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

Hepatitis C and type 2 diabetes mellitus (DM) are two rising epidemics with significant impact on each other. Hepatitis C-infected patients have a higher incidence of type 2 diabetes, and diabetic patients have a high prevalence of hepatitis C. There is mounting evidence that glucose abnormalities have a negative impact on the disease progression as well as antiviral therapy outcomes. Utilization of oral glucose tolerance testing has the potential to uncover previously undetected DM as well as impaired glucose tolerance or prediabetes in patients with chronic hepatitis C (CHC). Early detection of diabetes and prediabetes with oral glucose tolerance testing in CHC patients can lead to interventions, with significant positive impact on disease progression and antiviral therapy outcomes.
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PMID:Uncovering glucose abnormalities in people with hepatitis C infection: should oral glucose tolerance test become a standard of care? 1863 90

A 50-year-old woman with a 4-year history of type 2 diabetes history was treated with nateglinide (270 mg/day) and metformin hydrochloride (500 mg/day). The recipient was her 55-year-old husband whose diagnoses were liver cirrhosis with type C chronic hepatitis (Child-Pugh C, score, 10; Model for End-Stage Liver Disease: 15), hepatocellular carcinoma (solitary, 2 cm), and hepatic encephalopathy. Her body weight was 50 kg and body mass index 21.6 kg/m2. Laboratory examinations showed fasting blood glucose of 110 mg/dL and hemoglobin A1c (HbA1c) of 6.6% upon admission. Right liver lobectomy was performed of a 563-g graft. Operative time was 253 minutes and blood loss 50 mL. She was discharged at postoperative day 9 without any complications. We changed nateglinide and metformin hydrochloride to insulin aspart or human insulin after admission. Blood glucose level was strictly controlled using a sliding scale of insulin. She received regular glucose check-ups at our outpatient clinic after discharge. She stopped using insulin and returned to nateglinide and metformin hydrochloride on postoperative day 25. Her blood glucose level was 80 to 150 mg/dL and HbA1c was 5.8% at 5 months after surgery. This type 2 diabetic living liver donor showed good control of the postoperative glucose level without exacerbation or diabetic complications.
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PMID:Successful management of a type 2 diabetic donor in living-donor liver transplantation: a case report. 1892 79

To investigate how liver disease alter the serum glycated proteins as markers of diabetic control, we studied serum GA, A1c and especially GA/A1c ratio in 255 patients having over 35IU/L in ALT(transaminase) compared with those of 829 type 2 diabetes mellitus (DM) in cross sectional manner. 255 patients with liver diseases were divided into 69 patients with biopsy proven liver cirrhosis (LC), 66 patients with chronic hepatitis(CH) and 120 patients with fatty liver(FL) diagnosed by abdominal echography. The mean GA/A1c ratio (+/-SD) was significantly higher (p<0.0001) in LC group(3.71+/-1.03) than the other groups (3.03+/-0.45 for CH, 3.05+/-0.42 for DM), while the mean GA/A1c ratio in FL group was significantly lower(2.74+/-0.31) (p<0.0001)) than that of DM groups. In LC group the GA/A1c ratio increased significantly depending upon serum albumin and/or platelet reductions. The GA/A1c ratio was significantly correlated with the other laboratory data such as serum albumin, cholinesterase, total cholesterol levels and weakly correlated with serum hemoglobin level. We also followed the serum levels of GA and A1c and the GA/A1c ratio during about 13 months (5 times blood collections) in 18 patients enrolled in this study. Resultantly the coefficient of variation of GA/A1c ratio was the smaller than the others(GA, A1c). The ROC curve of GA/A1c ratio for LC versus FL group was the most reliable between four groups and the cut-off value for LC versus FL was 2.94. Theses results suggest that GA/A1c ratio could be an useful marker for different diagnosis when facing patients with abnormal serum ALT level in a clinical setting.
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PMID:[Relationship between glycated albumin (GA) and glycated hemoglobin (A1c) in 255 patients with liver diseases using cross-sectional laboratory data]. 1897 54

