Low dose amiodarone associated cirrhosis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Sahin Coban.
Explore the source record for details and available documents.
INTRODUCTION: Any organ in the human body may be affected by hydatid disease, but the liver and the lungs are most commonly affected. A rare localization of hydatid disease is within muscle tissue. Herein we present three patients with muscular hydatid disease who were successfully treated with a modified percutaneous approach. METHODS: Patients with Gharbi type III cysts were treated on an outpatient basis. All procedures were performed under ultrasound guidance in the ultrasonography unit of our department. After local anesthesia, percutaneous puncture was performed in a one-step procedure. After free drainage stopped, absolute ethanol and polidocanol were injected into the cyst cavity. After the procedure, the patient was observed for at least six hours for any adverse reactions and sent home. Patients were followed-up with ultrasonography. A positive treatment effect was characterized by a reduction of the cyst's pseudo-tumor pattern and size, and by detachment of the germinal membrane. RESULTS: The three patients in this report had a total of five hydatid cysts in muscle tissue and were all successfully treated with a modified percutaneous approach without recurrence. CONCLUSION: Percutaneous drainage without re-aspiration is simple, easy to apply, low cost, repeatable, and does not require hospitalization. There have been no reported deaths associated with the procedure and morbidity is very low. When the technique is applied properly, relapses do not occur. With its low complication rate and its suitability for outpatient treatment, this method can be an alternative to surgery or puncture, aspiration, injection, and re-aspiration (PAIR) in selected patients.
BACKGROUND/AIMS: RCAS1 is a novel tumor marker, and there are no sufficient data about the utility of this antigen as a serum tumor marker and about its tumor specificity. We aimed at measuring the serum levels of RCAS1 in patients with pancreatic cancer and at determining its diagnostic efficacy. METHODS: Sera collected from patients with pancreas adenocarcinomas (39 cases) and benign biliary and pancreatic diseases (19 cases) and from healthy volunteers (13 cases) were analyzed for RCAS1 and the results compared with CA19-9. The relation between serum RCAS1 and tumor stage was also evaluated. RESULTS: The serum RCAS1 levels exceeded the normal limit in 92.3, 26.3, and 23.0% of the patients with pancreatic cancer and benign biliary and pancreatic diseases and healthy volunteers, respectively. RCAS1 had a specificity similar to that of CA19-9 in pancreatic cancer, whereas RCAS1 had a higher sensitivity (p < 0.05). Both tumor markers had similar predictive values of positive and negative tests for pancreatic cancer. The RCAS1 level was less influenced than the CA19-9 level by biliary stenoses. The median serum levels of RCAS1 increased, as the tumor stage increased. CONCLUSIONS: RCAS1 is a valuable serum marker for the diagnosis of pancreatic cancer. The RCAS1 and CA19-9 levels increase the diagnostic efficiency of each other in pancreatic cancer.
Standard antituberculous therapy including isoniazid, rifampin, ethambutol, and pyrazinamide is widely used for the treatment of active tuberculosis. Its most important side effect is hepatotoxicity, ranging from asymptomatic transaminitis to fulminant hepatic failure. A 19-year-old woman was admitted to our unit due to jaundice and unconsciousness. According to her past medical history, she was diagnosed as having extrapulmonary tuberculosis and had been prescribed standard antituberculous therapy. The patient became icteric and unconscious on the fourth day after therapy initiation. She was diagnosed with drug-induced acute fulminant hepatic failure and underwent living-related liver transplantation. Nonhepatotoxic antituberculous therapy (cycloserine, ciprofloxacin, streptomycin, and ethambutol) and low-dose immunosuppressive therapy were started after transplantation. Currently the patient is very well with normal graft function 42 months after transplantation. Here we report a case of a patient with acute fulminant hepatic failure caused by isoniazid, rifampicin, or both, who was successfully treated with living-related liver transplantation and a relatively less hepatotoxic antituberculous therapy. In conclusion, liver transplantation is a feasible therapy for individuals with standard antituberculous therapy-induced hepatic failure. Nonhepatotoxic antituberculous therapy may achieve control of active tuberculosis in such individuals after transplantation.
BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) comprises a wide spectrum of liver injury, ranging from steatosis and steatohepatitis to cirrhosis. Reasons for the different natural course in individuals with NAFLD are still unclear. The aim of this study was to describe the natural course of disease in individuals with NAFLD who did not receive pharmacological therapy. METHODS: A total of 27 individuals with NAFLD (male/female ratio: 10/17, mean age 49.7 years) were prospectively enrolled. Management after diagnosis consisted of establishment of an appropriate diet and exercise (walking and jogging) program, treatment of associated metabolic conditions such as diabetes and dyslipidemia, and discontinuation of potentially hepatotoxic drugs if the patient was taking these. Liver tests were performed at diagnosis and at 3-month intervals during the follow-up period. Mean follow-up period was 43.3 months (range 36-49 months). RESULTS: From baseline to the end of the follow-up period, although there was no significant difference observed in terms of the mean body mass index, serum aminotransferase levels significantly improved (48.8+/-29.9 U/L to 31.6+/-16.0 U/L for aspartate aminotransferase [AST] and 66.3+/-38.3 U/L to 39.6+/-22.9 U/L for alanine aminotransferase [ALT]; P<0.05). No significant differences in platelet counts, serum albumin level or prothrombin time were observed (P>0.05). No patient developed signs of advanced liver disease during the follow-up period. CONCLUSION: A treatment strategy comprising diet, exercise and management of associated metabolic conditions is associated with improvement in aminotransferases among patients with NAFLD. Further investigation is needed to examine the long-term efficacy of this approach on liver histology and clinical outcomes.
BACKGROUND: Receptor-binding cancer antigen expressed on SiSo cells (RCAS1) is a novel tumour marker that has been described in various kinds of cancer. The majority of observations include immunohistochemical studies; however, there are not enough data about the utility of this antigen as a serum tumour marker and its tumour specificity. AIM: To measure the serum levels of RCAS1 in patients with gastrointestinal (GI) tract cancers and compare them with other GI tract tumour markers. PATIENTS AND METHODS: Sera collected from patients with GI cancers (14 esophagus, 32 gastric and 36 colon) and from healthy volunteers (30 individuals) were analyzed for RCAS1 and compared with carcinoembryonic antigen (CEA) and cancer antigen 19-9. The relationship between serum RCAS1, tumour stage and tumour grade was also evaluated. RESULTS: Mean serum RCAS1 level was higher in patients with GI tract cancers compared with the control group (P=0.001). Among GI tract cancers, RCAS1 had lowest and highest sensitivity for esophagus and colon cancer diagnosis, respectively. Serum RCAS1 had a higher sensitivity for malignancy, except in the colon, and lower specificity in all groups compared with CEA. In comparison with cancer antigen 19-9, serum RCAS1 was more sensitive but less specific for all GI cancer groups. Mean serum RCAS1 levels were not statistically significant among histopathological tumour types (P>0.05). Although serum RCAS1 levels were significantly higher in cases with lymph node involvement compared with lymph node-negative cases (P=0.009), there was no difference between cases with and without serosal involvement, vascular invasion and distant metastasis; no correlation was found between tumour size and RCAS1 levels. CONCLUSIONS: RCAS1 may be used and combined with CEA as a tumour marker in GI tract cancers.
BACKGROUND: The aims of this study were to determine the presence of trefoil factor family-3 (TFF3) expression in biliary epithelial cells (BECs) of chronic graft-versus-host disease (cGVHD) of the liver after allogeneic hematopoietic cell transplantation, to compare such expression in chronic liver diseases (CLD) with/without predominantly biliary disease, and to assess the effect of bile duct injury on the degree of TFF3 expression in BECs of cGVHD. METHODS: A total of 82 paraffin-embedded liver biopsy samples were reviewed. These samples were basically divided into two distinct groups according to the presence of ductal injury: group 1 with CLD and predominantly biliary disease (n=26: 17 cGVHD and 9 primary biliary cirrhosis [PBC]) and group 2 with CLD and predominantly parenchymal liver disease (n=56: 20 steatohepatitis and 36 chronic viral hepatitis). Group 2 was used as the controls. Immunohistochemistry was performed using a polyclonal anti-TFF3 antibody. Real-time quantitative PCR was used for the detection of TFF3 mRNA expression. RESULTS: Positive TFF3 immunohistochemical staining and the presence of TFF3 messenger RNA gene expression was demonstrably higher in group 1 than that in group 2 (P<0.0001 and P<0.05, respectively). No significant difference in terms of positive TFF3 stained BECs between GVHD and PBC samples was observed (P>0.05). The extent of TFF3 expression in GVHD samples with severe ductal injury were significantly more common than that of GVHD samples with mild/moderate ductal injury (P<0.0001). CONCLUSIONS: The expression of TFF3 in cGVHD of the liver is increased in response to bile duct damage and repair. Such expression seems to be related the severity of ductal injury.
