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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown both increased and decreased regional cerebral glucose metabolism-blood flow (rMRGlu-rCBF) values in diabetes. We sought to elucidate the influence of diabetes on rMRGlu-rCBF in 57 patients with pure cerebral microangiopathy. Sixteen of 57 patients had diabetes requiring therapy (11 NIDDM, 5 IDDM). Using a special head-holder for exact repositioning, rMRGlu (PET) and rCBF (SPET) were imaged and measured in slices, followed by MRI. White matter and cortex were defined within regions of interest taken topographically from MRI (overlay). Diabetic and non-diabetic microangiopathy patients were compared to 19 age-matched controls. The diabetic patients showed significantly lower rMRGlu-rCBF values in all regions than controls, whereas non-diabetic patients did not. There were no significant NIDDM-IDDM differences. rMRGlu-rCBF did not depend on venous blood glucose levels at the time of the PET examination. However, analysis of variance with the factors diabetes, atrophy and morphological severity of microangiopathy showed that lowered rMRGlu-rCBF in the diabetic group was due to concomitant atrophy only (P < 0.005), while neither diabetes nor microangiopathy had any influence on rMRGlu-rCBF (all P > 0.2). These results were confirmed by multivariate factor analysis. It can thus be concluded that a supposed decrease in rMRGlu-rCBF in diabetes mellitus is in fact only an artefact produced by the concomitant atrophy. All previous studies failed to correct for atrophy, and a critical reappraisal is required.
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PMID:Influence of diabetes mellitus on regional cerebral glucose metabolism and regional cerebral blood flow. 1071 98

A 37-year-old male patient with a diffuse pleomorphic B-cell-lymphoma, which has been diagnosed two month earlier with the primary site at the pterygopalatine fossa on both sides with infiltration of the clivus and cavernous sinus was referred to our hospital for continuation of the third course of CHOP chemotherapy. At admission he reported about a recent history of painful swallowing and intermittent substernal chest pain. Alleviation of the pain on swallowing and the chest pain was apparently only possible by drinking 10 to 15 l of cold coca cola throughout the day and night, a regimen that resulted in polyuria. Physical examination revealed extensive thrush stomatitis and soor esophagitis. Despite successful treatment with fluconazole, polydipsia continued unabated. The classic osmotic test of dehydration and exogenous vasopressin revealed hypothalamic diabetes insipidus (DI). Basal hormones and stimulated endocrine function tests of the adenohypophysis were found to be normal. MRI-scan revealed lymphoma infiltration of the neurohypophysis. After the third course of CHOP chemotherapy the patient surprisingly recovered completely from his excessive thirst. The present report shows that clinical disorders such as thrush stomatitis can mask diabetes insipidus caused by an early relapsing lymphoma.
Exp Clin Endocrinol Diabetes 2000
PMID:Diabetes insipidus in a patient with a highly malignant B-cell lymphoma and stomatitis. 1096 68

Exendin-4 is a 39 amino acid peptide produced in the salivary gland of the Gila monster lizard. It has a 53% amino acid homology to the incretin hormone glucagon-like peptide-1 (GLP-1). Exendin-4 induces insulin release through activation of the GLP- 1 receptor but is a much more potent insulinotropic agent than GLP-1. Of critical importance for its potential use as a treatment for diabetes is its much longer biological effect in vivo. Previous studies involving once daily administration of exendin-4 over 13 weeks to db/db mice demonstrated that it lowers hemoglobin A1c (HbA1c), a marker of mean blood glucose levels. Food consumption in the treated animals dropped over the first 4 days and then increased to a level comparable with that of the untreated animals. In this study, we initially examined the effect of once daily injections (over 14 days) on the food consumption of Zucker fatty rats. We observed an immediate reduction in food intake which then leveled off(after 5 days) to match that of the untreated animals. Subsequently we injected the same animals twice daily (treatment period of 56 days in total) and observed a sustained reduction in food intake and weight-gain. This was matched by a reduction in the critical parameters of HbA1c, fasting blood glucose and plasma insulin. MRI imaging of the abdominal regions of the animals showed that initially only the amount of fat deposited in the sc region was reduced after 4 weeks exendin-4 treatment. At the 8-week time point there was a corresponding decrease in the amount of visceral fat deposition. The combination of appetite reduction, decreased fat deposition and an improvement in the parameters associated with glucose intolerance makes a case for the use of exendin-4 as a treatment for diabetes.
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PMID:Exendin-4 decelerates food intake, weight gain, and fat deposition in Zucker rats. 1083 Feb 74

