Abstract: BACKGROUND/AIMS: Ulcerative colitis patients have increased risk for thromboembolic events. Factors predisposing to thrombosis in ulcerative colitis are poorly defined. The aim of this study was to evaluate possible thrombophilic abnormalities in patients with ulcerative colitis. METHODOLOGY: Fifty-one patients with ulcerative colitis and 51 healthy controls were studied. Disease activity, clinical and endoscopic, was assessed by standard criteria. Plasma levels of antithrombin, protein C, free protein S and activated protein C resistance were determined in both study groups. Genetic test for factor V Leiden was performed in cases with abnormal activated protein C resistance. Parameters of inflammation and fibrinogen were additionally measured in ulcerative colitis patients. RESULTS: Mean values of free protein S were significantly lower in ulcerative colitis patients (84.01 +/- 21.57) compared to healthy controls (100.17 +/- 24.7) (p < 0.001). Mean values of protein C were higher in ulcerative colitis patients (124.6 +/- 39.03) than healthy controls (100.19 +/- 19.86) (p < 0.001). No other significant differences were observed, but there was a trend towards higher prevalence of low values for antithrombin (9.8% vs. 0%, p = 0.056) and free protein S (19.6% vs. 5.9%, p = 0.072) in ulcerative colitis patients. Three ulcerative colitis patients and three healthy controls had low activated protein C resistance ratio. All these subjects were heterozygous for factor V Leiden. No correlation was observed between abnormalities in thrombophilic parameters and clinical, endoscopic or inflammatory parameters in ulcerative colitis group. CONCLUSIONS: Abnormalities in natural anticoagulants are more common in ulcerative colitis patients compared to healthy controls, irrespective of disease activity. Low activated protein C resistance ratio due to factor V Leiden is not more common in ulcerative colitis patients than in healthy controls.
Abstract: OBJECTIVE: The aim of this study was to investigate the incidence and long-term outcome of halitosis before and after eradication therapy in patients with functional dyspepsia and Helicobacter pylori infection. SUBJECTS AND METHODS: Halitosis and dyspepsia-related symptoms were investigated by way of a questionnaire. Only patients with functional dyspepsia, H. pylori infection and no histological evidence of atrophy were included in the study. A total of 18 patients fulfilled these criteria and completed the study. Four to six weeks after the end of eradication treatment, endoscopy or [(13)C] breath test was performed to check for H. pylori in the gastric mucosa. Halitosis and dyspeptic symptoms were re-evaluated during and at the end of follow-up. RESULTS: H. pylori infection was eradicated in all patients, in the 14/18 patients (77.8%) with triple drug therapy, and the 4/18 patients (22.2%) with quadruple drug therapy. During the follow-up period (mean 55.8 +/- 21.3 months (range 6-108 months)) resolution of halitosis was observed in 16/18 patients (88.9%), while 2 patients (11.1%) (p < 0.001) continued to present with halitosis. Also, eradication therapy resulted in statistically significant relief of all dyspeptic symptoms, except bloating. CONCLUSION: Eradication of H. pylori in patients with functional dyspepsia and halitosis results in sustained resolution of halitosis during long-term follow-up in the majority of cases. This finding supports the existence of a link between H. pylori infection and halitosis and suggests that H. pylori eradication might be considered in patients with halitosis.
Abstract: This study aimed to estimate the overall HCV genotype distribution and to reconstruct the HCV genotype-specific incidence in Greece during the recent decades. It also focused at the identification of genotype 4 subtype variability in Greek isolates. A total of 1686 chronically infected HCV patients with detectable serum HCV RNA by RT-PCR, belonging to different risk groups were studied. Amplified products from the 5'-noncoding region were typed using a commercially available assay based on the reverse hybridization principle. The HCV genotype-specific incidence was estimated using a previously described back calculation method. HCV genotype 1 was the most prevalent (46.9%) followed by genotype 3 (28.1%), 4 (13.2%), 2 (6.9%) and 5 (0.4%). A high prevalence of genotype 1 (66.3%) in haemophilia patients was recorded whereas HCV genotype 3 was found mainly among patients infected by I.V. drug use (58.2%). Data on the temporal patterns of HCV genotype-specific incidence in Greece revealed a moderate increase (1.3-1.6 times) for genotypes 1 and 4, and a decrease (1.5 times) for genotype 2 from 1970 to 1990, whereas there was a sharp (13-fold) increase for genotype 3. The molecular characterization of 41 genotype 4 HCV isolates belonging to various risk groups revealed that, subtype 4a was the most frequently detected (78%). Phylogenetic comparison of the Greek 4a isolates with all HCV-4a isolates reported worldwide so far revealed a topology which does not discriminate Greek isolates from the others. HCV-4 does not represent a recent introduction in Greece.
