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)

Sialadenosis (sialosis) has been associated most often with alcoholic liver disease and alcoholic cirrhosis, but a number of nutritional deficiencies, diabetes, and bulimia have also been reported to result in sialadenosis. The aim of this study was to determine the prevalence of sialadenosis in patients with advanced liver disease. Patients in the study group consisted of 300 candidates for liver transplantation. Types of liver disease in subjects with clinical evidence of sialadenosis were compared with diagnoses in cases who had no manifestations of sialadenosis. The data were analyzed for significant association. Sialadenosis was found in 28 of the 300 subjects (9.3%). Among these 28 cases, 11 (39.3%) had alcoholic cirrhosis. The remaining 17 (60.7%) had eight other types of liver disease. There was no significant association between sialadenosis and alcoholic cirrhosis (P = 0.389). These findings suggest that both alcoholic and non-alcoholic cirrhosis may lead to the development of sialadenosis. Advanced liver disease is accompanied by multiple nutritional deficiencies which may be exacerbated by alcohol. Similar metabolic abnormalities may occur in patients with diabetes or bulimia. Malnutrition has been associated with autonomic neuropathy, the pathogenic mechanism that has been proposed for sialadenosis.
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PMID:Sialadenosis in patients with advanced liver disease. 1964 42

We experienced two autopsy cases of fulminant sepsis due to anaerobes. Case 1: A 67-year-old female with uncontrolled diabetes mellitus (DM) was admitted to a hospital because of sudden onset of mid-abdominal pain. She was diagnosed with infectious colitis and given a laxative and an enema. However, 9h later, her blood pressure suddenly dropped with metabolic acidosis, and she died 20 h after admission. Autopsy revealed massive pneumohemia and a dark-brown colored mucosal surface from the terminal ileum to the sigmoid colon. Histopathological findings were compatible with marginal ischemic colitis. Anaerobes were positive in blood culture. Case 2: A 53-year-old male with alcoholic liver cirrhosis (LC) was found dead in his room. He had been alive 24 h before the discovery, but postmortem changes appeared to accelerate more rapidly than usual cases. Autopsy revealed severe LC with muddy ascites and many Gram-negative rods in several organs. These cases suggest the possibility of sepsis as causes of death, especially in immuno-compromised hosts when unexplained putrefactive changes are seen on forensic autopsy.
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PMID:Fulminant sepsis due to anaerobic bacterial infection in immuno-compromised state. 1964 68

Longer survival for orthotopic liver transplantation (OLT) patients over the last decade has focused emphasis on the metabolic complications that contribute to patient morbidity and mortality. The aim of our study was to analyze the prevalence of the metabolic syndrome (MS) and other risk factors after OLT among our patients at 1 year follow-up. From 2001 to 2008, we performed OLT in 210 patients with 62 exclusions leaving 148 patients for the study. We recorded age, gender, liver disease, smoking status, pre- and post-OLT body mass index, pre- and post-OLT arterial blood pressure, pre- and post-OLT fasting blood glucose, pre- and post-OLT high-density lipoproteins and triglycerides, family history of diabetes, hepatitis B and C virus status, immunosuppressive therapy, and corticosteroid bolus for rejection episodes. The MS was defined according to modified ATP III criteria. At month 12 after OLT, 29/148 patients (19.6%) developed the MS. The associated factors were obesity and hyperlipidemia pre-OLT, familial and personal history of diabetes as well as alcoholic cirrhosis. By multivariate analysis, pre-OLT body mass index (odds ratio, 3.7 [1.3-10.5]) and pre-OLT diabetes (odds ratio, 2.9 [1.1-7.9]) were independent risk factors.
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PMID:Risk of development of the metabolic syndrome after orthotopic liver transplantation. 2030 18

