Tenofovir disoproxil fumarate treatment in HbeAg-positive patients.

Tenofovir disoproxil fumarate (Tenofovir DF) is a nucleotide analogue. This multicentre study reports retrospectively the long-term efficacy and safety data with tenofovir DF treatment in nucleosid(t)e-naive, hepatitis B e antigen (HBeAg)-positive chronic hepatitis B patients. Thirty-one patients (11 females, 20 males) received 245 mg tenofovir DF per diem. All patients' initial serum hepatitis B virus (HBV) DNA levels were over 2,000 IU/ml. Serum alanine aminotransferase (ALT) levels, HBeAg, hepatitis B e antibodies (anti-HBe), hepatitis B surface antigen (HBsAg), hepatitis B surface antibodies (Anti-HBs), HBV DNA, creatinine and urea levels were evaluated at baseline, and at weeks 12, 24, 48 and 96 during therapy. Thirty-one patients completed 96 weeks of treatment. Mean age was 37.6 ± 9.4 years. The initial mean value of ALT was 79 ± 39.9 IU/L. At baseline, mean of fibrosis (Ishak) of liver biopsies was 2.3 ± 0.7. Two of the patients (5.9%) achieved HBV DNA less than 300 copies at week 12 of treatment and 97.1 % at week 96. HBeAg loss was observed in 6.7% of patients. At week 96, HBsAg loss was not observed in any of the patients. Mean ALT at week 48 was 32.7 U/L, at week 96 32.6 U/L. Renal safety was good. Creatinine remained stable. Tenofovir DF was well tolerated and produced potent, continuous viral suppression with increasing HBeAg loss.

Four-year study of entecavir efficacy and safety in nucleos(t)ide-naïve HBeAg positive chronic hepatitis B patients.

Entecavir is a guanosine analogue with activity against hepatitis B virus. The aim of this 4-year trial was to evaluate entecavir treatment in nucleos(t)ide-naïve HBeAg-positive chronic hepatitis B patients. Forty-nine patients received entecavir and nine of them withdrew from the trial at the end of week 96. The initial mean value of alanine aminotransferase was 79.4 +/- 41.5 IU/L, and at the end of the 4-year study period, 90% of patients had alanine aminotransferase values within the normal range. At week 96, 91.7% of patients had HBV DNA < 300 copies; at month 48, 90% of patients had HBV DNA < 50 IU/mL. HBeAg loss was recorded in 7.1% of patients at week 96 and in 12.5% at month 48. The rate of HBeAg seroconversion was 4.8% at week 96 and 7.5% at month 48. The rate of HBsAg seroconversion was 2.1% at week 96 and 2.5% at month 48. Entecavir as a potent and safe agent leading to continuous viral suppression proved to be safe and well tolerated therapy.

Primary retroperitoneal hydatid cyst: report of 2 cases and review of 41 published cases.

This paper gives an overview of the literature between 2000 and 2010 on primary retroperitoneal hydatid cyst. We reported 2 cases of primary retroperitoneal hydatid cyst, and studies published in English literature on hydatid cyst developing in the retroperitoneal space were accessed via Pubmed and Google Scholar databases. Forty-one published primary retroperitoneal hydatid cyst cases were evaluated, and 2 patients (1 man, 78 years old; 1 woman, 75 years old) who presented with abdominal mass caused by retroperitoneal hydatid cyst were reported. Twenty-five of the patients were men (including our patient), and 18 were women; patients ranged in age from 3 to 80 years, and the median +/- standard deviation age was 41.37 +/- 20.4 years. On presentation, 72% of the patients complained of back or abdominal pain; 13.9% had urinary tract symptoms, and 65.1% were determined as having a palpable mass. Ultrasonography was performed on 93% of the patients, computed tomography was performed on 81.4%, magnetic resonance imaging was performed on 18.6%, and intravenous pyelography test was performed on 13.9%. The results of these tests showed a cystoid mass located on the left in 32.5% of the patients, on the right in 37.2%, and in the retrovesical area in 16.2%. Serologic tests determined 67.8% of the patients were indirect hemagglutination positive, and 71.4% were positive on enzyme-linked immunosorbent assay. As a surgical approach, total exision was performed on 55.8% of patients, partial cystectomy was performed on 39.5%, and 4.6% of patients underwent unroofing. If a cystic lesion is determined in the retroperitoneal area in a patient living in an area of endemic hydatid disease, a differential diagnosis of hydatid cyst should be considered. Clinical, radiologic, serologic, and histopathologic evaluations should be made for a differential diagnosis.

