The importance of increasing the number of gastric biopsies in the diagnosis of Helicobacter pylori.

BACKGROUND/AIMS: The role of Helicobacter pylori in various gastroduodenal diseases is universally accepted. In this study, we aimed to determine the proper number and sites of the gastric biopsies in order to achieve the highest diagnostic yield through the use of a urease test and histopathology. We also compared the histological findings encountered in patients who had Helicobacter pylori (H. pylori) colonization. METHODOLOGY: Fifty patients referred for upper gastrointestinal endoscopy for dyspeptic complaints were included in the study. Our mapping protocol included 2 biopsies from antrum and 2 biopsies from corpus. We obtained 2 biopsies from each biopsy site for urease test and histopathological assessment. Golden standard positivity for the presence of H. pylori colonization was defined as concomitantly positive urease test and histologically detected bacteria found at the same biopsy site. RESULTS: Forty-three patients had H. pylori colonization. Colonization rates of H. pylori, sensitivities of urease testing, and histopathology in 4 biopsy sites were not statistically different. Sensitivity of urease testing was 81.4% for 1 biopsy and 100% for 4 cumulative biopsies. Sensitivities of histological assessment were 93% and 100% for 1 and 4 biopsies, respectively. CONCLUSIONS: Results of this study suggest that 2 biopsies for urease testing and 1 biopsy for histopathology obtained from the antrum or corpus of the stomach were sufficient to obtain the highest statistically significant diagnostic sensitivity.

Histopathological impacts of hepatitis virus infection in hemodialysis patients: should liver biopsy be performed before renal transplantation?

To evaluate the histologic changes in the livers of renal transplant candidates who were infected with hepatitis viruses, we performed a percutaneous liver biopsy in each of 74 regular hemodialysis patients. Forty percent of them were seropositive for the antibody to hepatitis C virus (anti-HCV) whereas 29.7% had anti-HCV and antibody to hepatitis B surface antigen (anti-HBs) concomitantly. Seven (9.5%) were seropositive for only hepatitis B surface antigen HBsAg. Histopathological examination revealed that 30% of patients had chronic active hepatitis (CAH), 11% had chronic persistent hepatitis (CPH), and 3% displayed histopathological evidence of cirrhosis. Eleven of 22 patients with CAH were positive for only anti-HCV, and 2 of 22 were positive for only HBsAg. One patient had HBsAg and anti-HCV together, and 8 of 22 had anti-HBs and anti-HCV concomitantly. None of the anti-HBs positive patients exhibited abnormal histopathological changes. We found no statistically significant difference in histopathological findings between the HBsAg positive and anti-HCV positive patients. As 32 of 74 patients (43%) had some degree of chronic liver disease, we concluded that it is prudent to evaluate liver histology in HBsAg and anti-HCV seropositive renal transplant candidates before transplantation.

Helicobacter pylori infection in haemodialysis patients and renal transplant recipients.

BACKGROUND: It is known that Helicobacter pylori (Hp) plays an important role in gastritis and peptic ulcer disease in the general population. Although dyspeptic complaints are frequent in haemodialysis (HD) patients and renal transplant recipients, there are few reports regarding the prevalence of Hp and its possible effects on this group of patients. This study was performed to examine the prevalence of Hp infection in patients on regular HD treatment and to detect its role in the pathogenesis of dyspepsia in this group of patients. METHODS: Two hundred and one patients with dyspeptic complaints were included in the study. The groups consisted of 47 HD, 54 renal transplant recipients, and 100 non-renal disease patients. Upper gastro-intestinal endoscopies were performed and gastric antral biopsies were obtained for urease test in all patients. RESULTS: Twenty-eight (60%) of the 47 HD and 38 (70%) of the 54 RTR were positive for Hp. Sixty-four (64%) of the 100 patients with various gastrointestinal complaints and known to have no renal dysfunction were positive for Hp. The Hp prevalences among the three groups were not significantly different (P > 0.05). The prevalence of Hp infection did not correlate with the haemodialysis duration nor the post-transplantation duration (P > 0.05). There was no correlation between the prevalence of Hp infection and duration of haemodialysis therapy or time post-transplantation. CONCLUSION: These findings suggest that HD patients are not protected against Hp infection as the Hp prevalences are as high as that for the non-renal disease group. The increased dyspeptic complaints may be partly related to Hp infection.

Congenital hepatic fibrosis associated with cavernous transformation of the portal vein.

