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Introduction and aims: International guidelines and routine clinical practice express concerns about antiviral treatment in intravenous drug users (IDUs). We analysed the effect of IDU and/or substitution therapy on chronic hepatitis C (CHC) treatment adherence and response. Patients and methods: Intravenous drug users with CHC were divided into three groups: (A) patients on a substitution programme; (B) active users; and (C) past IDUs. Patients were treated according to the standard of care and followed by a specialist team. Results: A total of 175 patients (mean age 39.4±8.8) were included. One hundred and forty-four (65%) were adherent to therapy (completing treatment and 6 months of follow-up). Twenty-two patients (36%) discontinued because of side effects, 28 (46%) discontinued on their own and 11 (18%) completed treatment but did not present at follow-up. Of 142 patients with available treatment outcome, 99 (69.7%) achieved a sustained virological response (SVR), with no differences among the study groups. Patients with genotypes 2–3 and those who completed the treatment schedule had 2.78-fold (95% CI: 1.3–5.8) and 6.4-fold (95% CI: 2.6–15.6) higher probability of achieving SVR. Conclusion: Active use of illicit drugs and/or drug substitution do not affect the treatment outcome in patients with CHC as long as they are closely followed and remain adherent to the treatment.

Pylephlebitis is a condition with significant morbidity and mortality. We review herein 100 relevant case reports published since 1971. Eighty-one patients were reported with acute pylephlebitis, while the remaining patients had chronic pylephlebitis. The most common predisposing infections leading to pylephlebitis were diverticulitis and appendicitis. Cultures from blood or other tissues were positive in 77%. The infection was polymicrobial in half of the patients and the most common isolates were Bacteroides spp, Escherichia coli and Streptococcus spp. Thrombosis was extended to the superior mesenteric vein (SMV), splenic vein, and intrahepatic branches of the portal vein (PV) in 42%, 12%, and 39%, respectively. Antibiotics were administered in all and anticoagulation in 35 cases. Patients who received anticoagulation had a favourable outcome compared to those who received antibiotics alone (complete recanalization 25.7% vs 14.8% (p > 0.05), no recanalization 5.7% vs 22.2% (p < 0.05), and death 5.7% vs 22.2% (p < 0.01)). Cases with complete recanalization had prompt diagnosis and management and two-thirds were recently published. Nineteen patients died; the majority of these (73.7%) died over the period 1971-1990. In conclusion, pylephlebitis remains an entity with high morbidity and mortality, but modern imaging modalities have facilitated an earlier diagnosis and have improved the prognosis. Anticoagulation has a rather beneficial effect on patients with pylephlebitis.

The clinical and imaging findings of primary hepatic actinomycosis are nonspecific and can mimic other diseases. This condition usually needs to be distinguished from other liver-occupying lesions, including malignancy. Review of the English language literature showed 67 cases of hepatic actinomycosis in immunocompetent, predominantly male patients. Infection was usually (75%) cryptogenic. The results of radiologic imaging showed that the lesion involved the right lobe in half of the cases, mimicked a liver tumor in 45%, and was single in two thirds of the cases. Hepatic actinomycosis coexisted with infections by common bacteria in 32% of cases reported. Diagnosis was usually achieved by microscopic examination of surgical or percutaneous specimens in 84.2% and 78.6%, respectively. Antibiotic therapy alone was used for treatment in approximately one half of cases and combined antibiotic treatment with surgical or percutaneous drainage procedure in the other half. The overall mortality rate was 7.6%. In conclusion, primary hepatic actinomycosis is a rare and usually cryptogenic infection. It is more common in men and immunocompetent subjects. It is well responsive to medical or combined medical and interventional treatment.

Apoptotic caspases are substantially activated in liver and serum caspase activity has been suggested as a marker of early liver injury.To investigate whether serum levels of caspase-generated fragments of cytokeratin-18 are associated with the severity of histologic lesions in chronic hepatitis C virus (HCV) infection and nonalcoholic fatty liver disease (NAFLD).We included 134 patients with chronic HCV infection and 58 patients with NAFLD, who consecutively underwent liver biopsy, and 40 healthy controls. Caspase-generated cytokeratin-18 fragment levels were blindly measured in stored serum samples.Median cytokeratin-18 fragment levels were lower in HCV-positive patients with minimal/mild than patients with moderate/severe histologic lesions (174 U/L vs. 223 U/L, P0.001) offering moderate accuracy for differentiation between the 2 groups (c-statistic: 0.74). Cytokeratin-18 fragments levels were lower in healthy subjects (148 U/L) than patients with simple fatty liver (174 U/L, P=0.013) than patients with nonalcoholic steatohepatitis (355 U/L, P0.001) offering excellent diagnostic accuracy for differentiation between the 2 latter groups (c-statistic: 0.87).Serum apoptotic caspase activity is associated with the severity of liver histologic lesions in both chronic HCV infection and NAFLD, but it has excellent diagnostic accuracy in NAFLD and moderate accuracy in chronic HCV patients.

To evaluate the prevalence and clinical burden of serendipitously discovered abnormalities in hospitalized patients, unrelated to their presenting symptoms and physical signs.A total of 478 patients consecutively admitted in the Department of Medicine were enrolled in the study. In the end of first diagnostic work-up, the previously undetected imaging or endoscopic asymptomatic abnormalities termed as incidental findings (IFs) were recorded and some of them were further investigated.One hundred thirty eight (28.8%) patients had IFs. The most common IFs were located in the kidney and genitourinary system followed by liver and gallbladder. The most common method of detection of IFs was ultrasonography (US) of the abdomen. The patients with IFs compared with those without, were older (P=0.007), had no previous hospitalizations (P0.001) and stayed longer in the hospital (P0.001). The 25 (18.1%) patients with IFs were not evaluated further. One hundred seventy seven IFs discovered in 113 patients were further evaluated by medical specialists and additional tests were performed if warranted. In the end of the diagnostic work-up, in a total of 113 patients with IFs, 78.7% had insignificant and 21.2% potentially significant IFs. The latter group had higher rate of IFs compared with the former group, usually more than 3 (P=0.017).IFs were prevalent in a hospital population. Hospitalized patients with IFs were more than 60 years old and had no previous hospitalization. A large number of IFs were potentially significant deserving further clinical management.