Screening for Celiac disease in Hodgkin and non-Hodgkin lymphoma patients.

BACKGROUND/AIMS: Celiac disease is an abnormal T cell-mediated immune response against dietary gluten in genetically predisposed individuals. The aim of our prospective study was to evaluate the frequency of Celiac disease in patients with lymphoma and to determine the usefulness of the anti-gliadin and anti-endomysial antibodies (EMA) for diagnosis of Celiac disease in this patient group. METHODS: We studied 119 patients with previously or newly diagnosed non-Hodgkin's lymphoma and 60 patients with Hodgkin's lymphoma who presented at the hematology and medical oncology divisions of Dicle University Hospital in Turkey between December 2002 and January 2006. Serological screening for Celiac disease was performed in all patients by searching for serum anti-gliadin immunoglobulin A and immunoglobulin G, and EMA immunoglobulin A and immunoglobulin G. RESULTS: In the Hodgkin's lymphoma group, anti-gliadin immunoglobulin A was detected in 9 (15%) patients (3 male, 6 female), and antigliadin immunoglobulin G was detected in 21 (35%) patients (15 male, 6 female). In the non-Hodgkin's lymphoma group, antigliadin immunoglobulin A was detected in 6 (5%) patients (2 M male 4 female), and anti-gliadin immunoglobulin G was detected in 30 (25.2%) patients (18 male, 12 female). EMA immunoglobulin A and immunoglobulin G were not detected in the Hodgkin's lymphoma and non-Hodgkin's lymphoma groups. CONCLUSIONS: Our report is the first to describe the frequency of Celiac disease in patients with lymphoma in the southeast region of Turkey. In our study, there was no evidence that Celiac disease is a pre-malignant condition for lymphoma. Serological screening for Celiac disease in lymphoma patients does not seem to be necessary.

Pyloric giant Brunner's gland hamartoma as a cause of both duodenojejunal intussusception and obscure gastrointestinal bleeding.

Obscure gastrointestinal bleeding is an important dilemma. Brunner's gland hamartoma is an extremely rare tumor generally localized in the duodenal bulb. We present a 34-year-old woman who had suffered from several episodes of melena for the past three years. Endoscopic examinations were normal. Computed tomography showed a large target lesion over the right abdomen and an image representing intestinal malrotation, which was supported by enteroclysis. At exploratory laparotomy, ligamentum of Treitz was located in the mid-to-right side of the columna vertebralis, and the duodenal bulb was found to be invaginated into the proximal jejunum. After longitudinal duodenotomy, a pedunculated ring-shaped large polyp originating from the pyloric ring was seen and excised. Histology was consistent with Brunner's gland hamartoma. This case with obscure bleeding was original with respect to its rarity and being a huge, ring-shaped tumor with pyloric localization. Moreover, the patient had a rare clinical presentation of duodenojejunal intussusception with accompanying intestinal malrotation.

Clarifying the relationship between ABO/Rhesus blood group antigens and upper gastrointestinal bleeding.

BACKGROUND AND AIM: The relationship between blood group antigens and peptic ulcer disease has been widely evaluated in the past. Data concerning the same association with upper gastrointestinal bleeding are very limited. We aimed to evaluate this association and we thought it was worthwhile to try to determine whether these components take some part in this complication. METHODS: The study population consisted of 1,098 adults (364 patients and 734 volunteer blood donors as controls). Demographic features, comorbid illnesses, and use of aspirin/nonsteroidal anti-inflammatory drugs (NSAIDs) were recorded. Blood groups were examined by gel centrifugation method. We included only patients with bleeding from peptic ulcer disease and erosive gastropathy. Ulcers were classified by using Forrest's classification system in terms of rebleeding risk. Helicobacter pylori was examined by histology. RESULTS: The gender distribution was similar in both groups. The ABO blood group phenotype distribution in patients and controls (respectively) was as follows: 46.2% versus 34.9% for group O, 32.4% versus 39.5% for group A, 15.7% versus 18.4% for group B, and 5.8% versus 7.2% for group AB. Blood group O was found to have higher frequency in the patient group than in the control group (P=0.004). Rh positivity was also higher in patients than in controls (P=0.007). H. pylori positivity was similar between blood groups among patients. The rebleeding and mortality rates between blood groups were also similar. CONCLUSION: ABO blood group O had an important role in patients with upper gastrointestinal bleeding. The impact of blood group on rebleeding and mortality may be a focus for further studies.