Insulin resistance and type 2 diabetes are associated with hepatitis C virus infection. A wealth of clinical and experimental data suggests that the virus is directly interfering with the insulin signalling in hepatocytes. In the case of at least one viral genotype (the type 3a), insulin resistance seems to be directly mediated by the downregulation of the peroxisome proliferator-activated receptor gamma. Whether and how this interaction may be manipulated pharmacologically, in order to improve the responsiveness to antivirals of insulin resistant chronic hepatitis C, patients remain to be fully explored.
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PMID:Peroxisome proliferator-activated receptors and hepatitis C virus-induced insulin resistance. 1913 31

This review focuses on the relationship between hepatitis C virus (HCV) infection and glucose metabolism derangements. Cross-sectional and longitudinal studies have shown that the chronic HCV infection is associated with an increased risk of developing insulin resistance (IR) and type 2 diabetes (T2D). The direct effect of HCV on the insulin signaling has been analyzed in experimental models. Although currently available data should be considered as preliminary, HCV seems to affect glucose metabolism via mechanisms that involve cellular pathways that have been implicated in the host innate immune response. IR and T2D not only accelerate the histological and clinical progression of chronic hepatitis C, but also reduce the early and sustained virological response to interferon-alpha-based therapy. Thus, a detailed knowledge of the mechanisms underlying the HCV-associated glucose metabolism derangements is warranted, in order to improve the clinical management of chronic hepatitis C patients.
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PMID:Hepatitis C virus and type 2 diabetes. 1934 Aug 95

In chronic hepatitis C, insulin resistance (IR) and type 2 diabetes mellitus (DM) are more prevalent than in healthy controls or in chronic hepatitis B patients. HCV infection promotes IR mainly through increased TNF-a and cytokine suppressor (SOCS-3) production. Both events inhibit insulin receptor and IRS-1 (insulin receptor substrate) tyrosine phosphorylation. Hepatic steatosis is also 2.5 fold more frequent in hepatitis C virus (HCV) infected patients as compared to the general population. Metabolic factors play a crucial role in the etiology of hepatic steatosis genotype non-3 related, which are also the genotypes with a greater association to IR. However, genotype 3, and particularly 3a, has a greater direct steatogenic capacity, and consequently, in those patients, the association with metabolic factors is weaker. Instead, in genotype 3, steatosis associates with viral factors like viral load. Those metabolic factors influence not only the natural history of HCV infection, as well as associate to an accelerated hepatic fibrosis progression, to a worse prognosis when hepatic cirrhosis is present, namely an increased risk of hepatocellular carcinoma, and to a lower sustained viral response rate. On the other hand, in patients who achieve viral eradication, IR and hepatic steatosis may regress, and return if viral infection recurs, which once again indicates an intrinsic steatosis and IR promoter action by HCV.
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PMID:Insulin resistance and steatosis in chronic hepatitis C. 1938 Nov 27

Non-alcoholic fatty liver disease (NAFLD) and chronic hepatitis C virus (HCV) infection are major causes of liver disease frequently described in outpatient patients with glucose abnormalities. Hyperferritinemia, which suggests that iron overload plays a decisive role in the pathophysiology of insulin resistance and hyperglycemia, is a common finding in both disorders. However, the role of the hepatic iron deposition differs from one to the other. In NAFLD, a moderate liver iron accumulation has been observed and molecular mechanisms, including the downregulation of the liver iron exporter ferroportin-1, have been described. Iron overload will enhance intrahepatic oxidative stress that promotes hepatic fibrosis, interfere with insulin signalling at various levels and may hamper hepatic insulin extraction. Therefore, liver fibrosis, hyperglycemia and hyperinsulinemia will lead to increased levels of insulin resistance and the development of glucose abnormalities. Furthermore, iron depletion by phlebotomy removes liver iron content and reduces serum glucose and insulin resistance in NAFLD patients. Therefore, it seems that iron overload participates in those glucose abnormalities associated with NAFLD. Concerning chronic HCV infection, it has been classically assumed that iron overload contributes to insulin resistance associated with virus infection. However, recent evidence argues against the presence of iron overload in these patients and points to inflammation associated with diabetes as the main contributor to the elevated ferritin levels. Therefore, glucose abnormalities, and specially type 2 diabetes, should be taken into account when evaluating serum ferritin levels in patients with HCV infection.
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PMID:Glucose abnormalities in non-alcoholic fatty liver disease and chronic hepatitis C virus infection: the role of iron overload. 1944 65