Background Survivin is a new member of the Inhibitor of apoptosis protein family that has a dual function as a mitotic regulator and apoptosis inhibitor. Survivin is prominently expressed in transformed cell lines and in many human cancers, including colorectal carcinoma. The aim of this study is to investigate the expression of survivin in colorectal carcinomas and its possible associations with clinicopathological parameters and patient survival. Materials and Methods Sections of formalin-fixed paraffin-embedded tissues from 77 colorectal carcinomas were immunohistochemistry stained for survivin. Results Survivin was mainly detected in the bottom of the glands of normal mucosa with mainly cytoplasmic localization. No survivin expression was found in infiltrating lymphocytes, fibroblasts, smooth muscle cells or neural tissue. Survivin staining was detected in 68/77 (88.3%) colorectal carcinomas. Survivin expression was found to be significantly associated with tumor differentiation (P = 0.02) but not with gender, age or Dukes stage. Survival did not differ according to survivin expression. Conclusion Survivin was found in the majority of colorectal carcinomas, suggesting that its expression is an early event in colorectal carcinogenesis. Its expression is statistically significantly associated with tumor differentiation but not with patient survival.

SUMMARY. Hepcidin is synthesized in the liver and has a crucial role in iron homoeostasis. Its synthesis is up-regulated in chronic inflammation and iron excess. We examined the determinants of serum hepcidin and liver hepcidin mRNA levels and their association with histological lesions in patients with chronic hepatitis C (CHC) and healthy controls. We studied 96 patients with CHC and 30 controls. Serum hepcidin levels were measured by an in-house competitive ELISA. Hepcidin mRNA levels were determined by a one-step qRT-PCR in total RNA extracted from liver biopsy specimens of 27 patients with CHC and six disease controls. Histological lesions were evaluated according to Ishaks classification. Serum hepcidin was significantly lower in patients with CHC than healthy controls (14.6 ± 7.3 vs 34.6 ± 17.3 ng/mL, P < 0.001). In patients with CHC, serum hepcidin correlated positively with aspartate aminotransferase (r = 0.334, P = 0.001) and insulin resistance (r = 0.27, P = 0.016) and had a trend for correlation with alanine aminotransferase (r = 0.197, P = 0.057) and serum haemoglobin (r = 0.188, P = 0.067) but not with ferritin. A significant positive correlation was also found between serum hepcidin levels and both necroinflammation (r = 0.259, P = 0.011) and fibrosis (r = 0.214, P = 0.036). Serum hepcidin was among others an independent predictor of cirrhosis (odds ratio: 1.145, P = 0.039). Liver hepcidin mRNA levels did not differ between patients and controls and were relatively lower in patients with than without cirrhosis (19.3 ± 21.7 vs 38.3 ± 26.0, P = 0.067). Patients with CHC have reduced serum hepcidin levels, which correlate with worse necroinflammation and fibrosis. The previously mentioned observations suggest a viral effect on hepatic hepcidin production, but might also support its involvement in the inflammatory process.

The pathogenetic mechanisms of development of non-alcoholic steatohepatitis (NASH) and fibrosis are not clear, although thrombosis of small intrahepatic veins has been suggested to trigger liver tissue remodelling and thrombotic risk factors have been associated with more advanced fibrosis in chronic viral hepatitis (CVH). We evaluated the prevalence of thrombotic risk factors (RFs) in non-alcoholic fatty liver disease (NAFLD) and their possible association with fatty liver or NASH.We included 60 patients with histologically documented NAFLD and a historical cohort of 90 patients with chronic hepatitis B (n=39) or C (n=51). Thrombophilic factors were evaluated on the day of the liver biopsy.One or more thrombotic RFs were detected in 37% of NAFLD patients, andor= 2 RFs were detected in 12% of NAFLD patients, being less frequently present than in CVH patients (37% and 68%, respectively; Por= 0.001). Among NAFLD cases, one or more thrombotic RFs were significantly more frequently present in NASH than simple fatty liver (56% vs. 8%; odds ratio [OR]: 13.8, 2.8-67.4, P0.001). In multivariate analysis, NASH was independently associated with moderate to severe steatosis (adjusted OR: 24.3; P=0.001) and the presence of one or more thrombotic RFs (adjusted OR: 38.7; P=0.002). Fibrosis stage was worse in NASH patients with than without thrombotic RFs (2.5+/-1.1 vs. 1.3+/-1.1; P=0.002).Thrombotic RFs are frequently present in patients with NAFLD and are associated with NASH and more advanced fibrosis. Such an association may have significant clinical implications, even though it is not clear yet whether it represents a primary or secondary phenomenon.

Chronic hepatitis C (CHC) induces insulin resistance (IR) and subsequently diabetes.To examine viral, metabolic and histological predictors of IR in 275 CHC patients to test the hypothesis that IR differs among HCV genotypes and that viral replication directly affects IR.We studied 275 nondiabetic treatment-naïve CHC patients. Histological lesions were evaluated according to Ishak. IR was assessed using homeostasis model assessment for insulin resistance (HOMA-IR).HOMA3.0 was found in 37% of patients, independently associated with higher BMI and GGT. In genotype non-3 patients, HOMA3.0 was associated with higher BMI and GGT values, while no significant association was noted in genotype 3 patients. In non-obese patients with minimal fibrosis, HOMA3.0 was found in 20% of cases without significant differences among genotypes. No association between HOMA3.0 and HCV-RNA levels was found. Severe fibrosis (stage 5-6) related to older age (OR:1.048), HOMA-IR (OR:1.177), necroinflammation (OR: 2.990) and higher ALT (OR: 1.009) and GGT (OR:1.006).IR develops at early stages of CHC without significant differences among genotypes. It is more frequent in obese patients with steatosis and contributes to fibrosis progression. However, IR does not seem to be associated with viraemia and therefore its exact pathogenetic mechanism in CHC remains elusive.

AIM Retinol-binding protein-4 (RBP4) has been proposed as a new adipokine that regulates insulin action in muscles and the liver, and contributes to the pathogenesis of insulin resistance. As non-alcoholic fatty liver disease (NAFLD) is related to insulin resistance, we aimed to evaluate RBP4 levels in the serum and liver of patients with NAFLD. METHODS Serum RBP4 was measured in 30 NAFLD patients and 30 matched healthy controls. RBP4 expression in the liver of NAFLD patients was shown by immunohistochemistry. RESULTS Serum RPB4 was significantly lower in NAFLD patients compared with controls (25.15 vs 34.66 microg/mL, P < 0.001) and there was no correlation with metabolic parameters or insulin resistance. RBP4 liver tissue immunostaining was more extensive and intense in NAFLD liver compared with normal liver and the RBP4 immunohistochemical score was positively correlated with the grade of steatosis, grade of non-alcoholic steatohepatitis activity and stage of fibrosis. CONCLUSIONS In NAFLD patients, serum RBP4 was significantly lower as compared with controls and did not correlate with insulin resistance. In contrast, RBP4 liver tissue expression was enhanced and correlated with NAFLD histology.

