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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acromegaly is caused by excessive secretion of growth hormone (GH), and a resultant persistent elevation of insulin-like growth factor-1 (IGF-1) levels. Diabetes mellitus is accompanied in some acromegalic patients with insulin resistance. We encountered a type-2 diabetic patient who had a poorly controlled glycemic state and was diagnosed as acromegaly with normal IGF-1 levels. The patient showed definite acromegalic features. However, in the first screening test, GH levels were high and IGF-1 levels were inappropriately normal so the results were not close to the diagnosis of acromegaly. After moderate glycemic control, an oral glucose suppression test was performed, showing no suppressed GH response. TRH test revealed paradoxical increases in growth hormone levels and a brain MRI discovered a pituitary adenoma. After several-months insulin treatment, IGF-1 levels were increased to the abnormal state and GH levels were decreased without treatment for acromegaly. Here we report the rare case of acromegaly that presents inappropriately normal IGF-1 levels at the time of diagnosis in uncontrolled type 2 diabetic patient and shows increased IGF-1 levels after glycemic control with insulin therapy. When evaluating acromegaly in type 2 diabetes under poorly controlled glycemia, cautious IGF-1 analysis is needed after sufficient glycemic control.
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PMID:Acromegaly associated with type 2 diabetes showing normal IGF-1 levels under poorly controlled glycemia. 1757 66

Diabetic muscle infarction (DMI) is a rare complication of longstanding, poorly controlled diabetes. Only a few cases have been reported in the literature. The case of a 34-year-old man with a 7-year history of type 2 diabetes mellitus, with sudden onset of left thigh pain, is described here. A final diagnosis of DMI was made, the pathophysiology of which remains unclear. MRI findings were diagnostic and characteristic. The management of this condition is usually symptomatic. Short-term prognosis is very good; however, the recurrence rate is high. Long-term prognosis is poor, with most patients dying from cardiovascular complications of diabetes within 5 years of diagnosis. This case supports the need for a high index of suspicion, when a poorly controlled patient with diabetes presents with non-traumatic limb pain.
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PMID:Diabetic muscle infarction. 1758 55

Diabetes mellitus is associated with end-organ complications in the peripheral and central nervous system. It is unknown if these complications share a common aetiology, and if they co-occur in the same patient. The aim of the present study was to relate different measures of peripheral neuropathy in patients with type 2 diabetes mellitus (DM2) to cognition and brain MRI. A standardized neurological examination and questionnaire, neuropsychological examination and brain MRI were performed in 122 patients with DM2 and 56 matched controls. Measures of peripheral neuropathy were vibration threshold, a sensory examination sum score and the Toronto Clinical Neuropathy Scoring System. Neuropsychological test scores were expressed in standardized z-values across five predetermined cognitive domains. White matter lesions and cortical and subcortical atrophy were rated on MRI. Overall 38% of the patients with DM2 and 12% of the controls were classified as having any neuropathy (p<0.001). Patients with DM2 had a lower performance on the neuropsychological tests, more white matter lesions (p<0.01) and more atrophy (p<0.01) than controls. Within the DM2 group none of the measures of peripheral neuropathy was related to MRI abnormalities or cognitive dysfunction (linear regression analyses, adjusted for age, education, sex). We conclude that peripheral neuropathy in patients with DM2 is not related to cognitive dysfunction and brain abnormalities. This indicates that central and peripheral neurological complications of DM2 might have different etiologies.
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PMID:Peripheral and central neurologic complications in type 2 diabetes mellitus: no association in individual patients. 1785 Aug 22