BACKGROUND/AIMS: Congenital hepatic fibrosis (CHF), which is one of the fibropolycystic diseases, occurs in various forms. Portal hypertension, a very common clinical feature of this condition, has been attributed to the compression of portal vein radicles in the fibrous bands. We investigated whether there are any other contributing factors in the development of portal hypertension in patients with CHF. METHODOLOGY: A total of 1285 patients with portal hypertension of different etiologies were studied using ultrasonography as the screening test. Forty-seven (including portal vein involvement and/or CHF) of these 1285 patients were prospectively studied to evaluate the etiology of the portal hypertension by portography, abdominal computed tomography, exploratory laparotomy, peritonoscopy, liver biopsy and laboratory tests. The patients with CHF were divided into two groups, according to whether or not they had portal vein involvement. RESULTS: Eleven (0.8%) of the 1285 patients with portal hypertension had CHF, and 41 (3.2%) had cavernous transformation of the portal vein (CTPV), resulting from different or unknown etiologies. Five patients had both pathologies (CTPV and CHF). In the 11 patients with CHF, there was CTPV in 5 patients, Caroli's disease in 2 patients, cholangiocarcinoma in 1 patient, inferior vena caval obstruction in 1 patient, and CHF in only 2 patients. There were statistically significant differences in the age of the CHF patients at clinical onset, the incidence of bleeding from esophageal varices, and laboratory findings between the 2 groups with and without CTPV. Despite a thorough investigation, we could not distinguish any predisposing factor in 25 of the 41 patients with CTPV. The incidence of CTPV was 48% in patients with CHF and 3.2% in patients with portal hypertension. CONCLUSIONS: These results suggest that the association of CTPV with CHF is not coincidental, but that CTPV may be associated with CHF and a new possible factor in portal hypertension, and that it can be a major factor in the manifestation of esophageal bleeding from varices.

Treatment of chronic hepatitis C infection with interferon alpha-2a in a Turkish population.

Recombinant interferon (IFN) alpha has been shown to normalize the aminotransferase levels in approximately half of patients with chronic hepatitis C virus (HCV) infection. Twenty four patients with chronic HCV infection were treated with IFN alpha-2a subcutaneously, three times a week for 6 months. All patients responded to IFN therapy with a decrease of alanine aminotransferase (ALT) level. Thirteen out of 24 cases (54.2%) had normal ALT levels at the end of the sixth month of therapy. However, four of these complete responders (30.8%) relapsed during the 12 month follow-up. Relapse was high in the partial responder group (45.5%). Overall relapse rate was 37.5% at 6 months. HCV genotype II, which is associated with a low response rate to IFN was prevalent (85-87%) in our patient population. This study shows that interferon therapy can be effective in reducing transaminase levels in patients with chronic hepatitis C in a population with a high prevalence of HCV type II. The relapse rate after discontinuation of treatment, however, remains a problem.

Interferon-induced vitiligo in a patient with chronic viral hepatitis C infection.

Vitiligo is an autoimmune disease characterized by depigmentation of the skin due to destruction of melanocytes. Interferons have been used for the treatment of chronic hepatitis C and some malignancies. We report interferon alpha-2a-induced vitiligo in a male patient with chronic active hepatitis C. All skin lesions disappeared completely without requiring therapy after discontinuation of interferon. This case suggests that vitiligo may be developed during interferon therapy as a side effect.

Recombinant alpha-interferon in renal allograft recipients with chronic hepatitis C.

BACKGROUND: Although chronic hepatitis C infection is one of the factors that can lead to morbidity and mortality in renal allograft recipients, treatment procedures have not been well documented. Interferon treatment has been shown to be effective in the normalization of biochemical hepatitis C and in the clearing of hepatitis C virus RNA. However, little is known concerning the efficacy and safety of interferon treatment in renal allograft recipients with chronic hepatitis C. Interferon has also been accused of increasing renal allograft rejection. METHODS: Recombinant alpha-interferon in a dose of 4.5 million units three times per week was given to five renal-allograft recipients with chronic hepatitis C for 6 months. Besides biochemical investigations, liver histopathologies before and after the treatment course were also studied. RESULTS: Interferon treatment was effective in two of the patients, in another two cases renal function deteriorated during the treatment. In the last case ALT increased again after cessation of interferon therapy. CONCLUSION: We conclude that interferon seems to be moderately effective in treating chronic hepatitis C in renal allograft recipients, but a risk of renal functional deterioration and rejection remains.

The "pseudo-cholangiocarcinoma sign" in patients with cavernous transformation of the portal vein and its effect on the serum alkaline phosphatase and bilirubin levels.