BACKGROUND/AIMS: Lamivudine improves liver histology in patients with chronic hepatitis B (CHB), but its effects on portal pressure remain unknown. We evaluated the effect of lamivudine monotherapy on hepatic venous pressure gradient (HVPG) in CHB-related cirrhosis with significant portal hypertension. METHODS: We studied 19 patients with cirrhosis due to HBeAg-negative CHB and HVPG >or=10 mm Hg treated with oral lamivudine (100mg daily). Liver biochemistry, Child-Pugh and MELD score were determined every 3 months, alpha-fetoprotein and HBV DNA every 6 months and HVPG at baseline and at 12 months after lamivudine initiation. Diuretics, beta-blockers, antibiotics and/or endoscopic therapy were used for routine indications. RESULTS: At 12 months, a significant reduction was observed in ALT (p=0.001), HBV DNA (p=0.002), Child-Pugh (p=0.012) and MELD score (p=0.006). Four patients developed virological breakthrough during treatment. At 12 months, HVPG decreased in all but one patient [baseline: 14.4+/-3.9 and 12 months: 12.4+/-3.3 mm Hg (p=0.007)]. HVPG decreased >20% or below the 12 mm Hg threshold in 10 of 13 patients with baseline HVPG >or=12 mm Hg. HVPG increased in a patient with hepatic flare after virological breakthrough. CONCLUSION: In conclusion, in patients with cirrhosis due to HBeAg-negative CHB, lamivudine monotherapy reduces HVPG, especially when virological suppression and biochemical remission is achieved.

SUMMARY. Despite several studies, the association of glucose intolerance with chronic hepatitis B (CHB) or C (CHC) virus infection remains controversial. We evaluated the prevalence of glucose intolerance by oral glucose tolerance test (OGTT) in patients with CHB or CHC in comparison with matched controls. In total, 189 consecutive outpatients with CHB or CHC and 189 subjects individually matched for age, sex and body mass index (BMI) were included. OGTT was performed in all cases, except in known diabetics, and glucose intolerance was defined as impaired glucose tolerance (IGT), OGTT-diabetes or known diabetes. Most patients with abnormal OGTT had normal fasting glucose (IGT: 69.8%, OGTT-diabetes: 54.5%). Compared with their own controls, CHB patients had a higher prevalence of IGT (13.6% vs 2.5%, P = 0.018) and family history of diabetes (34.6% vs 16.0%, P = 0.011), while CHC patents had higher prevalence of glucose intolerance (37.0% vs 15.7%, R = 0.001), mostly because of more frequent IGT (21.3% vs 6.5%, R = 0.003). After age and BMI adjustment, patients with CHC compared with those with CHB had significantly higher prevalence of glucose intolerance (37.0% vs 29.6%, P = 0.037). In conclusion, increased prevalence of glucose intolerance is documented by OGTT both in CHC and CHB patients compared with age, sex and BMI matched controls. Glucose intolerance is more frequent in CHC than CHB patients, regardless of known risk factors. An OGTT might be necessary at the baseline work-up of CHB or CHC patients, as a normal fasting glucose value does not exclude IGT or OGTT-diabetes.

Insulin resistance (IR) and metabolic syndrome have recently been implicated in the pathogenesis and progression of chronic liver diseases, especially chronic hepatitis C (CHC) and non-alcoholic fatty liver disease (NAFLD). In this review, we provide current information on their deleterious effect on the liver, with particular interest in those two entities. In NAFLD, IR causes both the accumulation of fat in hepatocytes and the progression to non-alcoholic steatohepatitis (NASH). Moreover, the presence of metabolic syndrome seems to be associated with severe fibrosis in NASH patients. In CHC, IR develops early in the course of the disease and precedes steatosis. It is also independently associated with histological severity and negatively affects treatment response, irrespective of genotype. Consequently, therapies targeting IR and metabolic syndrome could indirectly ameliorate the prognosis of both NAFLD and CHC. As specific therapies do not exist, patients with metabolic syndrome and CHC and NAFLD should be counseled to lose weight and ameliorate their glycemic control and lipid profile.

The results of retrospective studies suggest an association between smoking, insulin resistance, steatosis and fibrosis in patients with chronic hepatitis C (CHC); no data are available for chronic hepatitis B (CHB). The purpose of this study was to evaluate the relationship, if any, of such factors on liver fibrosis in a cohort of patients with CHB and CHC.The study prospectively included 271 consecutive patients with CHB (n=95) or CHC (n=176) who had undergone liver biopsies. Each patient completed a questionnaire on smoking habits; anthropometric measurements and laboratory examinations were carried out and histological lesions were recorded.In CHC patients, severe fibrosis was independently associated with a higher body mass index (BMI) (OR: 1.180, 95% CI: 1.028-1.354; p=0.019), heavy smoking (OR: 3.923, 95% CI: 1.356-11.348; p=0.012), higher alanine aminotransferase (ALAT) levels (OR: 1.010, 95% CI: 1.003-1.017; p=0.005) and alkaline phosphatase (ALP) levels (OR: 1.016, 95% CI: 1.001-1.030; p=0.03) and presence of necroinflammation (OR: 11.165, 95% CI: 1.286-96.970; p=0.029). Moreover, steatosis was independently associated with high gamma-glutamyl transpeptidase (GGT) values, heavy smoking and presence of necroinflammation. In CHB patients, no association between smoking habits and fibrosis or steatosis was noted.Heavy smoking is associated with severe fibrosis in CHC but not CHB. Heavy smoking is also significantly associated with steatosis in CHC and this could be the link between smoking and fibrosis progression.

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and can vary from benign steatosis to end-stage liver disease. The pathogenesis of non-alcoholic steatohepatitis (NASH) is currently thought to involve a multiple-hit process with the first hit being the accumulation of liver fat which is followed by the development of necroinflammation and fibrosis. There is mounting evidence that cytokines secreted from adipose tissue, namely, adipokines, are implicated in the pathogenesis and progression of NAFLD. In the current review, we explore the role of these adipokines, particularly leptin, adiponectin, resistin, tumor necrosis factor-a, and interleukin-6 in NASH, as elucidated in experimental models and clinical practice. We also comment on their potential use as noninvasive markers for differentiating simple fatty liver from NASH as well as on their potential future therapeutic role in patients with NASH.