Analysis of inherited thrombophilic mutations and natural anticoagulant deficiency in patients with idiopathic portal hypertension.

Idiopathic portal hypertension (IPH) is characterized by non-cirrhotic presinusoidal intrahepatic portal hypertension. The etiopathogenesis of the disease is poorly understood. Obliteration with microthrombosis of the small portal vein branches may lead to lesions underlying portal hypertension. We aimed to put forward a comprehensive thrombophilic mutation profile in IPH and its probable contribution to pathogenesis. Eleven patients and 12 controls were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen -455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. We also evaluated some blood parameters and protein C, protein S, AT-III levels using commercially available assays. IPH patients and controls were similar in respect to gender distribution (P = 1.000). Mean age was 31.2 in patients and 29.1 in controls (P = 0.622). Pica history was present in 54.5% of the patients. Mean protein C and AT-III levels were lower in patients than that of controls (P = 0.002 and 0.001, respectively). Factor XIII V34L, PAI-1, GPIIIa L33P, MTHFR C677T and MTHFR A1298C frequencies of genetic polymorphisms were found to be significantly higher among patients than that of controls. Apolipoprotein E2/E3/E4 analysis showed an inverse relationship with IPH when E2 plus E4 compared with E3. A higher frequency of Beta-Fibrinogen -455G-A mutation was observed in patients, but this difference did not reach a statistical significance. Our data represent the most comprehensive study to date with respect to thrombophilic gene polymorphisms in IPH. The data support a possible pathogenetic role in IPH, at least by some of the prothrombotic mutations. In order to confirm or refuse this proposal, a larger cohort of patients is needed.

The effects of nonsteroidal anti-inflammatory drugs on platelet function and severity of upper gastrointestinal haemorrhage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal (GI) damage primarily due to the inhibition of prostaglandin synthesis in gastric mucosa, which is an important factor in mucosa protection. Platelets are a cardinal feature of vascular repair. A variety of angiogenic stimulators are stored in platelets and are released during clotting at the wound. When there is a defect in any of these functions and/or platelet number, haemostasis is usually impaired and there may be an associated increased risk and severity of bleeding. While the mechanism of mucosal injury and bleeding are well documented with the use of NSAIDs, very little is known about the platelet function abnormalities and their effects on severity of upper GI bleedings. We performed a prospective analysis of 49 patients who had a history of NSAIDs use to investigate the association between the platelet function impairment associated with NSAIDs and severity of upper GI haemorrhages. Thirty-six of 49 patients (73.5%) had deteriorated platelet function. Mean severity score of patients with deteriorated platelet functions was 3.39, and that of patients with normal platelet functions was 2.46. Mean severity score was statistically significantly higher in patients with deteriorated platelet functions. In conclusion, impaired platelet functions associated with NSAIDs may cause more severe upper GI bleeding. Clinicians should be alert for GI complications especially in older patients and in those with a history of ulcer bleeding.

Two cases of bacterial meningitis accompanied by thalidomide therapy in patients with multiple myeloma: is thalidomide associated with bacterial meningitis?

