GAD 65 and IA2 autoantibodies in HCV seropositive schistosomal liver disease

Several immunological abnormalities characterize patients with schistosomal liver disease. Besides, hepatitis C virus [HCV] is known to induce extrahepatic autoimmune manifestations. The aim of this study was to determine if there is an increased risk in patients with schistosomiasis and associated HCV infection to have or to develop type 1 diabetes. Subjects and In this study, 25 untreated HCV seropositive together with 17 HCV seronegative schistosomal patients were examined to determine whether HCV seropositive compared to seronegative schistosomal patients, are at an increased risk to have associated type 1 diabetes by testing their sera for GAD65-abs and IA2-abs [levels >1 U/ml and >/= 0.75U/ml, respectively, were considered positive]. In HCV seropositive patients 1/25 [4%] had positive GAD65-abs, while 3/25 [12%] were positive for IA2-abs; one of them was the same patient positive for GAD65-abs. In HCV seronegative patients, none was positive for either GAD65-abs or IA2-abs. The mean value of GAD65-abs was nonsignificantly higher in seropositive compared to seronegative patients [0.36 +/- 0.66 and 0.21 +/- 0.15 U/ml, respectively], while the mean value of IA2-abs was significantly higher in seropositive than seronegative patients [0.41 +/- 0.28 and 0.23 +/- 0.08 U/ml, respectively; p =0.006]. The patients positive for abs were suffering from type 1 diabetes and were treated by insulin but none of them received any specific therapy for the associated HCV infection. Conclusions: The study concluded that HCV seropositive patients with schistosomal liver disease have increased levels of GAD65-abs and IA2-abs. As interferon therapy can precipitate type 1 diabetes in prone subjects, the risk of the disease should be considered, whenever interferon therapy is indicated

Hyperhomocysteinemia in cirrhosis is not a cardiovascular risk

The study aimed to evaluate and highlight the relationship between the serum Hcy concertrations in cirrhotic patients and some important risk factors for atherosclerotic cardiovascular disease, and to relate the findings with the severity of liver dysfunction. Subjects and A total of25 male patients with liver cirrhosis [mean age +/- SD= 38.16 +/- 9.89 years] and 10 age and sex matched healthy controle [mean age +/- SD= 34.80 +/- 8.53 years] were included in the study. Biochemical evaluation of serum Hcy, plasma PAI-1 antigen and vWF: antigen levels. HOMA-IR as well as serum lipid pattern were performed for patients and controls. A significant increase in mean serum Hcy levels was found in cirrhotic patients compared to controls, [24.12 +/- 17.65 versus 11.62 +/- 2.67 micro mol/L; P=0.002], and the increase was directly related to the severity of liver disease [r=0.887; P=0.001]. The mean plasma levels of PAI-1 and vWF: antigens levels were significantly higher in patients than controls [60.24 +/- 43.63 versus 29.50 +/- 9.33 ng/ml; P=0.002 and 4.67 +/- 0.92 versus 2.04 +/- 0.11 IU/ml; P<0.001 respectively] but did not correlate with other parameters. The fasting blood glucose, serum insulin and HOMA-IR were significantly elevated in cirrhotic patients compared to controls [5.29 +/- 1.34 versus 4.27 +/- 0.88 mmol/L; P=0.01, 15.09 +/- 9.59 versus 8.92 +/- 2.94 micro IU/ml; P=0.007 and 3.94 +/- 2.45 versus 1.71 +/- 0.65; P<0.001 respectively]. The serum lipids in patients revealed significant decrease in TC, TG, and HDL-C while the decrease was statistically nonsignificant in LDL-C in patients compared to controls [127.00 +/- 29.89 versus 174.73 +/- 19.00 mg/dl. 68.60 +/- 26.12 versus 101.30 +/- 9.49 mg/dl, 26.40 +/- 11.39 versus 68.41 +/- 3.43 mg/dl; P< 0.001 and 83.53 +/- 26.86 versus 86.06 +/- 18.99 mg/dl; P=0.756 respectively]. Conclusions: Patients with liver cirrhosis have elevted serum Hcy concentrations which correlated with the degree of liver disease. However, they are protected from the adverse effects of hyperhomocysteinemia on the cardiovascular system by many mechanisms; increased serum NO may be one of them. The possible role of hyperhomocysteinemia on liver fibrogenesis is proposed for further study in the future