Silent brain infarction (SBI) is often detected on MR imaging, however the pathogenesis is still unclear. We aimed to investigate and compare the association of soluble adhesion molecules and C-reactive protein levels with the prevalence of SBI in patients with and without diabetes mellitus. We recruited 130 patients (mean age 59.6 +/- 7.6 yrs) with type 2 diabetes and 130 age- and sex-matched non-diabetic subjects. All subjects underwent head MRI to determine SBI. We measured levels of soluble intercellular adhesion molecule 1(sICAM-1), vascular cell adhesion molecule 1(sVCAM-1), and high sensitivity C-reactive protein (hs-CRP) and evaluated intima-media complex thickness (IMT) in common carotid arteries by ultrasound B-mode imaging. SBI was present in 36 (27.7%) of the diabetic patients and 31 ( 23.8%) of the non-diabetic subjects. Levels of sICAM-1, sVCAM-1 and IMT were all significantly higher in diabetic patients than in non-diabetic subjects, and were significantly increased in both subjects with SBI. IMT was only positively correlated with sVCAM-1 levels in diabetic and non-diabetic subjects. On the other hand, hs-CRP levels were not significantly different in both subjects with and without SBI. In addition, sICAM-1 levels were associated with a significantly higher relative risk for the prevalence of SBI in diabetic patients after multivariate adjustment. Our study suggests that the associations between endothelial dysfunction and presence of SBI may be stronger in diabetic patients than in nondiabetic subjects. In particular, sICAM-1 may play an important role for the pathogenesis of SBI in patients with diabetes mellitus.
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PMID:Association of soluble adhesion molecule and C-reactive protein levels with silent brain infarction in patients with and without type 2 diabetes. 1847 26

The occurrence of diabetes and dementia is very high in older patients. The fact that both conditions are concurrent raises the question of a possible link between the two. Cognitive functions of non-demented patients with diabetes have been extensively studied. In type 1 diabetes, only a mild decrease of the speed of information processing and of the psychomotor efficiency has been shown. Cognitive decline seems to be related to poor metabolic control and not to hypoglycaemia. In older patients with type 2 diabetes, memory and executive functions have been found impaired. Longitudinal studies of the literature have shown that diabetic patients have a higher chance of developing dementia than non-diabetic patient, with a relative risk (RR) between 1.26 and 2.83. The risk of vascular dementia was increased in 3 out of 5 studies, with a RR ranging between 2 and 2.6. With regard to Alzheimer's disease, the results are conflicting. Half of the studies found an increased risk in diabetic patients (RR: 1.3-2). The possible causal mechanisms of dementia in diabetic patients remain hypothetical. MRI studies showed varying degrees of cortical atrophy, cerebral infarcts and deep white matter lesions. In neuropathological studies, senile plaques and neurofibrillary tangle were not found with higher severity in the brain of diabetic patients than in the brain of age-matched controls. Several hypotheses have been raised to explain the relationship between diabetes and cognitive decline. Micro and macrovascular changes in the brain could induce cerebral hypoxia and ischemic conditions resulting in cellular death or white matter lesions. The occurrence of vascular lesions might reduce the threshold at which dementia will occur in Alzheimer disease. The deposition of advanced glycation end products doesn't spare the brain and they have been found in senile plaques, where they can reduce the solubility of proteins such as the beta amyloid and Tau proteins. Some authors favour the hypothesis of a brain insulin resistance because, in a few small studies, insulin was found to improve memory.
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PMID:[Diabetes mellitus and cognition: is there a link?]. 1878 78

Treatment with angiotensin II receptor blockers is associated with lower risk for the development of type 2 diabetes mellitus compared with thiazide diuretics. The Mechanisms for the Diabetes Preventing Effect of Candesartan Study addressed insulin action and secretion and body fat distribution after treatment with candesartan, hydrochlorothiazide, and placebo. Twenty-six nondiabetic, abdominally obese, hypertensive patients were included in a multicenter 3-way crossover trial, and 22 completers (by predefined criteria; 10 men and 12 women) were included in the analyses. They underwent 12-week treatment periods with candesartan (C; 16 to 32 mg), hydrochlorothiazide (H; 25 to 50 mg), and placebo (P), respectively, and the treatment order was randomly assigned and double blinded. Intravenous glucose tolerance tests and euglycemic hyperinsulinemic (56 mU/m(2) per minute) clamps were performed. Intrahepatic and intramyocellular and extramyocellular lipid content and subcutaneous and visceral abdominal adipose tissue were measured using proton magnetic resonance spectroscopy and MRI. Insulin sensitivity (M-value) was reduced following H versus C and P (6.07+/-2.05, 6.63+/-2.04, and 6.90+/-2.10 mg/kg of body weight per minute, mean+/-SD; P<or=0.01). Liver fat content was higher (P<0.05) following H than both P and C. The subcutaneous to visceral abdominal adipose tissue ratio was reduced following H versus C and P (P<0.01). Glycosylated hemoglobin, alanine aminotransferase, aspartate aminotransferase, and high-sensitivity C-reactive protein levels were higher (P<0.05) after H, but not C, versus P. There were no changes in body fat, intramyocellular lipid, extramyocellular lipid, or first-phase insulin secretion. Blood pressure was reduced similarly by C and H versus P. In conclusion, visceral fat redistribution, liver fat accumulation, low-grade inflammation, and aggravated insulin resistance were demonstrated after hydrochlorothiazide but not candesartan treatment. These findings can partly explain the diabetogenic potential of thiazides.
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PMID:Hydrochlorothiazide, but not Candesartan, aggravates insulin resistance and causes visceral and hepatic fat accumulation: the mechanisms for the diabetes preventing effect of Candesartan (MEDICA) Study. 1925 58