Morbidity and mortality in multiple myeloma is often attributed to life-threatening infections. A defect in humoral immunity has been proposed for the predisposition to bacterial infections. Most of the infections are of bacterial origin, and the most serious are septicemia, meningitis, and pneumonia. Thalidomide is a drug with pleiotropic effects. The immunomodulatory effects of thalidomide are at least partially mediated through its ability to down-regulate the pathogenic over-production of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a cytokine that plays a central role in the regulation of the host immune and inflammatory response to infection. In the central nervous system, TNF-alpha is involved in induction of a fever response and triggers the release of other cytokines, and may also influence transport of compounds into the brain, leading to cerebrospinal fluid leukocytosis, increased protein influx, and lactate accumulation. Thalidomide has been shown to down-regulate the production of TNF-alpha. On the other hand, knowledge of the effects of thalidomide on granulocyte functions is limited. Thalidomide has been shown to attenuate neutrophil adhesion and chemotaxis. We present herein two cases of Streptococcus pneumoniae bacterial meningitis that developed soon after the initiation of thalidomide treatment, and discuss the effect of thalidomide on the immune system. Although, it is not clear whether thalidomide caused the development of the bacterial infections and meningitis, or what its pathogenetic mechanisms are, physicians should be alert for signs and symptoms of meningitis in patients with multiple myeloma who are treated with thalidomide, especially those in neutropenic states.

Thyroid and celiac diseases autoantibodies in patients with adult chronic idiopathic thrombocytopenic purpura.

The association of chronic idiopathic thrombocytopenic purpura (cITP) and thyroid autoimmune diseases (TAD) is a known but an uncommon condition. Celiac disease (CD), which is characterized by malabsorption and villous atrophy that occur as a consequence of the ingestion of wheat gluten may also be related to other autoimmune disorders. In this study, we investigated the prevalence of thyroid anti-microsomal (TAMA) and anti-thyroglobulin (TATA) auto antibodies, anti-gliadin (AGA) IgG, IgA, anti-endomisium (EMA) IgG and IgA antibodies in 74 patients with cITP and in 162 healthy controls. TATA positivity was found in 29, and TAMA positivity in 19 out of 74 patients; and in 16 and 18 out of 162 controls respectively (p < 0.0001 and p = 0.005, respectively). TAD was diagnosed in 29 of cITP patients. AGA IgG positivity was found in 17, and IgA was present in five out of 74 patients; and AGA IgG was found in 19, and IgA was detected in 4 out of 162 controls (p = 0.032 and p = 0.143, respectively). EMA IgG positivity was found in six out of 74 patients and in nine out of 162 control subjects (p = 0.566). EMA IgA positivity was found in two out of 74 patients and in one out of 162 controls (p = 0.232). We showed that the prevalence of TAD and related autoantibodies are higher in patients with cITP. We suggest that, patients with cITP should be followed up for development of TAD. In addition, all CD related auto antibodies were found to be more frequent in patients with cITP, but only the AGA IgG reached to the clinical significance. None of the CD related auto antibody positive patients developed clinically manifested CD. Large-scale designed studies are needed to clarify the long-term impact and importance of these CD related auto antibodies in patients with cITP.

The prevalence of primary and secondary Helicobacter pylori resistance to clarithromycin and probable contributing cofactors: data from southeastern Anatolia.

BACKGROUND/AIMS: Antibiotic resistance of Helicobacter pylori is the most important reason for failure in its eradication. We aimed to determine the prevalence of primary and secondary H. pylori resistance to clarithromycin in isolated H. pylori from dyspeptic patients in southeastern Anatolia and to evaluate the cofactors affecting this clinical problem. METHODOLOGY: The study involved adult patients who had already been diagnosed with symptomatic H. pylori infection based on rapid urease test, gastric histopathological examination and culture. H. pylori strains were isolated from antral biopsies taken during upper endoscopy in 142 dyspeptic patients with no previous therapy against the microorganism. MICs of clarithromycin were determined by E-test. Patients were treated for 14 days with standard triple-agent protocol. H. pylori eradication rate was assessed after 8 weeks. Each patient was re-interviewed to determine secondary resistance. Primary clarithromycin resistance was defined as pre-treatment resistance, while secondary as after treatment resistance. Strains were considered resistant to clarithromycin if the MIC > 1 microg/mL. RESULTS: In total 213-105 women and 108 men-patients was enrolled to the study. The mean age was 35.5+/-14.1 years. In 142 (66.7%) patients out of the total patients enrolled in the study, H. pylori was detected. H. pylori could be cultured from only 61 (43%) of them. In 16.4% of the cases, primary clarithromycin resistance was noted. After 8 weeks, seventy-seven (54.2%) of the 142 patients were reevaluated. Helicobacter pylori eradication could be achieved in 68.8% of them. The proportion of H. pylori eradication in clarithromycin-sensitive patients was 75.8% and the respective proportion was 10% for resistant cases. In the group where H. pylori was still positive the secondary resistance percentage was found to be 27.2%. CONCLUSIONS: The prevalence of primary clarithromycin resistance is relatively high in our geographical area. Secondary resistance rate was 27.2%. None of the criteria of age, gender, presence of endoscopic lesions, detected H. pylori concentration and gastritis activity showed any effect on the primary resistance.

