[1] karyotype. His parents were karyotypically normal. Microsatellite marker analysis on chromosome 14 demonstrated mosaic maternal segmental isodisomy for 14q21-q24. Although the parents had normal glucose regulation, the patient who finally returned to impaired glucose tolerance and his mother both have a deficiency in early postprandial insulin secretion. Since obesity was mild (body mass index, 24.1 kg/m2) and he was relatively young for type 2 diabetes, we speculated that his isodisomy 14 may have been involved in the onset of diabetes mellitus in this patient.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
6/34. Inaccurate glycosylated hemoglobin A1C measurements in human immunodeficiency virus-positive patients with diabetes mellitus.Persistent differences in blood glucose and serum glycosylated hemoglobin (HbA1C) measurements were observed in 4 human immunodeficiency virus-positive patients with diabetes mellitus, all of whom were taking drugs associated with hemolysis, which interferes with the reliability of HbA1C levels. Determination of fructosamine levels was a more accurate alternative for measuring average glycemic control in these patients.- - - - - - - - - - ranking = 2.5keywords = deficiency (Clic here for more details about this article) |
7/34. Permanent neonatal diabetes caused by glucokinase deficiency: inborn error of the glucose-insulin signaling pathway.Neonatal diabetes can be either permanent or transient. We have recently shown that permanent neonatal diabetes can result from complete deficiency of glucokinase activity. Here we report three new cases of glucokinase-related permanent neonatal diabetes. The probands had intrauterine growth retardation (birth weight <1,900 g) and insulin-treated diabetes from birth (diagnosis within the first week of life). One of the subjects was homozygous for the missense mutation Ala378Val (A378V), which is an inactivating mutation with an activity index of only 0.2% of wild-type glucokinase activity. The second subject was homozygous for a mutation in the splice donor site of exon 8 (intervening sequence 8 [IVS8] 2T-->G), which is predicted to lead to the synthesis of an inactive protein. The third subject (second cousin of subject 2) was a compound heterozygote with one allele having the splice-site mutation IVS8 2T-->G and the other the missense mutation Gly264Ser (G264S), a mutation with an activity index of 86% of normal activity. The five subjects with permanent neonatal diabetes due to glucokinase deficiency identified to date are characterized by intrauterine growth retardation, permanent insulin-requiring diabetes from the first day of life, and hyperglycemia in both parents. Autosomal recessive inheritance and enzyme deficiency are features typical for an inborn error of metabolism, which occurred in the glucose-insulin signaling pathway in these subjects.- - - - - - - - - - ranking = 3.5keywords = deficiency (Clic here for more details about this article) |
8/34. lipoma and opthalmoplegia in mitochondrial diabetes associated with small heteroplasmy level of 3243 tRNA(Leu(UUR)) mutation.We report a patient with mitochondrial diabetes mellitus associated with the A3243G mutation (MDM3243). The patient is a 77-year man with diabetes. At age 68, he noticed diplopia, due to superior rectus muscle palsy of the right eye. At age 70, he noticed lipoma on the right arm. The pathology of his muscle revealed some ragged-red fibers, and focal cytochrome c oxidase deficiency. Hence, he may have a pathogenetic mechanism in common with CPEO (chronic progressive external ophthalmoplegia) or mitochondria-related autoimmune disorder associated with mononeuropathy. He had the rate of 0.102% for heteroplasmy of 3243 mitochondrial dna mutation in leukocytes. This case's heteroplasmy level is the smallest among the reported cases of MDM3243 in the literature. 3243 mitochondrial dna mutation is known to induce a lack of uridine-modification in tRNA(Leu(UUR)) at the first letter of the anticodon, with which the third letter of the codon pairs, and decline of the pairing of the anticodon of tRNA with the codon of mRNA, suggesting the termination of polypeptide-elongation to generate premature proteins. Therefore, we speculate that these premature proteins may accumulate overtime, thereby affecting cells in target organs.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
9/34. Pancreatic pathology in pentamidine-induced diabetes in acquired immunodeficiency syndrome patients.An acquired immunodeficiency syndrome patient who was treated with pentamidine for a pneumocystis infection developed hypoglycemia followed by diabetes mellitus. The pathologic findings in the pancreas consisted of a significant decrease in the number of insulin-positive cells as measured by immunoperoxidase techniques when compared with comparable tissue from an age- and sex-matched control. There was also a decrease in the staining intensity of the insulin-positive cells, an absolute increase in the glucagon-positive cells, and no significant change in the number of somatostatin-positive cells. Routinely stained histologic sections showed morphologic changes in the islets with features different from those described in insulin-dependent diabetes mellitus or those caused by the toxin Vacor. The islets had increased vascular spaces, no islet cell necrosis, no fibrosis, and no lymphocytic infiltrates when compared with an age-matched control.- - - - - - - - - - ranking = 2.5keywords = deficiency (Clic here for more details about this article) |
10/34. diabetes mellitus associated with late onset congenital adrenal hyperplasia: coincidence or causality?diabetes mellitus and late onset congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency were observed in two female siblings aged 51 and 60 years. Not only coincidence but also causality (hyperinsulinism, glucose intolerance due to hyperandrogenism) should be considered when explaining the association of diabetes mellitus with late onset congenital adrenal hyperplasia.- - - - - - - - - - ranking = 0.5keywords = deficiency (Clic here for more details about this article) |
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