Insulin resistance and liver fibrosis progression in patients with chronic hepatitis C virus infection

Hepatitis C virus [HCV] infection can predispose to development of insulin resistance before diabetes occurs. Such a potential link is particularly cogent in light of recent date indicating that diabetes might be associated with increased hepatic fibrosis progression in patients with chronic HCB infection. This study aims to determine the prevalence of insulin resistance in non-diabetic patients with chronic hepatitis C and its relation to liver fibrosis. This study included a cohort of 38 patients with chronic liver diseases. They were subdivided into two groups: chronic hepatitis C [CHC] with elevated liver enzymes and CHC with normal liver enzymes. Twelve age- and sex-matched healthy subjects were considered as the control group. The cohort was subjected to careful history and complete examination stressing upon the signs and symptoms of chronic liver diseases. Investigations include liver function test, viral markers [anti-HCV antibodies and polymerase chain reaction [PCR] for HCV], serum fasting glucose, serum fasting insulin and homeostasis model assessment [HOMA], liver biopsy and abdominal ultrasound. Liver fibrosis was found to be considerably more severe among HCV patients elevated serum transaminases levels. No correlation between viral load and hepatic fibrosis in HCB-infected patients was found. Insulin resistance was present in HCV-infected cases compared with the control group and it correlated with liver fibrosis positively. The present data support the hypothesis that insulin resistance may increase the rate of fibrosis progression in non-diabetic patients with chronic HCV. Follow-up of hyperinsulinaemia by serial measurements of HOMA test in non-diabetic HCV-infected patients may be a biochemical indicator for progression of liver fibrosis

Spontaneous bacterial peritonitis: clinico-epidemiological and microbiological study

Spontaneous bacterial peritonitis [SBP] is a frequent severe and potentially life-threatening complication of cirrhotic patients with ascites. The clinical presentation of SBP depends on the stage at which the infection is diagnosed. In early stages, most patients are asymptomatic or present with insidious, non specific symptoms. As the disease progresses, patients show signs and symptoms of peritoneal infection. To determine the prevalent pathogens responsible for SBP in our locality and their sensitivity pattern, to test the efficiency of different culture techniques in microbial isolation, and to study the diagnostic predictors of such cases. Two hundred fifteen adults with cirrhotic ascites consecutively admitted to Tropical Medicine Unit Mansoura University Hospital were screened for SBP. One hundred eight SBP episodes from 92 adult patients were compared to 88 cirrhotic ascites patients cross-matched with age and sex without SBP. Diagnosis of cirrhosis was based on clinical biochemical radiological and/or histo-pathological data. Ascitic fluid was subjected to cytological biochemical examination and culture on both conventional and blood culture bottles at the bedside for bacterial identification and antimicrobial susceptibility testing. Diagnosis of SBP and its variants were made depending on ascitic fluid poly-morphnuclear count >/= 250 cell/ mm[3] and/or monomicrobial growth in ascitic fluid culture without evidence of an infra-abdominal surgically treatable source of infection, and no recent use of antibiotics. A total of 432 diagnostic paracentesis were performed in 215 cirrhotic patients with ascites. The prevalence of SBP was 25.02%. History of previous episode of SBP or history of paracentesis were significantly more frequent in SBP patients [P=0.000 and P=0.001] respectively also, Abdominal wall edema and redness [cellulitis], presence of ascetic fluid with numerous fine internal hyper-echoic particulates by ultrasonography and the aspiration of slightly turbid ascites were significantly more frequent in SBP patients [P= 0.01, P=0.031 and P=0.035] respectively. Ascitic fluid protein levels and serum albumin levels were significantly lower and serum creatinine levels were significantly higher in SBP patients. [P=0.009, P=0.03, and P= 0.003] respectively. Applying the model of logistic regression analysis between SBP and Non SBP clinical and laboratory data revealed that; previous SBP episode, low ascitic fluid protein levels, high serum creatinine and low serum albumin levels were significant predictors of SBP [P-0.000]. Fourty-nine [45.37%] episodes of SBP were detected by the conventional culture compared to 79 [73.15%] by modified technique with a significant P value <0.001. Gram-negative bacteria were the cause of SBP in 46 [58.23%] culture positive episodes while Gram-positive bacteria were the isolated organisms in 33 cases [41.77%]. Escherichia coli and Staphylococcus aureus were the most commonly detected organisms in 40 [50.63%] and 26 [32.91%] cases respectively. In this study, 31.65% of cultures were highly sensitive to Levofloxacin, 29.11% were sensitive to Cefotaxime, 20.25% were sensitive to Amoxicillin-Clavulanic acid, 18.99% were sensitive to Meropenem, 17.72% were sensitive to Ciprofloxacin and 15.19% were sensitive to Ceftazidime. On the other hand, antibiotic resistant rates to Ciprofloxacin were 25.32%, 24.05% to Ceftazidime and 21.52% to Cefotaxime. Previous SBP episode, low ascetic fluid protein levels, high serum creatinine, and low serum albumin levels, all had a significant prediction of SBP. Beside cytological and biochemical examination, culture of ascitic fluid in blood culture bottles at bedside increases the sensitivity of SBP detection and must be a routine in every hospitalized patient with cirrhotic ascites. Gram-negative organisms still, the prevalent microorganisms causing SBP but there is a significant recent increase in Gram-posittue pathogen with emergence of maltidrug resistance especially for Ciprofloxacin, Ceftazidime and Cefotaxime. These recent changes may have an impact on guidelines for management and treatment of SBP in oar locality

Hepatitis C virus Infection and Diabetic microvascular complications

The microvascular complications are the important cause of mortality and morbidity of either type 1 or 2 DM. Great efforts have been made to recognize the possible susceptibility or etiologic factors of these complications; whether genetic or environmental. Hepatitis C virus infection is another prevalent problem in our community. The present work aimed to study the possible impact, if any of HCV infection on microvascular complications. A total 70 diabetic patients 17 type 1 and 53 type 2, were included [20 males and 50 females] with age ranging from 13 to 72 years and 30 healthy volunteers with matched age and sex were taken as a control group. Complete history taking and full clinical examination were done. Laboratory work up was done for patients and control including urinalysis, blood sugar, serum creatinine, urinary albumin excretion, lipogram, liver function tests, HbAlc and HCV antibodies. Fundus examination was done for patients and control. Diabetics were found to have a prevalence rate of HCV infection of 32%. Prevalence of microvascular complication, nephropathy, retinopathy and neuropathy were found to be relatively higher in diabetics with HCV infection. Advanced grades of microvascular complication were more prevalent in HCV-positive diabetics. It was concluded that HCV infection is possibly a potential aggravating factor for microvascualr complications