Lamivudine for the prevention of hepatitis B virus reactivation in hepatitis-B surface antigen (HBSAG) seropositive cancer patients undergoing cytotoxic chemotherapy.

Hepatitis B virus (HBV) is one of the major causes of chronic liver disease worldwide. Cancer patients who are chronic carriers of HBV have a higher hepatic complication rate while receiving cytotoxic chemotherapy (CT) and this has mainly been attributed to HBV reactivation. In this study, cancer patients who have solid and hematological malignancies with chronic HBV infection received the antiviral agent lamivudine prior and during CT compared with historical control group who did not receive lamivudine. The objectives were to assess the efficacy of lamivudine in reducing the incidence of HBV reactivation, and diminishing morbidity and mortality during CT. Two groups were compared in this study. The prophylactic lamivudin group consisted of 37 patients who received prophylactic lamivudine treatment. The historical controls consisted of 50 consecutive patients who underwent CT without prophylactic lamivudine. They were followed up during and for 8 weeks after CT. The outcomes were compared for both groups. Of our control group (n= 50), 21 patients (42%) were established hepatitis. Twelve (24%) of them were evaluated as severe hepatitis. In the prophylactic lamivudine group severe hepatitis were observed only in 1 patient (2.7%) of 37 patients (p < 0.006). Comparison of the mean ALT values revealed significantly higher mean alanine aminotransferase (ALT) values in the control group than the prophylactic lamivudine group; 154:64 (p < 0.32). Our study suggests that prophylactic lamivudine significantly decreases the incidence of HBV reactivation and overall morbidity in cancer patients during and after immunosuppressive therapy. Further studies are needed to determine the most appropriate nucleoside or nucleotide analogue for antiviral prophylaxis during CT and the optimal duration of administration after completion of CT.

Familial Mediterranean fever gene mutations in the Southeastern region of Turkey and their phenotypical features.

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent inflammatory attacks of serosal membranes. Several studies have focused on the differences between frequency of the mutations and their phenotypical manifestations. The aim of this study was to evaluate whether or not this phenotypical variation is associated with the existence of particular mutations. Twelve MEFV (Mediterranean fever) gene mutations were investigated in 119 patients suffering from FMF. Heterozygote M694V (21/119), heterozygote E148Q (21/119), homozygote M694V (17/119) and heterozygote V726A (12/119) mutations were the most common mutations. Patients were grouped according to the presence of the M694V mutation: group I was M694V/M694V, group II was M694V/others, and group III was other/other. Mean severity scores for the groups were 13.94 +/- 4.10, 10.79 +/- 3.01 and 8.31 +/- 2.26, respectively. There were statistically significant differences between the mean severity scores of groups I and II (p = 0.029), groups I and III (p < 0.0001), and groups II and III (p < 0.0001). Diagnosis of amyloidosis was established in four (23%) patients of group I, and three (8%) patients of group II, but in none of the patients in group III. There was also a statistically significant difference between groups I and III (p = 0.046), but not between groups II and III (p = 0.083) and groups I and II (p = 0.317) in terms of amyloidosis development. In conclusion, we found a higher disease severity score and higher prevalence of amyloidosis in FMF patients who were M694V mutation carriers. Many ethnic groups live in Anatolia and more ethnic origin-based studies are needed to determine the real effect of these mutations on disease severity and amyloidosis.

Pseudoxantoma elasticum, as a repetitive upper gastrointestinal hemorrhage cause in a pregnant woman.