OBJECTIVES: The goal of this study was to identify the underlying disorder responsible for portal venous thrombosis and cavernous transformation of the portal vein (CTPV). All patients with this finding underwent a thorough medical examination with intent to determine the cause and biochemical consequences of CTPV. METHODS: During an 8-yr period, a total of 1247 patients with clinical evidence of portal hypertension were examined using ultrasonography. Forty four of these 1247 patients were found to have CTPV. In each case, the finding of CTPV was confirmed by portography using either splenoportography or arterial portography, with digital subtraction angiography. These 44 patients were studied in an effort to determine the etiology of the cavernous transformation. In addition, the specific reason for the increased serum bilirubin and alkaline phosphatase levels in 35 of the 44 cases was evaluated by endoscopic retrograde cholangiopancreatography (ERCP) (34 patients), percutaneous transhepatic cholangiography (one patient), and by CT in 19. The surgical findings in 10 of these 44 patients, who ultimately underwent splenectomy and portal venous decompression for bleeding, were reviewed in light of the ultrasonographic, portographic, and ERCP findings in the same 10 patients. RESULTS: The underlying disorder responsible for cavernous transformation was found to be Behcet's disease in seven patients, chronic liver disease in four, congenital hepatic fibrosis in five, congenital protein C deficiency in one, and a prior abdominal operation for cholelithiasis in one patient. Despite a full clinical, radiological, hematological, and chemical evaluation, no etiology for CTPV was found in the remaining 26 patients. All of these later cases had no indication for liver biopsy or evidence for parenchymal liver disease. In these 26 patients, the serum levels of bilirubin and alkaline phosphatase ranged from mild to moderately increased compared with the moderately to markedly increased levels present in the 18 patients having an identifiable underlying liver disease. Irregular, undulating narrowing and nodular extrinsic defects, the so-called "pseudo-cholangiocarcinoma sign" was present in 33 of the 35 patients who underwent either ERCP or percutaneous transhepatic cholangiography. No such findings were observed in 10 control cirrhotic patients with portal hypertension but without CTPV, who also underwent ERCP. CONCLUSION: The results of this study indicate that mildly increased serum alkaline phosphatase and direct reacting bilirubin levels occur in cases with CTPV associated with a pseudo-cholangiocarcinoma sign. Presumably, these enzyme elevations are a result of compression of the biliary tree by the venous collaterals that run along the extrahepatic biliary tree. None of the 33 cases with this sign had cholangiolar carcinoma. Thus, when a patient with splenomegaly but without documentable parenchymal liver disease demonstrates an increase in the serum direct reacting bilirubin and alkaline phosphatase levels, CTPV and the presence of large extrahepatic venous collaterals partially obstructing the biliary tree should be suspected.

Cavernous transformation of the portal vein: a common manifestation of Behçet's disease.

Behçet's disease (BD) is a chronic, multisystem inflammatory disorder of unknown etiology, which is characterized by recurrent aphthous ulcers of the mouth and genitalia, uveitis with hypopyon, and a diffuse vasculitis that involves the arterial and venous systems. From January 1968 to July 1993, 66 of 844 patients with BD seen at the Hacettepe University Hospital, Ankara, Turkey, experienced a vascular complication other than peripheral thrombophlebitis. The vascular complication in each case was identified based upon a combination of clinical data, digital subtraction angiography, CT, and ultrasonography findings. Six of these 66 (9.1%) had cavernous transformation of the portal vein. Five of these six had additional large vein involvement resulting in the Budd-Chiari syndrome with or without inferior vena caval obstruction. Based upon this experience, it can be concluded that portal vein thrombosis is not a rare complication of BD. When patients with BD are found to have or develop splenomegaly, portal vein thrombosis should be suspected and investigated. If hepatomegaly and ascites are detected, Budd-Chiari syndrome due to hepatic vein thrombosis should be suspected. Finally, if hepatosplenomegaly, ascites, and dependent edema of the lower body are present, thrombosis of the inferior vena cava should be suspected.

Interferon treatment of chronic active hepatitis C in patients with end-stage chronic renal failure.

Alpha interferon has been shown to be effective in the treatment of chronic hepatitis C virus infection. We studied the efficacy of alpha 2a-interferon in chronic active hepatitis C patients with end-stage chronic renal failure (CRF). Thirteen patients with CRF and 12 patients with a normal renal function were included in the study. The patients received interferon 3 million units three times a week subcutaneously for 6 months. All patients with CRF and 6 patients without CRF had a complete response, defined as a decline in serum alanine aminotransferase levels to the normal range. One patient had a decrease in alanine aminotransferase of more than 50%, and 5 patients were nonresponders. A relapse was observed in 4 patients with and in 4 without CRF. Three patients had renal transplantation, and the alanine aminotransferase levels were normal after 12-14 months. This preliminary study shows that interferon is effective in the treatment of patients with chronic hepatitis C and CRF.