Abstract: BACKGROUND/AIMS: Osteoporosis has been recognized in patients with liver cirrhosis, although the prevalence and the exact mechanisms vary considerably in the literature. We have studied the prevalence of bone disease in cirrhotic patients, the pathogenesis and the relation to the etiology and the severity of liver failure. METHODOLOGY: The study included 83 hospitalized patients with various types of cirrhosis, where 25 healthy individuals served as controls. Patients were classified according to Child-Pugh's stages as follows: Child A: 49, Child B: 20, Child C: 14. Serum levels of iPTH, 250HD, LH, FSH, SHBG, testosterone, estradiol, IGF-I, osteocalcin and urine levels of cross-linked N-telopeptides of collagen type 1 (NTX) were measured in all patients. Bone mineral density (BMD) was measured by DEXA at the spine of both patients and controls. RESULTS: The prevalence of osteoporosis was higher in patients (26/83) 31.3% than in controls (4/25) 16%. Osteopenia was positively related with the elevated levels of crosslinked N-telopeptides (p=0.048). There were no differences in BMD between the types of cirrhosis. BMD was found to be significantly lower in Child B and C male patients than in Child A (p=0.043). Patients' groups B, and C had lower testosterone levels with a trend to contribute to the low BMD (p=0.15). 250HD and IGF-1 were significantly lower in decompensated cirrhosis (p<0.002), but did not correlate with BMD. CONCLUSIONS: Cirrhosis is a major cause of osteoporosis and the degree of osteopenia is related to the severity and not the etiology of the liver disease. The biochemical markers of bone remodeling suggest a high-turnover osteoporosis in cirrhosis.
Abstract: AIM: To study the prevalence and clinical significance of hyperhomocysteinemia (hHcys), an independent factor for arterial and venous thrombosis, in a group of patients with ulcerative colitis (UC). METHODS: Fasting homocysteine (Hcys), folate, and vitamin B(12) serum levels were measured in 40 UC patients and 50 healthy controls. Clinical data regarding UC were gathered. RESULTS: Median serum Hcys levels in UC patients were similar to controls (12.26 micromol/L vs 12.32 micromol/L), but the prevalence of hHcys was higher in UC patients than in controls (30% vs 10%, P = 0.028). UC significantly increased the risk of hHcys (adjusted odds ratio: 4.125; 95%CI: 1.26-13.44). Multivariate regression analysis showed that male sex, folate and vitamin B(12) deficiency or lower serum values were significant independent predictors of higher Hcys levels in UC patients (r(2) = 0.4; P<0.001). CONCLUSION: HHcys is common in UC patients and it is related to folate and vitamin B(12) deficiency or lower serum values. It would be reasonable for patients with UC to receive folate and vitamin B complex supplements as a prophylactic measure.
Abstract: AIM: To evaluate the plasma von Willebrand factor (vWF) levels in patients with ulcerative colitis (UC) and to investigate their relationship with disease activity, systemic inflammation and coagulation activation. METHODS: In 46 patients with ulcerative colitis (active in 34 patients), clinical data were gathered and plasma vWF levels, markers of inflammation (ESR, CRP, and fibrinogen) and thrombin generation (TAT, F1+2, and D-dimers) were measured at baseline and after 12 wk of treatment. Plasma vWF levels were also determined in 52 healthy controls (HC). The relationship of plasma vWF levels with disease activity, disease extent, response to therapy, acute-phase reactants (APRs) and coagulation markers (COAGs) was assessed. RESULTS: The mean plasma vWF concentrations were significantly higher in active UC patients (143.38+/-63.73%) than in HC (100.75+/-29.65%, P = 0.001) and inactive UC patients (98.92+/-43.6%, P = 0.031). ESR, CRP and fibrinogen mean levels were significantly higher in active UC patients than in inactive UC patients, whereas there were no significant differences in plasma levels of D-dimers, F1+2, and TAT. UC patients with raised APRs had significantly higher mean plasma vWF levels than those with normal APRs (144.3% vs 96.2%, P = 0.019), regardless of disease activity. Although the mean plasma vWF levels were higher in UC patients with raised COAGs than in those with normal COAGs, irrespective of disease activity, the difference was not significant (141.3% vs 118.2%, P = 0.216). No correlation was noted between plasma vWF levels and disease extent. After 12 wk of treatment, significant decreases of fibrinogen, ESR, F1+2, D-dimers and vWF levels were noted only in UC patients with clinical and endoscopic improvement. CONCLUSION: Our data indicate that increased plasma vWF levels correlate with active ulcerative colitis and increased acute-phase proteins. Elevated plasma vWF levels in ulcerative colitis possibly reflect an acute-phase response of the perturbed endothelium due to inflammation. In UC patients, plasma vWF levels may be another useful marker of disease activity or response to therapy.