Pseudoxantoma elasticum is a rare, hereditary, multisystemic disease affecting the skin, eye, and cardiovascular system. A twenty-eight-year-old female has presented to emergency unit with the complaint of gastrointestinal hemorrhage. This patient, who had been monitored in the gastroenterology clinic more than 10 times in the past 8 years, noted a repetitive hemorrhage during her previous pregnancy in her history. The examination of the patient revealed the following signs and symptoms: atrophy in the epithelium of the retina pigment; typical angioid streaks and peau d'orange finding in the fundus; thinning of the retinal nerve fiber in OCT (optic coherence tomography); bilateral and reticular papillary lesions with yellowish-color in the neck region (plucked chicken appearance); presence of bleeding foci in fundus; and nephrocalcinosis in kidneys. In light of these symptoms, the patient was diagnosed with pseudoxantoma elasticum. Skin biopsy confirmed the pseudoxantoma elasticum diagnose. PXE is an uncommon, hereditary disease. Early diagnosis of pseudoxantoma elasticum cases, is important for minimalizing systemic complications and informing the other family members through genetic counseling.

Epidemiological and clinical aspects of liver cirrhosis in adult patients living in Southeastern Anatolia: leading role of HBV in 505 cases.

BACKGROUND/AIMS: Liver cirrhosis is the terminal condition of liver disorders resulting from various causes. Literature lacks data on epidemiological and clinical aspects of liver cirrhosis in Turkey. We aimed to evaluate the main features of liver cirrhosis in this study. METHODOLOGY: We included in the study a total of 505 patients referred to Dicle University Hospital in the last five years and evaluated retrospectively. Demographic features, etiology, clinical findings, disease severity, complications and mortality rates were all recorded. RESULTS: Of the patients, 136 (27%) were female and 369 were (73%) male. Mean age was 50.4. The etiologic spectrum consisted of 368 HBV (72.9%), 41 HCV (8.1%), 12 alcohol (2.4%). Rate for cryptogenic cirrhosis (CC) was 11.1% with mean age of 45.4. HDV superinfection was present in 17.8%. Most of the patients were in Child-Pugh class B. Number of decompensated cirrhosis cases was 278 (55%). Hepatocellular cancer (HCC) was seen in 8.9% of patients and 88% had HBV with a mean age of 60. HCC was seen more commonly in HDV superinfected patients (p = 0.035). In-patient mortality was observed in 13.2%. CONCLUSIONS: HBV is the leading etiological factor of liver cirrhosis in Southeastern Anatolia and strict measures must be taken against perinatal or horizontal transmission of contagious pathogens. Alcohol had a marginal role in cirrhosis in our region. Although HDV superinfection is decreasing with time, it may increase HCC risk. Patients with cryptogenic cirrhosis were younger and had lower Child-Pugh scores.

Long-term conventional interferon alpha in combination with lamivudine for chronic hepatitis B: data from Turkey.

BACKGROUND/AIMS: Standard interferon or lamivudine monotherapy has been shown to induce a low response rate in patients with chronic hepatitis B infection. Genotype D represents almost the whole of chronic HBV infection of Turkish population. The aim of this study was to evaluate the efficacy and safety of the long-term interferon-alpha plus lamivudine on these patients, and thereafter the co-effect of maintenance therapy by lamivudine. METHODOLOGY: This prospective study was carried out between the late 1999 and 2005. A total of 37 (24 HBeAg-positive and 13 HBeAg-negative) patients were enrolled in the study. These patients received standard interferon-alpha (9/10 MU) three times sc. a week plus lamivudine 100mg po. daily, for 52 weeks. After the interferon discontinuation, lamivudine monotherapy was assigned to be given until 4-6 months after the occurrence of HBeAg seroconversion in the HBeAg-positive patients and at least three years in HBeAg-negative patients. Response-1 was defined as the response at the end of combination therapy at the 52nd week, and Response-2 as response at the end of the follow-up period under lamivudine monotherapy. An intention-to-treat analysis was performed. RESULTS: Patients' follow-up ranged between 7-67 months, with a mean duration of 29.64 +/- 14.01 months. Twenty-six patients (70.3%) had a Response-1, both virological and biochemical. A biochemical Response-2 was achieved in 24 patients (64.9%), while virological Response-2 in 17 (45.9%). Response-1 and Response-2 were similar between HBeAg-positive and HBeAg-negative patients (p = 0.262 and p = 0.734, respectively). HBeAg seroconversion was achieved only in 8 (33.3%) of HBeAg-positive patients. Clinical resistance to lamivudine developed only in 9 (24.3%) of the patients. Decompensation or hepatocellular carcinoma did not observe in any case. CONCLUSIONS: This study showed the efficacy of the 'long-term' anti-viral maintenance along with the combination therapy in genotype D predominant chronic hepatitis B patients. A low clinical resistance rate to lamivudine was achieved.