Osteoporotic changes in Egyptian cirrhotic patients

Aim: Hepatic osteodystrophy occurs in most patients with chronic liver disease. Subjects and In this study, bone density, measured by dual energy X-ray absorptiometry [DEXA], and some biochemical markers of bone turnover were studied in 30 Egyptian schistosomal patients classified equally into 3 groups according to the Child-Pugh score of severity of liver disease. Patients showed significant reduction of BMD in both lumbar spine and femoral neck [LS: -2.87 +/- 1.39; FN: -0.54 +/- 1.13, p< 0.001]. Osteoporosis was found in 56.7% of patients. Urinary D-Pyr/cr, as a marker of bone resorption, showed marked significant increase in Child B and C patients [p<0.001], while serum B-AP and serum PICP, as markers of bone formation, showed less changes. Serum B-AP was significantly increased in the patient group [p<0.05], while serum PICP was insignificantly decreased in patients as compared to controls. The rate of bone loss, determined by the ratio of urinary D-Pyr/cr to PICP, was increased in Child A, B, and C patients. Serum testosterone was significantly decreased in both Child B and C patients and was markedly decreased in the whole patient group [p<0.001]. Conclusions: These results suggest that increased bone resorption is the predominant cause of hepatic osteodystrophy and its risk increases with the severity of liver disease. It also provides bone biomarkers as useful alternatives to bone biopsy in evaluating hepatic bone changes

Altered serum leptin and lipoproteins pattern in Egyptian patients with liver cirrhosis

Aim: Leptin is implicated in the regulation of several body functions including liver metabolism, in addition, the liver plays a key role in serum lipoproteins synthesis and metabolism. This study aimed to assess serum leptin levels, serum lipids and lipoproteins pattern in Egyptian patients with liver cirrhosis, and to relate the findings with the body composition and the severity of liver disease. Subjects and Thirty male patients with liver cirrhosis, together with 15 age and sex-matched control subjects were enrolled in the study. Clinical and biochemical investigations included: clinical examination, ultrasonic scanning and /or liver biopsy, liver function profile, viral markers, measurement of serum leptin, serum lipids, and serum apolipoproteins B and A-1. Sixteen patients were positive for hepatitis C antibodies, 9 were positive for hepatitis B surface antigen, and 5 were positive for both viral markers, while schistosomal hepatic fibrosis was present in 22 patients. Serum leptin was significantly decreased in patients compared to controls [mean +/- SD= 1.34 +/- 0.16 and 3.94 +/- 0.55 ng/ ml respectively; P< 0.05], it correlated directly with BMI in both patients and controls [r= 0.60; P< 0.01 and r= 0.337; P< 0.05 respectively] and with the triceps skinfold thickness in both groups [r= 0.384 and 0.376 respectively; P< 0.05], but did not correlate with the severity of liver disease. Serum lipids showed a significant decreased levels in both TC and TG in cirrhotic patients compared to controls [mean +/- SD = 172.00 +/- 17.24 and 86.60 +/- 64.51 mg/dl in patients versus 192.27 +/- 32.33 and 136.13 +/- 70.86 mg/dl in controls; P < 0.05], serum HDL-C and LDL-C levels showed non significant differences between the two groups, while apo A-1 and apo B were significantly lower in patients than controls [mean +/- SD= 130.84 +/- 40.64 and 38.37 +/- 15.34 mg/dl in patients versus 197.00 +/- 42.05 and 53.39 +/- 3.79 mg/dl in controls; P< 0.001]. Serum lipids did not correlate with the severity of liver disease, however, apo A-1 correlated directly with both prothrombin activity and serum albumin [r= 0.368 and 0.372 respectively; P< 0.05], and inversely with both ALT and AST [r= -0.472; P< 0.01 and r= -0.448; P< 0.05 respectively]. Conclusions: It was concluded that in Egyptian patients with liver cirrhosis, serum leptin level was decreased and did not correlate with serum lipids nor with the severity of liver disease, however it correlated directly with BMI and triceps skinfold thickness in both patients and controls. Serum TC, TG, apo B, and apo A-1 levels were decreased significantly in patients than controls. Although no correlation was found between serum lipids and the degree of liver function, yet, apo A-1 correlated directly with both prothrombin activity and serum albumin, thus it could be regarded as a good parameter for synthetic liver function