A retroperitoneal tumor in the region of the adrenal gland was diagnosed in a 56-year-old woman. The patient had been suffering from a dull abdominal pain for nearly four weeks before consulting her family physician. Ultrasound, CT and MRI scans revealed a giant tumor of the right adrenal gland. Endocrine activity could not be demonstrated. The size of the tumor was suggestive of an adrenal carcinoma. The patient was referred for adrenalectomy and complete exstirpation of the retroperitoneal mass. The histological examination revealed characteristical findings of a benign schwannoma.
Exp Clin Endocrinol Diabetes 2000
PMID:Retroperitoneal schwannoma presenting as an adrenal tumor. 1096 66

The thiamine transporter gene SLC19A2 was recently found to be mutated in thiamine responsive megaloblastic anaemia with diabetes and deafness (TRMA, Rogers syndrome), an early onset autosomal recessive disorder. We now report a novel G1074A transition mutation in exon 4 of the SLC19A2 gene, predicting a Trp358 to ter change, in a girl with consanguineous parents. In addition to the typical triad of Rogers syndrome, the girl presented with short stature, hepatosplenomegaly, retinal degeneration, and a brain MRI lesion. Both muscle and skin biopsies were obtained before high dose thiamine supplementation. While no mitochondrial abnormalities were seen on morphological examination of muscle, biochemical analysis showed a severe deficiency of pyruvate dehydrogenase and complex I of the respiratory chain. In the patient's fibroblasts, the supplementation with high doses of thiamine resulted in restoration of complex I activity. In conclusion, we provide evidence that thiamine deficiency affects complex I activity. The clinical features of TRMA, resembling in part those found in typical mitochondrial disorders with complex I deficiency, may be caused by a secondary defect in mitochondrial energy production.
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PMID:A novel mutation in the thiamine responsive megaloblastic anaemia gene SLC19A2 in a patient with deficiency of respiratory chain complex I. 1097 58

We herein report a rare case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and diabetes mellitus with ketoacidosis. An 18-year-old female patient was diagnosed to have diabetes mellitus and insulin therapy was thereafter initiated. At 26 years of age, she was hospitalized for diabetic ketoacidosis, soon followed by a loss of consciousness, left-sided dysmetria, and ataxic speech. MELAS was diagnosed because of the presence of ragged red fibers in a muscle biopsy. At 33 years of age, she was admitted to our hospital because of ketoacidosis and partial status epilepticus. A blood gas examination revealed as follows; arterial pH, 6.88; bicarbonate, 2.1 mmol/l; base excess - 29.8 mmol/l. The serum level of glucose had also increased to 30 mmol/l. The serum levels of lactate and B-hydroxybutyrate were elevated to 11.4 mmol/l and 1,990 micromol/l, respectively. Ketoacidosis improved by fluid replacement and continuous intravenous insulin infusion. A brain MRI demonstrated hyperintensity areas on FLAIR images in the bilateral temporal lobes and the cerebellum. A proton MRS demonstrated the abnormal lactate accumulation in the bilateral temporal and occipital lobes. Since epileptic seizures are rare in patients with diabetic ketoacidosis, such seizures may indicate the existence of MELAS syndrome.
Diabetes Metab 2000 Nov
PMID:Ketoacidosis accompanied by epileptic seizures in a patient with diabetes mellitus and mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). 1111 21

Involvement of the central nervous system is uncommon in progressive systemic sclerosis, with only 2 reported cases associated with intracerebral hemorrhage detected by neuroimaging. A 55-year-old woman with a 10-year history of scleroderma presented with left occipital lobe hemorrhage manifesting as headache and vomiting. She had no signs of hypertension, diabetes mellitus and hyperlipidemia. CT and MRI, on admission, showed left occipital lobe hemorrhage with ventricular rupture and acute left subdural hematoma. Serial cerebral angiography was performed on day 0, day 7 and day 14, and found no evidence of aneurysm, arteriovenous multiformation or tumor stain in the left occipital lobe. However, the bilateral anterior cerebral arteries showed increasing segmental narrowing suggestive of vasculitis. Histological examination of a section from the brain cortex adjacent to the hemorrhage revealed no evidence of vasculitis, fibrinoid degeneration or amyloid deposition. Focal vasculitis may have occurred secondary to the homorrhagic lesion.
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PMID:[A case of left occipital lobe hemorrhage in a patient with progressive systemic sclerosis: evaluation of cerebral angiography and histology]. 1112 85

