Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of histologic, immunohistochemical and ultrastructural examination of pulmonary vessels of 85 necropsy cases (65 patients had diabetes and 20 were controls with atherosclerosis). In the lung vessels in diabetes the changes in the arteries of the elastomuscular and muscular types were frequently found (73.8 and 81.5%, respectively) which were regarded as manifestations of diabetic macroangiopathy, as well as those of arterioles, capillaries (81.5 and 55.4%, respectively) which are the expression of diabetic macroangiopathy. Macroangiopathy is represented by thickening of the endothelial basal membrane, destruction of the internal elastic lamina, its mucoid edema. An extreme manifestation is lipogranulomatosis of the arteries of muscle type. These changes are frequently associated with arterial thrombosis. Diabetic microangiopathy is characterized by plasmorrhagy and hyalinosis of the wall (lipohyaline) with the development of the nodular arteriolo-hyalinosis, the thickening of the endothelial basal membrane and frequent necrosis of capillary pericytes. A specific feature of the diabetic angiopathy is lipidosis of all cells in the lung artery system and its extracellular structures combined with lipidosis of type II pneumocytes producing surfactant and phagocyting alveolar macrophages and polinuclear leukocytes.
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PMID:[Diabetic macro- and microangiopathy of the lungs]. 208 71

A 59-year-old woman, one of 5 cases with familial type III hyperlipoproteinemia reported at our clinic to date, had nephrotic syndrome and diabetes mellitus, but had neither coronary atherosclerosis nor xanthoma. A renal biopsy specimen revealed a massive cluster of foam cells containing apolipoprotein B and E in the mesangial region of the kidney. A restricted diet intake combined with lipid-lowering drugs such as cholestyramine, clinofibrate, and bezafibrate, in addition to methylprednisolone was not very effective in lowering serum triglyceride and cholesterol levels within physiological ranges. Therefore, plasmapheresis, using a dextran sulfate-cellulose column, was performed. Repeated plasmapheresis resulted in a marked decrease in both serum total cholesterol and triglyceride. A second renal biopsy specimen performed 2 years later revealed a marked reduction in foam cells with concurrent improvement in her nephrotic syndrome and glucose intolerance. These results suggest that familial type III hyperlipoproteinemia may be responsible for glomerular lipidosis resulting in nephrotic syndrome. They also indicate that plasmapheresis using a dextran sulfate-cellulose column is very effective in the removal of abnormal lipoproteins such as beta-very low density lipoprotein and intermediate density lipoprotein in a case of familial type III hyperlipoproteinemia.
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PMID:Effects of plasmapheresis on familial type III hyperlipoproteinemia associated with glomerular lipidosis, nephrotic syndrome and diabetes mellitus. 231 Apr 24

Six fractions of serum apolipoproteins (apolipoprotein A-I, A-II, B, C-II, C-III and E) obtained from 100 patients with diabetes mellitus not administered any antihyperlipidemic drugs were measured to clarify the relationship between diabetes mellitus and the abnormal lipidosis. The serum concentrations of apolipoprotein B, C-II and C-III were significantly higher in these diabetics than in the controls (p < 0.05), and that of apolipoprotein E was significantly lower (p < 0.01). The serum concentrations of apolipoprotein C-II, C-III and E (p < 0.05) as well as HbA1C and FRA (p < 0.001) were significantly higher in the insufficient control group (FPG > or = 140 mg/dl) of diabetes mellitus. The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). The serum concentrations of apolipoprotein B, C-II, C-III and E were significantly higher (p < 0.01) in the high cholesterol group (> 220mg/dl) and the high triglyceride group (> 150mg/dl) among the diabetic groups, but no significant differences were observed in the concentrations of apolipoprotein A-I and A-II.
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PMID:[Evaluation for serum apolipoproteins in patients with diabetes mellitus]. 813 26

Hypophosphatemia associated with hemolytic anemia was diagnosed in five cats with diabetes mellitus and in one cat with idiopathic hepatic lipidosis. The hematocrit began decreasing within 24 to 48 hours after documented hypophosphatemia in each case. The anemia resolved in all five surviving cats. Because of the temporal relationship and lack of other detectable causes, hemolytic anemia was presumed to be caused by hypophosphatemia. There were increased Heinz bodies in three of six hypophosphatemic cats during episodes of hemolysis. Intravenous potassium phosphate administration corrected the hypophosphatemia in four of five cats. The effective dosages of intravenous phosphate ranged from 0.011 to 0.017 mmol of phosphate/kg/h for 6 to 12 hours. Hypocalcemia (5.4 to 8.7 mg/dL) occurred in four of five cats treated with intravenous phosphate; however, only one cat developed clinical signs attributable to hypocalcemia. Based on this retrospective study, we recommend monitoring serum phosphorus concentration every 6 to 12 hours in cats likely to become hypophosphatemic. Treatment of hypophosphatemia in cats is warranted because of the apparent increased susceptibility of cats to hypophosphatemia-induced hemolysis. Cats with severe hypophosphatemia (< or = 1.5 mg/dL) should be given oral or parenteral phosphate if contraindications do not exist.
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PMID:Hypophosphatemia and hemolytic anemia associated with diabetes mellitus and hepatic lipidosis in cats. 826 44