Acute exacerbations in HBeAg negative patients with chronic hepatitis B virus (HBV) infection are invariably associated with concurrent increases in the index of IgM class antibodies against the core protein (anti-HBc) of the virus. This study aimed to investigate whether this was related to the clearance of variants from the quasispecies pool and the appearance of new ones, with aminoacid substitutions in well recognized B-cell epitopes. In this study, 5 HBeAg negative patients (A to E) with 13 sequential serum samples (A1-A2, B1-B2-B3, C1-C2, D1-D2-D3, E1-E2-E3) were investigated after amplification of the entire core encoding region followed by cloning/sequencing studies. The sequences at different time points were compared with those from a single HBeAg positive patient with no apparent acute exacerbations. The results from sequence comparison showed that virus variants emerged in all (A2, B3, C2, D3, E2, and E3) but two (B2 and D2) subsequent sera with amino-acid substitutions affecting B-cell epitopes. It is concluded that the rise in the values of IgM anti-HBc may be attributed to the alteration of the antigenic epitopes leading to new antibody production in the majority of the cases. However, it appears that increases in IgM anti-HBc indexes in a few cases may relate to other possible mechanisms which are discussed.

Background Adverse drug reactions (ADRs) are a significant cause of morbidity and mortality. Methods A prospective study was conducted over a 6-month period. All patients consecutively admitted were enrolled in the study. Analysis included: (1) an evaluation of the frequency of ADR-related hospital admissions and their causality, severity, and preventability; (2) a description of the type of drugs involved; (3) a report of the most common clinical manifestations related to these ADRs; and (4) an assessment of the factors that were predictive of ADRs. Results Seventy of the 548 admissions (12.8%) were related to an ADR. Hemorrhage represented the most common ADR (37.3%), followed by metabolic and renal events (10.8% each). The drugs most often involved were non-steroid anti-inflammatory drugs (NSAIDs), followed by diuretics, aspirin, oral anticoagulants, and oral hypoglycemic agents. A comparison between ADR and non-ADR-related admissions showed that mean number of medications and age were significantly higher for patients admitted for an ADR than for those who were not. Gender, chronic disease at admission, days of hospitalization, cognitive impairment, renal insufficiency, physical activity impairment, and use of psychoactive drugs did not differ between the two groups. In the multivariate analysis, number of drugs was the only independent predictor of ADR-related hospital admission (OR = 1.064, 95% CI 1.019–1.109). In 13 of 70 (18.6%) ADR-related hospital admissions, ADRs were coded as severe. Conclusions ADRs are common causes of hospital admissions and may have important consequences. The most important determinant for ADR-related hospital admissions is the number of drugs taken.

The diagnosis of hepatitis B e antigen (HBeAg)-negative chronic hepatitis B indicating therapeutic intervention currently requires serum hepatitis B virus (HBV) DNAor=2,000 IU/mL. We evaluated the severity of liver histology and the presence of histological indication for treatment in patients with HBeAg-negative chronic HBV infection focusing on those with low viremia and/or normal alanine aminotransferase (ALT). In total, 399 patients with increased ALT and detectable serum HBV DNA (chronic hepatitis B patients) and 35 cases with persistently normal ALT and HBV DNA2,000 IU/mL (inactive carriers) were included. Histological indication for treatment (grading scoreor=7 and/or stageor=2 in Ishak's classification) was found in 91% (185/203), 82% (75/91), 75% (47/63), and 62% (26/42) of chronic hepatitis B patients with HBV DNAor=200,000, 20,000-199,999, 2,000-19,999, and2,000 IU/mL, respectively (P0.001). Histological indication for treatment was more frequent in chronic hepatitis B patients with persistently elevated ALT (86% or 275/321), but it was also found in 74% (58/78) of those with transiently normal ALT (P = 0.025). All inactive carriers had HBV DNA20,000 IU/mL. Histological indication for treatment was present in 17% (6/35) of inactive carriers always due to moderate (stage 2) fibrosis without active necroinflammation.HBeAg-negative chronic HBV patients with persistently or transiently increased ALT and HBV DNAor=20,000 IU/mL almost always require therapeutic intervention, but histological indications for treatment are also present in the majority of such cases with HBV DNA20,000 and even2,000 IU/mL. In contrast, minimal histological lesions are observed in the majority of HBeAg-negative patients with persistently normal ALT and HBV DNA2,000 IU/mL, who may not require immediate liver biopsy and treatment but only close follow-up.

Introduction: In Western countries, the most frequent aetiology of acute liver failure (ALF) is acetaminophen overdose, while in developing countries viral infections [hepatitis A virus and hepatitis B virus (HBV)] predominate. Aim: To evaluate the epidemiology, clinical characteristics, outcome and prognostic factors of survival of patients with ALF in Greece during the last 6 years. Results: A total of 40 patients, 28 females (70%), with a median age of 37.4±18.6 years (range: 15–84) with ALF were studied. HBV infection was the cause in 53% of them (compared with 74% from a previous study reported in the early 1980s), drug toxicity in 15% and undetermined in 13%. The overall survival was 57.5%, including 94% with and 15% without liver transplantation. Forty-five per cent of our patients had emergency liver transplantation in European Centers within a median time of 3.3 days (1–9) from admission. The total bilirubin level at admission and the development of infections were found to be significantly associated with poor outcome. Conclusions: Hepatitis B virus still remains the most important cause of ALF in Greece, but shows a significant decrease as compared with studies in the early 1980s. Almost half of our patients needed emergency liver transplantation and had a very good survival rate. The other 15% of the patients presented spontaneous survival only with intensive medical support.

Aim We investigated whether changes of liver and muscle enzymes activity are associated with rigor of several causes and have any prognostic significance. Methods Seventy-five patients with rigor were prospectively evaluated. Serum enzymes were measured at the onset of rigor and during the three following days. Results Causes of rigor were bacteremia ( n = 28), cholangiitis ( n = 12), protozoan infections ( n = 9), viral infections ( n = 10) and platelet transfusions ( n = 16). Increases in enzymes activity were observed with rigors from infectious causes, but not with that following platelet transfusions. Patients with cholangiitis demonstrated the highest ALT elevations, while those with viral infections the highest CPK levels. In bacteremia, CPK values increased significantly only in cases with dehydration and hypokalemia. Conclusions Rigor per se does not cause increases in muscle or liver enzymes activities. Rather these changes are associated with the rigor's causative agent (infectious or not), the patient's general condition and the severity and extent of the underlying disease.