Chronic hepatitis C virus infection is a well-recognized risk factor for occurrence of hepatocellular carcinoma (HCC). In Europe, Oceania and America, chronic hepatitis C and alcoholic cirrhosis are the main risk factors for HCC. In Latin America, a few retrospective and one prospective study have also shown the predominant role played by hepatitis C in this setting. Furthermore, the incidence of HCC has been increasing in industrialized countries in the last decades; partially as a consequence of the increase in HCV-related cirrhosis (as the long-term sequel of the peak of infections occurring 2-4 decades ago). The main risk factor for HCC development in patients with hepatitis C is the presence of cirrhosis. Among patients with hepatitis C and cirrhosis, the annual incidence rate of HCC ranges between 1-8%, being higher in Japan (4-8%) intermediate in Italy (2-4%) and lower in USA (1.4%). Some studies have also found that HCC may be the first complication to develop and the more frequent cause of death in the compensated HCV-associated cirrhosis. Other risk factors for HCC occurrence are older age at infection, male gender, decreased platelet count, esophageal varices, presence of porphyria cutanea tarda, liver steatosis or diabetes, infection with genotype 1b, coinfection with hepatitis B virus or with HIV and chronic alcoholism. Many studies and also meta-analysis have reported that antiviral therapy based on interferon may reduce the incidence of HCC in chronic hepatitis C, especially in patients with sustained virologic response. Patients with HCV-related cirrhosis should undergo surveillance for HCC.
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PMID:Hepatitis C and hepatocellular carcinoma. 2071 8

A 53-year-old man presented with high fever and urinary retention. The patient had diabetes, and alcoholic liver cirrhosis. Clinical diagnosis was prostatic abscess by magnetic resonance imaging (MRI), and we performed anti-biotic therapy. Because there was no improvement of symptoms, we performed percutaneous cystostomy and transurethral resection (TUR) of the abscess walls. Drainage by TUR is suggested to be a useful strategy for prostatic abscess.
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PMID:[A case of prostatic abscess]. 2127 12

Ureteral obstruction may develop in immunocompromised patients with an Aspergillus fungal infection. Infections can progress to invasive aspergillosis, which is highly lethal. We report a case of a 56-year-old man with alcoholic cirrhosis of the liver and diabetes. He had ureteral aspergilloma, discovered as a saprophytic whitish mass. It was treated by ureteroscopic removal, however, he refused antifungal treatment. His condition progressed to invasive aspergillosis, and died from sepsis and hepatorenal syndrome.
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PMID:Invasive aspergillosis arising from ureteral aspergilloma. 2178 56

Apolipoprotein C3 (ApoC3) is synthesized in liver so that levels or isoform distributions may constitute indicators of liver pathogenesis. The glycoforms of intact protein ApoC3 in serum or plasma can be readily analyzed by matrix-assisted laser desorption/ionization-time of flight mass spectrometry after a one-step extraction using a C4 reverse-phase ZipTip. Glycoform distributions were sensitive to severe systemic diseases such as sepsis or liver diseases such as chronic hepatitis C and alcoholic liver cirrhosis. Glycoisoform distributions were also altered in persons with elevated body mass index and were corrected to normal distribution by metformin, a common drug used for diabetes therapy. This simple method may offer an approach to analysis of health and the mechanism of drug therapies.
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PMID:Glycoproteins and glycosylation: apolipoprotein c3 glycoforms by top-down maldi-tof mass spectrometry. 2290 14

Residual hepatic functional reserve in cirrhotic patients is generally evaluated by a multivariate scoring system (Child-Pugh classification), which includes serum albumin levels as a variable. However, several patients show discrepancies between serum albumin levels and the progression of liver fibrosis, especially those with alcoholic cirrhosis. To assess whether hepatic capacity of protein synthesis varies with the etiology of cirrhosis, serum albumin and cholinesterase levels, and prothrombin time were compared between alcoholic cirrhosis and hepatitis C virus (HCV)-related cirrhosis. To minimize the influence of malnutrition and extrahepatic platelet destruction, patients with hepatocellular carcinoma, uncontrolled diabetes, appetite loss and/or splenal longitudinal size >15 cm were excluded. The patients with compensated liver cirrhosis were divided into three groups as follows: alcohol(+)/HCV(+) (alcohol + HCV group; n=31), alcohol(-)/HCV(+) (HCV group; n=31) and alcohol(+)/HCV(-) (alcohol group; n=27). These groups were adjusted with respect to age, gender, body mass index and platelet count. Serum albumin levels in the alcohol group were significantly higher than those in the HCV group, with a difference of approximately 0.5 g/dl in every class of platelet count. The correlation of the alcohol + HCV group was intermediate between the alcohol and HCV groups. On the other hand, the correlations between serum cholinesterase levels and platelet counts were similar among the three groups. The prothrombin time was also comparable among the groups. Accordingly, serum albumin levels were higher in patients with alcoholic cirrhosis and alcohol consumption should be carefully considered when evaluating hepatic functional reserve.
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PMID:Serum albumin is present at higher levels in alcoholic liver cirrhosis as compared to HCV-related cirrhosis. 2296 47