Does adding misoprostol to standard intravenous proton pump inhibitor protocol improve the outcome of aspirin/NSAID-induced upper gastrointestinal bleeding?: a randomized prospective study.

Aspirin and nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal bleeding is recognized as an important health problem. We performed a single-center randomized clinical trial to compare the effect of high-dose intravenous proton pump inhibitor (omeprazole) alone (group 1) with omeprazole in combination with a low-dose prostaglandin analog (misoprostol; group 2) on clinical outcomes in patients with aspirin/NSAID-induced upper gastrointestinal bleeding. Additionally, we evaluated the contribution of Helicobacter pylori eradication therapy on the late consequences. Patients were recruited to the study if they had upper gastrointestinal bleeding with history of taking aspirin or other NSAIDs within the week before the onset of bleeding. All were evaluated in terms of probable risk factors. After the standard treatment protocol, patients with histologically proven H pylori infection were prescribed a triple eradication therapy for 14 days. The primary end points were recurrent bleeding, surgery requirement, and death rates before discharge and at the end of follow-up period. This study lasted for 2 years. A total of 249 patients with upper gastrointestinal bleeding were admitted, and 49.7% of these patients were users of aspirin/NSAIDs. There were 67 patients in group 1 and 56 in group 2. The distributions for gender, age, comorbidity, H pylori infection, and high-risk ulcer rate were similar in both groups. Among aspirin/NSAID users, endoscopy revealed duodenal ulcer in 47 (38.2%), gastric ulcer in 10 (8.1%), and erosive gastropathy in 33 (26.8%). The overall rebleeding occurred in 12.2%, death in 2.4% of the patients. The in-hospital death (P=.414), rebleeding (P=.925), and surgery (P=.547) rates were similar in both treatment groups. After the follow-up period of 3 months, overall rebleeding occurred in 4.1%, and death in 4.8% of the patients. The overall mortality rate was highest in those >65 years old, who were chronic low-dose aspirin users with comorbidity. One died of transfusion-related graft-versus-host disease. In this pilot study, we indicated that adding misoprostol (600 microg/day) to standardized proton pump inhibitor treatment did not improve or change the rebleeding or mortality rates of patients with upper gastrointestinal bleeding related to aspirin/NSAID use. Other prospective studies on higher doses of misoprostol are needed to establish the coeffect. One should bear in mind that all blood products must be irradiated before transfused to the host.

A comprehensive analysis of 12 thrombophilic mutations and related parameters in patients with inflammatory bowel disease: data from Turkey.

BACKGROUND: Possible association of inflammatory bowel disease (IBD) with the most common inherited prothrombotic conditions has been the focus of many investigations. Advance in modern molecular biology is expanding the thrombophilia evaluation steadily. We tried to put forward a comprehensive thrombophilic profile in IBD and to see the probable role of this profile in pathogenesis. METHODS: A total of 60 adults (33 patients and 27 healthy controls) were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen-455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. Besides, we evaluated many related blood parameters such as protein C, protein S, AT-III, IL-6, TNF-alpha, Apo-A1, Apo-B100, homocysteine (tHcy) etc. using commercially available assays. RESULTS: The frequencies of genetic polymorphisms were found to be statistically insignificant among patients and controls, except for three: Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D. Two patients with a history of deep venous thrombosis had more than one polymorphism. Patients with MTHFR C677T and MTHFR A1298C gene mutations had a similar mean tHcy levels with controls. Patients with Apolipoprotein B R3500Q and Apolipoprotein E4 gene mutations had similar mean LDL-cholesterol levels. Mean total cholesterol and triglyceride levels were similar in patients and controls of Apo E2, E3, E4 alleles. CONCLUSION: Predominantly, the presence of genetic mutations that predispose to hypercoagulable states does not appear to be in correlation with IBD. There was a statistical difference between the proportions of the mutated allele frequencies of Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D in IBD.