Currently available options for the treatment of chronic hepatitis B virus (HBV) infection include standard and pegylated interferon alfa and four oral antiviral agents (lamivudine, adefovir, entecavir, and telbivudine). These treatment strategies are either therapies of finite duration that aim to achieve sustained off-therapy responses, or long-term treatments that aim to maintain on-therapy remission. Pegylated interferon alfa may offer higher sustained off-therapy responses after 1 year, but most patients do not respond. Oral antivirals are the only candidates for long-term treatment of patients with chronic HBV infection. Viral suppression has favourable effects on patients' outcome and modifies the natural history of the disease. Viral resistance is the main drawback of long-term antiviral therapy. Lamivudine monotherapy is associated with higher resistance (year 1, 10-27%; year 2, 37-48%; year 4, 60-65%) than adefovir (year 1, 0%; year 2, 3%; year 5, 29%) or telbivudine (year 1, 3-4%; year 2, 9-22%). Entecavir resistance is rare in naive individuals (year 4

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. Activating mutations in tyrosine kinase receptors KIT or platelet-derived growth factor receptor alpha (PDGFRA) are the main mechanisms causing the disease. Patients generally present with non-specific symptoms, while a number of tumors are discovered incidentally and may be metastatic at the time of diagnosis. Aggressive GISTs have a defined pattern of metastasis to the liver or throughout the abdomen, or both. Though GISTs rarely present systemic or isolated paraneoplastic reactions, a few cases have been reported in the literature. We present the case of a 54-year-old patient with metastatic GIST at diagnosis and the emergence of paraneoplastic manifestations during follow-up.

A 47-year-old woman presented with severe hemolytic uremic syndrome (HUS) followed by heart failure. An echocardiogram showed an ejection fraction of 20%, and a cardiac catheterization followed by a myocardial histologic evaluation demonstrated dilated cardiomyopathy. Plasma exchange and hemodialysis were performed regularly. The later outcomes of renal function and cardiomyopathy were favorable. A review of the literature confirmed the rare and severe nature of cardiac lesions occurring in the course of HUS. This case indicates the importance of cardiac monitoring in HUS and the need for prolonged support.

Background/aims Hepatic steatosis has not been adequately studied in chronic hepatitis B, while it is considered to be a cardinal feature in chronic hepatitis C and to be mainly metabolically induced in patients infected with genotype 1. We investigated the prevalence of and the parameters associated with steatosis in HBeAg-negative chronic hepatitis B. Methods We studied 213 patients with HBeAg-negative chronic hepatitis B and compared them with 163 patients with genotype-1 chronic hepatitis C. Steatosis was semi-quantitatively graded. Results Steatosis was significantly less frequent in chronic hepatitis B than chronic hepatitis C (60% versus 72%, P = 0.016), but there was no difference in the prevalence of moderate/severe steatosis. In chronic hepatitis B, steatosis was associated only with higher body mass index (P = 0.002), while moderate/severe steatosis was associated only with higher body mass index (P = 0.043) and diabetes (P = 0.031). Steatosis was relatively less frequent in chronic hepatitis B than chronic hepatitis C non-diabetic, normal-weight patients (45.6% versus 62.5%, P = 0.063), but it did not differ in diabetic and/or overweight/obese patients with chronic hepatitis B or chronic hepatitis C. Conclusions Hepatic steatosis in HBeAg-negative chronic hepatitis B (a) is less frequent than in genotype-1 chronic hepatitis C, (b) is mainly associated with presence of host metabolic factors, such as high body mass index and diabetes and (c) does not seem to be associated with the severity of liver histological lesions.

Autoimmune thyroid diseases have been correlated with a variety of autoimmune diseases also affecting the skin. A 56-year-old patient with a history of vitiligo is presented who was admitted for hyperthyroidism (Graves disease) and a blistering eruption. Clinical and histological appearance of the skin disorder, rapid response to corticosteroids, recurrence and remission of the lesions with discontinuation and reintroduction of corticosteroids, respectively, were all suggestive of an autoimmune blistering disease accompanying autoimmune hyperthyroidism and vitiligo.

Cytotoxin-associated gene A (CagA) diversity with regard to EPIYA-A, -B, -C, or -D phosphorylation motifs may play an important role in Helicobacter pylori pathogenesis, and therefore determination of these motifs in H. pylori clinical isolates can become a useful prognostic tool. We propose a strategy for the accurate determination of CagA EPIYA motifs in clinical strains, based upon one-step PCR amplification using primers that flank the EPIYA coding region. We thus analyzed 135 H. pylori isolates derived from 75 adults and 60 children Greek patients. A total of 34 cases were found to be EPIYA PCR negative and were consequently verified as cagA negative by cagA -specific PCR, empty-site cagA PCR, and Western blotting. Sequencing of the remaining 101 PCR-positive amplicons confirmed that an accurate prediction of the number of EPIYA motifs on the basis of size distribution of the PCR products was feasible in all cases. Furthermore, our assay could identify closely related H. pylori subclones within the same patient, harboring different numbers of EPIYA repeats. The prevalence of CagA proteins with three EPIYA motifs (ABC) or four EPIYA motifs (ABCC) was the same within the adult and children groups. However, CagA species with more than four EPIYA motifs were observed exclusively within adults (8.6%), suggesting that CagA-positive strains may acquire additional EPIYA-C motifs throughout adulthood. Our strategy requires no initial cagA screening of the clinical isolates and can accurately predict the number of EPIYA repeats in single or multiple closely related subclones bearing different numbers of EPIYA motifs in their CagA, which may coexist within the same patient.

Hepatic granulomas have been reported in 2-15% of unselected liver biopsies, with a wide clinical profile responsible for their presence. To date, no series concerning the prevalence and the etiology of granulomas from Greece has been reported.To evaluate the prevalence and the etiology of hepatic granulomas and to investigate whether there has been an alteration in distribution of diagnoses in our series compared with those published so far in the literature.The results of liver biopsy specimens performed in a Department of Medicine, between 1999 and 2004, were retrospectively reviewed and the cases revealing hepatic granulomas had their medical notes and the liver biopsies recorded.Over the study period, 1768 liver biopsies were performed. Hepatic granulomas were identified in 66 (3.7%). Of those, 51 were female with a mean age of 57 years (range 34-74 years) and 15 were male with a mean age of 42 years (range 18-78 years). Autoimmune liver diseases including primary biliary cirrhosis, overlap syndrome and autoimmune hepatitis accounted for the majority of cases (68%), followed by sarcoidosis (7.5%), chronic hepatitis B virus and hepatitis C virus infection (7.5%), idiopathic (6%), drugs (3%) and other miscellaneous causes (7.5%).Our series showed that autoimmune liver diseases, mainly primary biliary cirrhosis was the most common cause of granuloma formation, a finding rather similar to that stated in the studies from Western countries. A rather small number of idiopathic cases were recorded. Chronic viral hepatitis and sarcoidosis rates were equal, a finding possibly reflecting a fairly high proportion of viral hepatitis in our sample.