Silibinin is the most active component of a complex of flavonoids -silymarin contained in fruit milk thistle (Sylibum marianum). Its mechanism of action is complex and highly beneficial in protecting hepatocytes. On the one hand this compound blocks the penetration of various toxins (for example amanitin) into the hepatocytes not allowing in this way for the cell death and on the other hand, it prevents apoptosis through intracellular. It protects the liver from oxidative intracellular free radicals by increasing the activity of enzyme superoxide dismutase and peroxidase, as well as by increasing the concentration of glutathione and the activity of the peroxidase. Silibinin strengthens and stabilizes the cell membranes, inhibits the synthesis of prostaglandins associated with the lipid peroxidation and promotes regeneration of liver through the stimulation of protein synthesis and effect on the production of new hepatocytes. A particularly interesting topic from the perspective of a toxicologist is the application of silibinin in Amanita phalloides poisoning. Clinical trials conducted in this respect are very encouraging. The other beneficial application of silibinin is in therapy of the alcoholic liver cirrhosis. The evidence shows that the use of silymarin leads to a significant reduction in liver-related mortality and even reduction in the number of patients with encephalopathy in the course of the disease. Application of silibinin goes beyond liver disease and expands in the direction of cancer and even diabetes. What is interesting is the fact, that the substance of herbal origin occurring in the environment is so strong, favorable, beneficial and multidirectional. Science has contributed to improving the bioavailability of silibinin thus making it more effective.
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PMID:[Silibinin and its hepatoprotective action from the perspective of a toxicologist]. 2324 23

Unsafe use of alcohol results in approximately 2.5 million deaths worldwide, with cirrhosis contributing to 16.6% of reported deaths. Serum insulin levels are often elevated in alcoholism and may result in diabetes, which is why alcoholic liver disease and diabetes often are present together. Because there is a sizable population with these diseases alone or in combination, the purpose of this study was to determine whether transporter expression in human liver is affected by alcoholic cirrhosis, diabetes, and alcoholic cirrhosis coexisting with diabetes. Transporters aid in hepatobiliary excretion of many drugs and toxic chemicals and can be determinants of drug-induced liver injury. Drug transporter expression and transcription factor-relative mRNA and protein expression in normal, diabetic, cirrhotic, and cirrhosis with diabetes human livers were quantified. Cirrhosis significantly increased ABCC4, 5, ABCG2, and solute carrier organic anion (SLCO) 2B1 mRNA expression and decreased SLCO1B3 mRNA expression in the liver. ABCC1, 3-5, and ABCG2 protein expression was also upregulated by alcoholic cirrhosis. ABCC3-5 and ABCG2 protein expression was also upregulated in diabetic cirrhosis. Cirrhosis increased nuclear factor E2-related factor 2 mRNA expression, whereas it decreased pregnane-X-receptor and farnesoid-X-receptor mRNA expression in comparison with normal livers. Hierarchical cluster analysis indicated that expressions of ABCC2, 3, and 6; SLCO1B1 and 1B3; and ABCC4 and 5 were more closely related in the livers from this cohort. Overall, alcoholic cirrhosis altered transporter expression in human liver.
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PMID:Alcohol cirrhosis alters nuclear receptor and drug transporter expression in human liver. 2346 98


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