We evaluated the prevalence and the risk factors for gallstone disease in patients with chronic hepatitis C infection. We investigated 453 consecutively admitted patients with chronic infection with hepatitis C virus (HCV) (cirrhosis excluded) and 879 patients without liver disease (October 2006-April 2007). Gallstone disease was diagnosed if gallstones were present at ultrasonography or if there had been a previous cholecystectomy. Variables evaluated were age, gender, gallstone heredity, body mass index, waist circumference, parity, serum lipids, fatty liver, arterial hypertension, diabetes mellitus and metabolic syndrome (International Diabetes Federation criteria). Informed consent was obtained from all patients. We found that 88 of 453 (19%) patients with chronic HCV hepatitis (age 50.1 +/- 11.7 years) and 153 of 879 (17%) controls (age 60.6 +/- 12.6 years) had gallstone disease (GD). Abdominal obesity (OR = 2.108, 95% CI 1.287-3.452) and steatosis (OR = 3.699, 95% CI 2.277-6.008) were risk factors for GD in HCV patients. Gallstone heredity, dyslipidaemia, type 2 diabetes mellitus and metabolic syndrome increased the risk for GD in controls vs HCV patients. Our study shows that even HCV patients with chronic hepatitis but not cirrhosis have an increased prevalence of gallstones. Compared with controls, gallstones are present in HCV patients at a younger age and are associated with central obesity and liver steatosis, but not with gallstone heredity, dyslipidaemia, diabetes mellitus or metabolic syndrome. Although we could not establish a temporal relationship, the association between HCV infection and gall stone disease is real and appears to be causally linked, at least in predisposed individuals (obese and with liver steatosis).
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PMID:Hepatitis C virus infection is a risk factor for gallstone disease: a prospective hospital-based study of patients with chronic viral C hepatitis. 1948 79

Lymphangioleiomyomatosis (LAM), is an uncommon, progressive, cystic lung disease which predominantly affects young women of childbearing age. Our patient is a 36-year-old female diagnosed with LAM by open lung biopsy in January 1995. Her past history included a spontaneous left-sided pneumothorax in June 1994 which required chest tube for resolution. The last episode occurred on October. 2002. A chest CT scan at this time presented multiple cystic lesions. Followup with pulmonary function studies every 6 months since 1997 have shown a decrease in force expiratory volume in 1 second (%FEV 1) from 100% to an actual of 53%. The force volume capacity (%FVC) decreased from 105% to 85%, with a FEV1/FVC ratio of 49%. The patient's past medical history also includes a Wilm's tumor, resulting in left nephrectomy at age 6, left adnexal abscess requiring surgery in 2002, complicated with iliac and femoral vein thrombophlebitis and left iliac artery stenosis. A small pericardial effusion occurred in 2003, which resolved spontaneously. Osteoporosis of the spine was documented with a T score of -4.9. A hysterectomy was performed during her first gestation in 1992 due to the presence of ruptured ovarian cysts. She required blood transfusions during this intervention, acquiring chronic hepatitis C infection. She has two brothers and three sisters. One brother and one sister have bronchial asthma; her paternal grandfather had stomach cancer and her grandmother was diagnosed with type II diabetes mellitus. No family history of pulmonary disorders was identified. The chest CT scan showeds many small lung cavities compatible with moderate LAM. Our patient is one of three patients living in Puerto Rico who is currently followed by the NIH sponsored LAM registry.
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PMID:A clinico-pathologic presentation of a 23-year old-female with lymphangioleiomyomatosis and Wilm's tumor. 1961 May 58

The paper presents the results of the statistical processing that comprises the calculation of the basic numerical statistics, the analysis of an association of signs, the estimation of Pearson's paired correlation coefficient, and the testing of its statistical significance, the construction of logit models, and the regression analysis of 350 case histories of inpatients with nephrotuberculosis treated at Samara Regional Tuberculosis Hospital One in 2002-2006. The results of the study proved it possible to simulate a clinical diagnosis for urinary tract tuberculosis. It can be simulated using the following indices: the presence of chronic renal failure, urinary leukocytes, blood urea, excretory urographic data, the electrocardiographic signs of essential hypertension, and the presence of non-tuberculous comorbidity (type 2 diabetes mellitus, gastric peptic ulcer, chronic hepatitis).
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PMID:[Diagnosis simulation in urinary tract tuberculosis]. 1969 54


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