We describe a case of a long-standing, untreated achalasia with a huge sigmoid esophagus in a 58-year-old Caucasian man who declined surgery. All means of classical endoscopic approach for pneumatic dilation, including the use of an overtube, were impossible because any attempt to propel the balloon dilator made the guide wire pull back out of the stomach because of the large loops and the tortuosity of the esophagus. For this reason, we used, for the first time, a combined approach of percutaneous gastrostomy and endoscopy in order to fix the guide wire at two points, achieving a pneumatic dilation in this way. A few months later, a significant improvement in the symptoms and nutritional status of the patient were observed.

We assessed the value of the recently developed aspartate aminotransferase to platelet ratio index (APRI) for predicting significant fibrosis or cirrhosis in patients with chronic hepatitis C or HBeAg-negative chronic hepatitis B.In total, 489 patients (chronic hepatitis C, 284 patients; HBeAg-negative chronic hepatitis B, 205 patients) were included. APRI values of 0.50 or less and greater than 1.50 were evaluated for predicting significant fibrosis, and APRI values of 1.00 or less and greater than 2.00 for predicting cirrhosis. Liver biopsies were evaluated according to the Ishak's classification. Fibrosis was considered to be significant in cases with scores 3-6, and cirrhosis to be present in cases with fibrosis scores of 5 and 6.Significant fibrosis was observed in 56/148 (38%) patients with APRIor = 0.50, 130/227 (57%) patients with 0.50APRIor = 1.50 and 84/114 (74%) patients with APRI1.50 (P10). Cirrhosis was observed in 47/311 (15%) patients with APRIor = 1.00, 29/93 (31%) patients with 1.00APRIor = 2.00 and 37/85 (44%) patients with APRI2.00 (P10). The areas under receiver-operating characteristic curves were 0.65 and 0.70 for prediction of significant fibrosis or cirrhosis, respectively. The combination of APRIor = 0.50 and APRI1.50 classified correctly 36% of patients with or without significant fibrosis, while the combination of APRIor = 1.00 and APRI2.00 classified correctly 62% of patients with or without cirrhosis. There was no significant difference in the predictive values of APRI between patients with chronic hepatitis C and chronic hepatitis B.APRI is significantly associated with the extent of fibrosis, but it does not classify correctly 40-65% of patients with chronic hepatitis C or HBeAg-negative chronic hepatitis B, and thus it cannot replace liver biopsy.

Background/aims Treatment of chronic delta hepatitis is long and difficult and better monitoring is needed. Methods In this study, hepatitis delta virus (HDV) RNA, hepatitis B surface antigen (HBsAg) and hepatitis B virus (HBV) DNA were retrospectively quantified in 53 patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis delta. Twenty-one had received 28 courses of 3–5 MU interferon-α2b (IFN-α2b) thrice weekly for a median of 12.6 months (interquartile range [IQR]: 7.3–31.6), five had received eight courses of 100 mg lamivudine (LAM) daily for 23.6 months (IQR: 8.4–61.5) and 27 were untreated. The controls were 54 untreated, randomly selected, HBeAg-negative chronic hepatitis B patients without delta infection. Quantification of serum HDV RNA, HBsAg and HBV DNA were performed at baseline, during and at the end of treatment and end of follow up. Results Untreated patients had significantly higher median HBsAg levels than controls (5,872 vs 3,501 IU/ml; P=0.046), but lower median HBV DNA levels (2.933 vs 6.459 log10 copies/ml; P10 copies/ml) was similar in IFN-α2b-treated, LAM-treated and untreated patients. At the end of treatment, IFN-α2b significantly suppressed in paired measurements HDV RNA ( P=0.012) and HBsAg ( P=0.043), but LAM was inefficient. In IFN-α2b-treated patients, HDV RNA became undetectable in five patients within a median of 30 months (IQR: 8–90), followed by a slower decrease in HBsAg. Conclusions In untreated chronic delta hepatitis, suppressed HBV replication is associated with significantly increased HBsAg serum levels. IFN-α2b significantly suppresses both HDV RNA and HBsAg, but LAM has no effect. Long-term IFN-α2b treatment (IQR: 1.5–5.0 years) appears necessary for undetectable serum HDV RNA and further treatment is required for HBsAg loss. Monitoring of HDV RNA and HBsAg serum levels in patients with chronic delta hepatitis provides insight during treatment.

Background and Aim: It has been suggested that propranolol may have a protective effect on the development of spontaneous bacterial peritonitis by increasing the motility of the bowel and lowering the pressure of the portal vein. The aim of this study is to evaluate the association between the use of propranolol and development of spontaneous bacterial peritonitis in patients with cirrhosis and ascites. Methods: We retrospectively evaluated 134 patients with cirrhosis and ascites admitted consecutively for a period of 2 years. Diagnosis of spontaneous bacterial peritonitis was based on an ascitic fluid neutrophilic count of >250/mm3 and/or a positive culture without evidence of secondary peritonitis. Results: Spontaneous bacterial peritonitis was diagnosed in 39 of 134 (29%) patients and 12 of 39 (31%) patients died in hospital compared to only 4% (four of 95) of those without spontaneous bacterial peritonitis (P

Background & Aims: The aim was to systematically review the interactions between Helicobacter pylori (HP) infection and NSAID use on the risk of uncomplicated or bleeding peptic ulcer. Methods: All relevant full articles published in MEDLINE from January 1989–June 2004 were included. Sensitivity analyses for type of controls or use of aspirin or non-aspirin NSAIDs were performed. Results: In 21 studies involving 10,146 patients, uncomplicated peptic ulcer was more common in HP-positive than HP-negative patients (pooled odds ratio [OR], 2.17) or in HP-positive than HP-negative NSAID users (OR, 1.81). In 6 age-matched controlled studies, ulcer was more common in HP-positive than HP-negative patients (OR, 4.03), irrespective of NSAID use, and in NSAID users than non-users (OR, 3.10), irrespective of HP status; the risk of ulcer was 17.54-fold higher in HP-positive NSAID users than HP-negative non-users. The use of aspirin or non-aspirin NSAIDs did not affect the results. Ulcer bleeding was evaluated in 17 studies involving 4084 patients. NSAID use was more frequent in bleeding patients than control subjects (OR, 5.13), irrespective of HP status and type of controls. In contrast, HP infection in bleeding patients compared with control subjects was less frequent in the 8 studies with ulcer cases as control subjects (OR, 0.40) and more frequent in the 9 studies with uninvestigated subjects as controls (OR, 2.56). In the latter studies, presence compared with the absence of both HP and NSAIDs increased the risk of bleeding 20.83-fold. Conclusion: HP infection and NSAID use represent independent and synergistic risk factors for uncomplicated and bleeding peptic ulcer.