Hypophosphatemia is uncommon in cats, but it has been reported in association with diabetes mellitus and hepatic lipidosis, where it can cause hemolysis, rhabdomyopathy, depression, seizures, and coma. The purpose of this article is to describe 9 cats that developed low serum phosphorus concentrations (< 2.5 mg/dL) subsequent to enteral alimentation. Serum biochemical analyses from more than 6,000 cats were reviewed. The medical records of all cats with hypophosphatemia were examined for history of enteral alimentation; diabetic cats were excluded from the study. Nine cats, ranging in age from 3 to 17 years, were identified. All cats had normal serum phosphorus concentrations before tube feeding began. Onset of hypophosphatemia occurred 12 to 72 hours after initiation of enteral alimentation, and the nadir for phosphorus concentrations ranged from 0.4 to 2.4 mg/dL. Hemolysis occurred in 6 of the 9 cats. Hypophosphatemia secondary to enteral alimentation is an uncommon clinical finding in cats. Cats with high alanine aminotransferase activity, hyperbilirubinemia, and weight loss should be closely monitored for hypophosphatemia during the first 72 hours of enteral alimentation.
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PMID:Hypophosphatemia associated with enteral alimentation in cats. 852 19

The axl tyrosine kinase receptor is aberrantly expressed on myeloid cells of many individuals afflicted with chronic myelogenous leukemia (CML) and other myeloid leukemias. Although previous studies demonstrated this kinase to have oncogenic potential, it is not known whether axl actively participates in the onset and/or progression of CML. We addressed this question by generating transgenic mice possessing constitutive ectopic expression of human axl throughout cells of the myeloid hematopoietic lineage through the use of the granulocyte colony-stimulating factor (GCSF) receptor promoter. The transgenics did not exhibit hematopoietic malignancies, but did exhibit phenotypic characteristics associated with noninsulin-dependent diabetes mellitus (NIDDM) including hyperglycemia and hyperinsulinemia, severe insulin resistance, progressive obesity, hepatic lipidosis, and pancreatic islet dysplasia. The obese-diabetes phenotype was similar to that observed in the agouti and melanocortin-4(-/-) mutants, however the axl transgenics were not hyperphagic. Axl transgenic animals expressed elevated serum tumor necrosis factor (TNF)-alpha levels that were further enhanced upon in vitro lipopolysaccharide (LPS) stimulation of peripheral blood. Administration of the axl ligand, gas6, to peripheral transgenic blood samples eliminated excessive TNF-alpha production in response to LPS stimulation. As a means to better understand axl-gas6 biology, transgenic animals were produced which systemically expressed the gas6-binding axl proteolytic cleavage product. A more severe NIDDM phenotype occurred in these mice. The observed phenotypes may be related to the axl receptor or proteolytic cleavage product competing with related axl family receptors for binding of the gas6 ligand. We conclude that axl expression in myeloid cells in itself does not lead to the onset or progression of leukemia and suggest that ectopic axl expression affects endogenous modulation of TNF-alpha production indirectly resulting in the NIDDM phenotype.
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PMID:Noninsulin-dependent diabetes mellitus occurs in mice ectopically expressing the human Axl tyrosine kinase receptor. 1052 29

Five callitrichids (three common marmosets -Callithrix jacchus -, a black tufted-eared marmoset -C. penicillata-, and a saddle-back tamarin -Saguinus fuscicollis) were diagnosed with islet hyperplasia by histopathology and immunohistochemistry. All were privately-owned, unrelated callitrichids ranging from 2- to 4-year-old. Relevant findings were anorexia (3/5), vomiting (2/5), ptyalism (1/5), polyuria/polydipsia (1/5), respiratory distress (1/5), hyperglycemia (2/3) and glycosuria (1/1); hyperglycemia and glycosuria were associated with pregnancy in a common marmoset and resolved after reducing simple carbohydrates in diet. All five animals died, three of them after few premonitory signs; in two cases, other concurrent diseases unrelated to islet hyperplasia were considered the cause of death. Additional animals from two facilities had high weight (4), physical obesity (3), polyuria/polydipsia/polyphagia/uriposia (1), hyperglycemia (1), and/or glycosuria (2). Pathologic findings in the deceased callitrichids were: islet hyperplasia (5/5); hemosiderosis (5/5); lipomatosis (4/5) of several tissues (atria, 3/5; pancreas, gall bladder, intestine, esophagus, and thyroid, 2/5; liver, 1/5); pancreatic necrosis or steatonecrosis, and/or acute pancreatitis (3/5); and vacuolation of hepatocytes and renal tubular cells most likely consistent with hepatorenal lipidosis (2/5). The islets of Langerhans were more numerous and larger than in a control, and morphologically normal in all cases, except in a common marmoset that had a few cells with a foamy cytoplasm and shrunken hyperchromatic or picknotic nucleus. Insulin (5/5), glucagon (3/5), and somatostatin (3/5) immunohistochemistry revealed that most cells stained positively for insulin diffusely in their cytoplasm (5/5) (staining restricted to the vascular pole of b-cells in the control). These findings suggest that obesity, insulin resistance and/or type II diabetes may be implicated and thus a prospective study on these diseases in callitrichids is necessary to determine their etiopathogenesis.
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PMID:Islet hyperplasia in callitrichids. 1214 99