Diabetic muscle infarction is a rare complication of diabetes mellitus. However, idiopathic compartment syndrome in the diabetic patient is even a rarer disease, which has been reported only in three cases up to date. The disease seems to occur in patients affected by type 1 diabetes mellitus with a history of poorly controlled glucose levels. MRI aids in the diagnosis by delineating the edema of the muscle. However, definitive diagnosis is made using the Stryker needle unit. Treatment is accomplished by immediate two-incision fasciotomy. We present a case where a 34 yr-old female with a long standing history of poorly controlled Type 1 diabetes mellitus presented with a painful right lower extremity and was diagnosed with compartment syndrome. In our patient, a single incision fasciotomy to release the pressure was sufficient and might be considered as an alternative and less morbid procedure in the diabetic patient with already poorly healing tissues. We conclude that the muscle infarction in these patients is from diffuse microangiopathic disease leading to muscular infarction and fluid accumulation in the cells causing a decrease in the space in the compartment in question causing compartment syndrome.
Diabetes Metab 2000 Dec
PMID:Review and case report of idiopathic lower extremity compartment syndrome and its treatment in diabetic patients. 1117 20

Aceruloplasminemia is a newly recognized autosomal recessive disorder of iron metabolism that causes neurodegeneration of the retina and basal ganglia, as well as diabetes mellitus. The neurological symptoms in affected patients include involuntary movements, ataxia, and dementia reflecting the sites of iron deposition detected by MRI, and the regions of neurodegeneration observed at autopsy. Excess iron functions as a potent catalyst of biologic oxidation. CSF from affected patients revealed a threefold increased iron concentration associated with increased superoxide dismutase activity and lipid peroxidation products. We found that the amount of iron accumulated in various regions of the brain and visceral organs is correlated with the levels of the oxysterols, including 7-hydroxycholesterol, and 7-ketocholesterol, which are directly produced from cholesterol by active oxygen species. Positron emission tomography done on brains of aceruloplasminemia patients showed cortical glucose hypometabolism. Enzyme activities in the mitochondrial respiratory chain of the cerebral cortices of the patients were reduced to approximate 62% and 71%, respectively, for complexes I and IV. These findings suggest that iron-mediated free radicals contribute to lipid peroxidation and the impairment of mitochondrial energy metabolism in aceruloplasminemia.
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PMID:[Neuronal cell damage in aceruloplasminemia]. 1121 1

Our understanding of gastric motility disorder--diabetic gastroparesis has advanced in the last ten to fifteen years, but the published data regarding pathogenesis are confusing and show conflicting results. The pathogenesis is sometimes linked with hyperglycemia, autonomic neuropathy, gastrointestinal hormone or myogenic mechanism. Antral hypomotility is often associated with hyperglycemia which is often accompanied by reduction in duodenal waves. Varying level of motilin, a gastrokinetic hormone has been reported. However none of the mechanism could explain the exact pathogenesis. The relationship of this mortality disorder with clinical symptoms is not always established, however nausea and vomiting lasting for days or weeks are the prominent symptoms. Other symptoms are post-prandial fullness, early satiety, bloating, belching, and vague abdominal discomfort. In a few cases, it may be the cause of poor nutrition, uncontrolled diabetes and recurrent ketoacidosis. Last one or two decades have seen some advancement in the investigational procedures like scintigraphy, radio-opaque markers, breath test, electrogastrography and MRI. Which can lead to a proper diagnosis. Such objective assessment is all the more important as nearly half of the patients do not have any symptom. Symptomatic improvement of gastroparetic patients should be the aim and in asymptomatic patients, treatment is often not recommended. Some dietary advice and prokinetic agents like metoclopramide, cisapride etc. are often prescribed but much needs to be further known as management is not always uniformly rewarding.
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PMID:Diabetic gastroparesis. 1122 21


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