Ulcerative jejunoileitis (UJI) is a rare condition which usually develops in patients with established or simultaneously diagnosed coeliac disease (CD) and has been suggested to represent cryptic low-grade enteropathy-associated T-cell lymphoma (EATL). We report a case of a 78-year-old male patient with UJI and CD diagnosed at the same time. He presented with abdominal pain, diarrhoea and weight loss and had serological, endoscopical, radiological and histological findings compatible with the diagnoses of both UJI and CD. The possibility of EATL was carefully excluded. The patient exhibited significant symptomatic improvement with a gluten-free diet, probably indicating an early stage of disease despite his old age. In conclusion, this rather unusual case of an elderly patient presenting with UJI and CD without evidence of EATL supports the great heterogeneity of these diseases not only in their clinical presentation but even in their course and complications.

Fludarabine is used widely for the treatment of chronic lymphocytic leukaemia, but not as yet implicated in the emergence of hepatitis B surface antigen (HBsAg) variants following hepatitis B virus (HBV) reactivation. Such a variant was detected in a 78-year-old female who was HBsAg(-)/anti-HBc(+)/anti-HBs(+)/anti-HBe(+), and with normal ALT levels, who developed HBV reactivation after fludarabine treatment. She had high HBV-DNA levels, and became positive for HBeAg, in the absence of detectable HBsAg. HBV-DNA was extracted from serum and the HBsAg encoding region of the genome was amplified by PCR, followed by cloning and sequencing. The HBV strain appeared to be subtype adw, but had higher nucleotide homology with ayw than adw isolates, supported further by phylogenetic tree analysis. Amino-acid sequence comparisons over the alpha determinant region revealed the following substitutions: C124N, G130R, and N146S. There were also unique substitutions outside the alpha determinant. All these mutations appeared to have a profound effect on the antigenicity of this region, which resulted in failure to detect HBsAg by commercially available diagnostic assays. It is concluded that a surface variant emerged in an HBsAg(-)/anti-HBs(+) patient with chronic lymphocytic leukaemia following fludarabine treatment, with an unprecedented number of amino-acid substitutions in the alpha determinant region of HBsAg, including a subtype switch.

We performed a study to investigate the difference between serum and plasma potassium concentration in patients with increase in one or more of the cellular components of blood.This study was performed in two phases. During the first phase, we performed a cross-sectional comparison of the difference between serum and plasma potassium concentration (Dk) in 341 patients with the various clinical conditions where pseudohyperkalemia has been described, as well as with secondary or spurious erythrocytosis and in 30 normal controls. A cut-off value of Dk discriminating polycythemia vera from other erythrocytoses was estimated. In the second phase we studied the significance of this cut-off value as predictor of polycythemia vera in 90 naive patients who were referred with an elevated hematocrit.Dk was significantly increased in the groups with platelet, erythrocyte or with a mixed type disorder compared to the controls (P0.01). Among these groups, Dk was significantly increased in the groups with thrombocytosis and mixed type disorder, compared to the group with erythrocytosis (both P0.01). A cut-off value of Dk discriminating polycythemia vera from other erythrocytoses was estimated (0.70 mmol/L). Dk (or = 0.70 mmol/L), platelet and white blood cell count were identified as significant independent predictors of polycythemia vera.The Dk is increased in patients with erythrocytoses, thrombocytoses or both. This phenomenon is more profound in patients with a mixed type disorder, such as polycythemia vera patients, compared to those with erythrocytoses alone.

Aim: To evaluate the characteristics and possible recent changes of the microbial causes of spontaneous bacterial peritonitis (SBP) in cirrhotic patients. Methods: We retrospectively evaluated 42 cirrhotic patients with positive ascitic fluid culture and without evidence of secondary peritonitis who were admitted consecutively to our Department between 1998 and 2002. Results: Twenty (48%) of 42 patients with positive ascitic fluid culture were diagnosed during 1998–1999 (period A) and the remaining 22 (52%) patients during 2000–2002 (period B). Gram-negative bacteria were the cause of SBP in 15 (75%) of the 20 patients during period A and in only nine (41%) of the 22 patients during period B (P=0.026). SBP patients with Gram-positive bacteria compared with those with Gram-negative bacteria were less frequently in Child class C (P=0.058) and had significantly higher ascitic fluid protein (P=0.014) and albumin concentrations (P=0.009) and lower ascitic fluid neutrophil count (P=0.008). Resistance to quinolones was detected significantly more frequently in the isolated Gram-positive than Gram-negative bacteria (P

Polymorphic variability in Helicobacter pylori factors CagA and VacA contributes to bacterial virulence. The presence of one CagA EPIYA-C site is an independent risk factor for gastroduodenal ulceration (odds ratio [OR], 4.647; 95% confidence interval [CI], 2.037 to 10.602), while the presence of the vacA i1 allele is a risk factor for increased activity (OR, 5.310; 95% CI, 2.295 to 12.287) and severity of gastritis (OR, 3.862; 95% CI, 1.728 to 8.632).

Objective The aim of the study was to assess the efficacy of a regimen consisting of 1 week of low-dose triple therapy with lansoprazole, amoxicillin, and clarithromycin followed by lansoprazole alone for an additional 3 weeks in the eradication of Helicobacter pylori and the healing of peptic ulcer. Methods Patients aged ≥16 years with active peptic ulcer diagnosed by endoscopy and H pylori infection were eligible for this prospective, open-label, 3-center study. A triple-drug regimen was used that consisted of lansoprazole 30 mg once daily, amoxicillin 1 g BID, and clarithromycin 250 mg BID for 7 days. Ulcer healing and H pylori eradication were assessed endoscopically 8 to 9 weeks after the start of treatment. H pylori was determined to be eradicated if both histologic examination and rapid urease testing (4 biopsy samples, antrum [2] and body [2]) were negative. Results Fifty-five patients who tested positive for H pylori , 49 with duodenal ulcer (DU) and 6 with gastric ulcer (GU), aged 16 to 78 years, were enrolled in the study. Ten patients were lost to follow-up and 1 withdrew from the study because of side effects; 44 patients were included in the per-protocol analyses. H pylori was eradicated in 34 patients, 62% (95% CI, 0.477–0.746) and 77% (95% CI, 0.662–0.885) in the intent-to-treat and perprotocol analyses, respectively. Ulcers were healed in a total of 38 patients (34 DU, 4 GU), 69% in the intent-to-treat population (95% CI, 0.552–0.809) and 86% in the per-protocol population (95% CI, 0.727–0.948). In patients with DU, the rate of healing was 69% in the intent-to-treat analysis (95% CI, 0.546–0.817) and 89% in the per-protocol analysis (95% CI, 0.752–0.971). Conclusions One week of therapy with lansoprazole 30 mg once daily, amoxicillin 1 g BID, and clarithromycin 250 mg BID, followed by 3 weeks of treatment with lansoprazole 30 mg once daily, effectively healed peptic ulcer but was only moderately effective in eradicating H pylori .