The diabetes (db/db) genotype mutation induces a hyperglycemic-hyperinsulinemic endometabolic state in C57BL/KsJ mice, manifesting a type II NIDDM diabetes-obesity syndrome (DOS) associated with intrinsic leptin receptor expression defects. The severity of the DOS-induced premature pancreatic dysfunction and cytoatrophic involution has been linked to the severity of hypercytolipidemia which develops in pancreatic islets following systemic lipoidosis. The current studies define the cytochemical changes associated with pancreatic islet and acinar vesicular degranulation (deproteinization), cytoinvolution and B-cell dysfunction relative to the onset of cellular (nuclear DNA fragmentation) apoptosis in 20- to 26-week-old chronic db/db mutants relative to control (+/?) indices. The db/db mutation induced dramatic increases in body weights, blood glucose as well as serum and tissue triglyceride concentrations relative to +/? parameters. In contrast, pancreatic tissue weights and insulin concentrations were significantly decreased in db/db groups in association with premature islet cytoatrophy relative to +/? indices. Concurrent elevations in db/db tissue triglyceride concentrations and islet cytolipid depositions accompanied the progressive pancreatic cytoatrophic alterations. Diminished B-cell vesicular (insulin) granulation was pronounced in atrophic pancreatic islets, which were also characterized by hyperplasic acinar cellular intrusion and subsequent proteolytic B-cell dissolution coincident with 3'-DNA fragmentation-indexed (TUNEL-labeled) nuclear apoptosis. The chronic expression of the db/db mutation exacerbated these pancreatic islet B-cell atrophy indices, characterized by insulin vesicular degranulation, suppressed systemic insulin concentrations, invasive hypercytolipidemia, progressive cellular atrophy and hyperplasic acinar proteolytic dissolution, culminating in islet volume/mass reduction and chronic db/db-related pancreatic involution. The results of these studies indicate that pancreatic islet B-cell apoptosis is coincident with the progressive hypercytolipidemia component of the type II DOS promoted by the db/db genotypic mutation. These data suggest that the severity of progressive pancreatic lipoapoptosis disrupts regulatory cellular metabolic cascades, resulting in nuclear fragmentation, organelle dissolution and the subsequent promotion of a nonhomeostatic cytochemical milieu which ultimately renders islet B-cell populations susceptible to acinar proteolytic dissolution and progressive pancreatic involution.
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PMID:Cytochemical analysis of pancreatic islet lipoapoptosis: hyperlipidemia-induced cytoinvolution following expression of the diabetes (db/db) mutation. 1586 Sep 29

A 2-year-did ferret was referred with a diagnosis of diabetes mellitus. The animal died despite insulin therapy and was submitted for necropsy. Light microscopic examination revealed a mild hepatic lipidosis and pancreatic lesions consisting of a diffuse vacuolation of the Langerhans' islet cells with a periodic acid-Schiff positive material compatible with glycogen.
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PMID:Histopathologic lesions of diabetes mellitus in a domestic ferret. 1645 80

The diagnosis of drug-induced liver injury (DILI) is a challenging problem, often confounded by incomplete clinical information and the difficulty of eliciting exposure to herbal products, over-the-counter agents and toxins. The task is further rendered difficult on biopsy, as drugs can mimic all the patterns found in primary liver disease. Acute hepatitis, with or without cholestasis, is the most common histological pattern of DILI, and drugs such as acetaminophen are the leading causes of acute liver failure. Most cases of DILI resolve on discontinuation of the drug, but recovery can take months or rarely the disease can progress despite drug withdrawal. Drugs such as methotrexate can lead to chronic hepatitis and cirrhosis, while others such as minocycline, nitrofurantoin and methyldopa are implicated in autoimmune hepatitis. Prolonged cholestasis and ductopenia resembling primary chronic biliary disease can occur. Drug-induced steatohepatitis is also an uncommon pattern, but is well described with drugs such as amiodarone and irinotecan. In the presence of risk factors such as obesity and diabetes, some drugs such as tamoxifen, oestrogens and nifedipine can precipitate or exacerbate steatohepatitis. Other observed patterns include granulomatous hepatitis, vascular injury (eg, sinusoidal obstruction syndrome), Ito cell lipidosis and neoplasms (eg, adenomas).
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PMID:Histological patterns in drug-induced liver disease. 1947 52


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