Abstract: BACKGROUND: An acute and potentially life-threatening complication of hypertriglyceridemia (HTG) is acute pancreatitis (AP). Hypertriglyceridemia, usually severe, may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, and use of drugs. STUDY: The efficacy of treatment to prevent relapses in 17 patients with AP attributed to HTG was investigated in the current prospective study. The mean follow-up period of patients was 42 months. Hypertriglyceridemia-induced AP comprised 6.9% of all patients with AP (n = 246) hospitalized in our clinic during the study (6 years). RESULTS: Causative conditions of HTG-induced AP were familial HTG in eight patients, HTG caused by uncontrolled diabetes mellitus in five, HTG aggravated by drugs in two (one by tamoxifen and one by fluvastatin), familial hyperchylomicronemia (HCM) in one, and lipemia of pregnancy in one. During the acute phase of pancreatitis, patients underwent standard treatment. Thereafter, HTG was efficiently controlled with high dosages of fibrates or a fibrate plus acipimox, except for the patient with HCM, who was on a specific diet (the only source of fat was a special oil consisting of medium chain triglyceride) and taking a high dosage of acipimox. One of the patients died during the acute phase of pancreatitis with acute respiratory distress syndrome. During follow-up, maintenance treatment was successful and only one patient relapsed, because he discontinued diet and drug treatment. CONCLUSION: Appropriate diet and drug treatment, including dose titration, of severe HTG is very effective in preventing relapses of HTG-induced AP.
Abstract: BACKGROUND/AIMS: Adverse effects of NSAIDs (nonsteroidal antiinflammatory drugs) on the upper gastrointestinal tract and small intestine are well described. Evidence is also accumulating that implicate NSAIDs in inducing and exacerbating damage in the distal gastrointestinal tract. In this article we describe eight cases of colonic inflammation associated with nonsteroidal antiinflammatory drug administration; our aim is to stress the importance of an underestimated entity by clinicians. METHODOLOGY: Over a five-year period at two clinics, eight cases of NSAID-colopathy have been diagnosed. Crohn's disease, ulcerative and infections colitis have been excluded from this analysis. In all these subjects a careful drug history has been taken in a prospective manner and colonic inflammation appeared to be directly related to NSAID administration. There was a time interval (mean: 20 months) between initiation of treatment with NSAID and presentation with diarrhea, rectal hemorrhage and tenesmus. RESULTS: A correct diagnosis of colopathy associated with NSAIDs administration was made on careful drug history, pathological findings, stool cultures and biochemical changes which were insignificant, in contrast to the protracted troublesome symptoms. Resolution of symptoms was observed on discontinuation of NSAID medication. CONCLUSIONS: Our report is further evidence that NSAIDs administration is associated with significant mucosal injury in the distal gastrointestinal tract, despite is underestimated by most physicians.
Abstract: BACKGROUND: The aim of this study was to evaluate the effectiveness of endoscopic sphincterotomy for preoperative and postoperative complications of hepatic hydatid disease. METHODS: Nineteen patients underwent endoscopic treatment for complications of hepatic hydatid disease. Indications for ERCP in 5 patients treated before surgery (Group A) were obstructive jaundice in 1 and acute cholangitis in 4. In 14 patients treated after surgery (Group B), the indication was acute cholangitis in 6, obstructive jaundice 2, and persistent external drainage in 6 patients. OBSERVATIONS: In group A, ERCP detected hydatid vesicles within the bile duct. All patients underwent endoscopic sphincterotomy and clearance of the duct with no complications. The 6 patients in Group B with persistent external drainage had biliary fistulas that resolved after endoscopic treatment within 10 to 20 days. Among the 8 patients with postoperative obstructive jaundice or acute cholangitis, 7 had cyst remnants obstructing the bile duct and 1 had findings of sclerosing cholangitis. All underwent endoscopic sphincterotomy and clearance of the bile duct without complications. After treatment, all patients, with the exception of the one with sclerosing cholangitis, remained asymptomatic. CONCLUSION: Endoscopic sphincterotomy is a safe and effective treatment for biliary complications of hepatic hydatid disease.
Abstract: This report describes two patients who developed jaundice within two weeks of receiving an amoxycillin-clavulanate potassium combination. Causes of jaundice, other than drug administration, were excluded. The patients' jaundice and clinical symptoms did not respond to stopping the drug. Ursodeoxycholic acid (750 mg/day) led to a prompt and sustained improvement in their hyperbilirubinaemia and symptoms such as pruritus and fatigue. These cases suggest that ursodeoxycholic acid may be an effective treatment for drug-associated cholestasis.
Abstract: Four patients who developed endometriosis at the episiotomy scar are reported. The latent period varied from 6 months to 10 years before the onset of symptoms. Three of them experienced cyclic pain at the site of the lesion during their menses and one patient had bloody discharge from the scar during menstruation. All patients were managed surgically and no one had recurrence during the follow-up period which ranged from 2 to 5 years. The pathogenesis of endometriosis is discussed as a clinical entity; the literature is also reviewed.
Abstract: We report the cases of two women who had testicular feminization with remnants of Müllerian ducts and whose mothers had received diethylstilbestrol (DES) during the first trimester of pregnancy. At laparotomy, masses were removed which had the microscopic appearances of testes and Fallopian tubes, and were confirmed as such at histology. There were three possible explanations for these genetic abnormalities: deficient antimüllerian hormone (AMH) secretion (or lack of sensitivity of Müllerian ducts to AMH); early testicular descent with regression of Müllerian ducts beyond the efficacy margin of AMH; exposure to DES in utero during the first trimester of pregnancy. In these two women, the most likely explanation seems to be the last one.