Background and Aims: The validity of the rapid urease (CLO) test to diagnose Helicobacter pylori infection in patients with bleeding ulcers has been questioned. The aim of this paper is to evaluate the validity of the CLO test in comparison with histology in diagnosing H. pylori infection in patients with acute upper gastrointestinal bleeding (UGB), irrespective of non-steroidal anti-inflammatory drug (NSAID) use. Methods: Upper gastrointestinal endoscopy was performed within 24 h of admission for all patients with UGB admitted to the Department of Pathophysiology, Medical School, Athens, for a period of 12 months. Patients with variceal bleeding, previous gastric operation, recent treatment with proton pump inhibitors (< 2 months) and those with a history of H. pylori eradication therapy were excluded from the study. At least four biopsies (two from the antrum and two from the body) were obtained for the CLO test and histology (modified Giemsa). Results: Seventy-two consecutive patients (aged 18–90 years, 51 men, 21 women) were included. Forty-six patients (64%) used NSAID. Thirty-two patients (44%) were found to be positive for H. pylori infection by the CLO test, while 44 patients (61%) were found to be positive on histology (P < 0.045, 95% CI, 0.004–0.331). The sensitivity and specificity of the CLO test were 68 and 93% respectively; positive and negative predictive values were 94 and 65%, respectively. The age of the patient and visible blood in the stomach did not inflence results of either the CLO or histology. Conclusions: The CLO test, performed within 24 h of hospital admission in patients with UGB, irrespective of NSAID use, is unreliable for the detection of H. pylori infection. The age of the patient and the presence of blood in the stomach do not seem to influence these results.

Carnitine palmitoyltransferase II (CPT2) deficiency is an inherited disorder associated with rhabdomyolysis. The adult form of CPT2 deficiency is usually "benign", characterized by episodes of rhabdomyolysis without extramuscular manifestations and with a good outcome, while the infantile type characteristically presents with severe metabolic symptoms such as hypoketotic hypoglycemia. We present here a case of severe rhabdomyolysis with acute renal failure and hypoglycemia in an adult patient with CPT2 deficiency.

Brucella endocarditis is a rare and life threatening complication of brucellosis. It usually involves the aortic valve and successful management requires a combination of medical treatment and valve replacement. We describe a case of tricuspid valve and defibrillator lead brucella endocarditis induced by the implantation of the defibrillator itself. Our patient was admitted to hospital with a 2-week history of fever, back pain and night sweats. One month prior to admission, due to episodes of syncope, he was hospitalized at the Cardiology Department and because of a low grade fever he underwent complete investigation with no result. His original symptoms relapsed 2 days after dischargement. Although serological tests were not indicative, blood cultures grew Brucella melitensis and transesophageal echocardiography showed a vegetation on tricuspid valve, which was mildly regurgitant. Fever subsided 2 days following start of triple antibiotic therapy and 2 weeks later the defibrillator and the pacemaker were surgically explanted.

Pseudohyperkalemia, a rise in serum potassium concentration with concurrently normal plasma potassium concentration, is an in vitro phenomenon that was first described 50 years ago. It was originally attributed to the release of potassium from platelets during platelet aggregation and degranulation, and a significant correlation between pseudohyperkalemia and platelet count was established. During the last decade, new data were added to this phenomenon. In particular, pseudohyperkalemia was defined when serum potassium concentration exceeded that of plasma by more than 0.4 mmol/L provided that samples are collected under strict techniques, remain at room temperature and are tested within 1 hour from blood specimen collection. Moreover, it is positively correlated to (1) thrombocytosis due to the release of potassium from platelet granules during coagulation, (2) erythrocytosis due to the dilution of the released potassium in smaller volumes of serum, and (3) the presence of activated platelets, which have the capability of aggregation at a higher speed and release more potassium during degranulation. However, pseudohyperkalemia may be "masked" when in a state of hypokalemia because potassium moves back into the intracellular space in vitro, and the phenomenon is ameliorated or even not detected.

A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described. Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor. No specific treatment was administered. The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.

Although autopsy series report liver granulomas in up to 70% of patients, computed tomography detection of hepatic and splenic lesions is described in 5% and 15% of sarcoidosis cases, respectively. A rather rare case of liver sarcoidosis mimicking macronodular cirrhosis is presented by this current article. Imaging findings in our patient were in compliance with the diagnosis of liver cirrhosis, although liver biopsy findings eventually revealed sarcoid granulomas located in the portal and lobular areas without fibrotic lesions. Histological and imaging modalities in liver sarcoidosis are discussed.

A prospective study was undertaken to investigate the potential value of morphometry and artificial neural networks (ANN) for the discrimination of benign and malignant gastric lesions. Two thousand five hundred cells from 23 cases of cancer, 19 cases of gastritis and 58 cases of ulcer were selected as a training set, and an additional 8524 cells from an equal number of cases of cancer, gastritis and ulcer were used as a test set. Images of routine processed gastric smears stained by the Papanicolaou technique were processed by a custom image analysis system. The application of the learning vector quantization (LVQ) classifier enabled correct classification of > 97% of benign cells and > 95% of malignant cells, obtaining an overall accuracy of > 97%. This study presents the capabilities of ANN, and also indicates that ANN and image morphometry may offer useful information on the potential of malignancy in gastric cells.

Sixty patients with advanced gastric carcinoma who refused to receive cytotoxic chemotherapy were examined for serum immunoglobulin levels (IgG, IgM, IgA, IgE). Three samples were obtained every two months thereafter. The group of patients who had above-normal values of one or more of the examined immunoglobulins had a longer survival than the other (p

Osteomyelitis of the pubic symphysis or pubic osteomyelitis is a rare entity that is encountered in certain groups of people such as athletes, intravenous drug users, patients with pelvic malignancy, and patients who have undergone surgical manipulations of the genitourinary system. The most frequent causative organism is Staphylococcus aureus. K pneumoniae is a common pathogen in diabetic patients, but pubic osteomyelitis due to K pneumoniae has not previously been described. We present a diabetic patient with pubic osteomyelitis caused by K pneumoniae without known predisposing factors.