There is emerging evidence from healthy individuals, as well as direct and indirect evidence from psychiatric and neurological patients with disease-related hippocampal atrophy, linking the cortisol awakening response (CAR) to hippocampal volume. Type 2 diabetes mellitus (T2DM) is a metabolic disease that is also accompanied by hippocampal atrophy, and therefore can serve as a model for ascertaining the relationship between CAR and hippocampal volume. We contrasted a group of 18 individuals with T2DM with 12 matched controls on MRI-based hippocampal volume and salivary diurnal cortisol profile including CAR. Individuals with T2DM had smaller hippocampal volumes and exhibited a blunting of the CAR relative to controls, while diurnal cortisol was not affected. Across all subjects, fasting insulin and hippocampal volume were associated with the CAR, independent of diagnosis. Our findings support the hypothesis that hippocampal integrity is an important predictor of the CAR.
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PMID:A blunted cortisol awakening response and hippocampal atrophy in type 2 diabetes mellitus. 1916 31

The prognosis and management of liver disease greatly depends on the amount of liver fibrosis. Non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), is emerging as a major cause of liver disease in Western countries because of the increasing prevalence of obesity and type 2 diabetes. A key issue in patients with NAFLD is the differentiation of NASH from simple steatosis. It is particularly important to identify NASH patients as they are at greatest risk of developing complications such as cirrhosis, liver failure and hepatocellular carcinoma. The limitations of liver biopsy (invasive procedure, sampling errors, interobserver variability and non-dynamic fibrosis evaluation) have stimulated the search for non-invasive approaches for the assessment of steatosis and liver fibrosis in patients with NAFLD. A variety of methods, including serum markers, imaging techniques such as ultrasound, CT, MRI and measurement of liver stiffness by transient elastography, have been proposed for the non-invasive assessment of steatosis and hepatic fibrosis. This review discusses the advantages and limitations of these different methods in clinical practice.
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PMID:Non-invasive diagnosis of steatosis and fibrosis. 1919 29

Diabetic muscle infarction is a rare complication of diabetes. Since first reported in 1965, approximately 130 patients have been reported, with only 2 cases described affecting the upper extremity. We report on 3 men (age, 40-63) with diabetic muscle infarction involving the arm. The patients had symptoms 4 to 18 days before presenting to the emergency department and all required admission for their pain. Only 1 of the patients was febrile. The patients had type 2 diabetes mellitus for 10 to 25+ years, and 2 were on chronic hemodialysis, with the third starting peritoneal dialysis shortly after admission. Hemoglobin A1c ranged from 0.049 to 0.095. Creatine kinase levels ranged from 69 to 483 U/L and the white blood cell count ranged from 9.6 to 12.0 x 10(3)/microL. None of the patients required surgery nor had biopsies, and the patients were managed with rest, transdermal fentanyl, and later physiotherapy. Diagnoses were supported by MRI images in 2 patients and serial ultrasounds in the third patient. Although rare, the condition may be under-recognized. Pathophysiology, which may have some unique features in patients on hemodialysis, is briefly discussed.
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PMID:Upper extremity diabetic muscle infarction in three patients with end-stage renal disease: a case series and review. 1926 53

A 63-year-old male with type 2 diabetes mellitus was admitted to our hospital with fever and chest pain. An echocardiogram, chest CT and MRI showed the gas-containing pericardial abscess located posteriol to the right atrium. He was initially treated by thoracoscopic pericardial fenestration to set a drainage tube in the pericardial abscess. However, the surgical treatment was discontinued because of a large amount of bleeding from the abscess wall. The patient was then treated by continued administration of antibiotics and gamma-globulin. The inflammatory reactions improved and shrinkage of the abscess was confirmed.
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PMID:Gas-containing pericardial abscess in a type 2 diabetic patient. 1950 39


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