OBJECTIVE: To report a case of possible levofloxacin-induced acute fulminant hepatic failure. CASE SUMMARY: An unconscious 55-year-old woman was hospitalized with the diagnosis of hepatic encephalopathy. The patient had received levofloxacin 500 mg daily for 10 days because of an upper respiratory infection. Her past medical history revealed hepatitis B surface antigen positivity as an asymptomatic hepatitis B virus carrier for 10 years. After hospitalization, treatment included plasmapheresis and supportive care. The patient's consciousness improved on the second day of treatment. Other etiologies of fulminant hepatic failure were ruled out, suggesting levofloxacin-induced fulminant hepatic failure. Although the patient received supportive treatment, her condition gradually deteriorated and she died 12 weeks after admission to our hospital. An objective causality assessment revealed that the adverse event was possibly related to levofloxacin. DISCUSSION: Levofloxacin is widely used because of its broad spectrum of antimicrobial activity. As of August 9, 2005, to our knowledge, only one case of fulminant hepatic failure in relation to levofloxacin has previously been published. We believe that, in our patient, the relationship between levofloxacin and her illness is clear because of the negative results in the etiological studies, the short time between the drug's administration and the development of disease, and the pathologic findings suggestive of drug-induced hepatitis. CONCLUSIONS: Clinicians should be aware of the possibility of severe hepatic injury associated with levofloxacin when prescribing this drug.
Our aim was to analyze patients diagnosed with left-sided portal hypertension prospectively and to document the complications at follow-up. Twenty-four patients with isolated splenic vein thrombosis (diagnosed by ultrasonography or angiography or intraoperatively) and/or isolated fundal varices (diagnosed by endoscopy or endosonography) were involved in this study. Demographics, clinical presentation, diagnostic and therapeutic procedures, and morbidity and mortality were recorded in their follow-up. There were 11 and 13 left-sided portal hypertension cases associated with pancreatic diseases and nonpancreatic disorders, respectively. Chronic abdominal pain and gastrointestinal bleeding were the two most common complaints. All patients except one had isolated esophageal (2 cases) or fundal (21 cases) varices. Thirteen patients had splenomegaly on ultrasonography. On Doppler sonography, the splenic vein could be evaluated in 21 of the 24 patients (9 and 6 had complete and partial occlusion, respectively, and 6 had patent blood flow). Urgent intervention with therapeutic endoscopy and splenectomy was performed for two patients each. Medical therapy was begun for three patients according to the underlying diseases. Three patients underwent elective surgery. Two patients were lost to follow-up after the first visit and the mean follow-up of the remaining 22 patients after diagnosis of left-sided portal hypertension was 20 months. Only one patient (with pancreas cancer) had gastrointestinal bleeding at follow-up. All patients with pancreas and gastric cancer died within 2-12 months. Left-sided portal hypertension has various etiologies. It may be difficult to diagnose this entity both endoscopically and radiologically. Treatment should be directed at the underlying diseases. Recurrent hemorrhage due to left-sided portal hypertension is not usual and the prognosis depends mainly on the underlying etiology.
Explore the source record for details and available documents.
Cytomegaloviral enterocolitis is an uncommon infection that can complicate inflammatory bowel disease. A case of a patient with a three-year history of Crohn's disease is reported. He had been in a stable condition on mesalamine 4 g/day and methylprednisolone 10 mg/day for three years until four weeks before admission. The patient was admitted with complaints of fever, abdominal pain and watery diarrhea. A diagnosis of an exacerbation of Crohn's disease was established. The radiological examination revealed narrowing of the terminal ileum. Multiple fistulas and abscess-like images were observed. The patient then underwent ileocolic resection and ileostomy. The histopathological examination revealed Crohn's ileocolitis with superimposed cytomegalovirus infection. In patients with rapidly deteriorating inflammatory bowel disease, cytomegalovirus infection should be kept in mind as one of the differential diagnoses.
BACKGROUND: Hepatocellular carcinoma is a common malignancy for which chronic hepatitis B infection has been defined as the most common etiologic factor. The most frequent metastatic sites are the lung, bone, lymphatics, and brain, respectively. Metastases to the chest wall have been reported only rarely. CASE PRESENTATION: We report a patient with hepatocellular carcinoma who presented with an isolated metastatic mass on the left anterolateral chest wall in the axillary region. CONCLUSIONS: Metastasis of HCC should be included in the differential diagnosis of rapidly growing lesions in unusual localizations, particularly in patients with chronic liver disease even if a primary tumor can not be radiologically identified.
OBJECTIVE: To present a single case of sulbactam/ampicillin-induced chronic cholestasis and a literature review of antibiotic-associated chronic cholestasis. CASE SUMMARY: A 74-year-old man with Hodgkin's disease in remission developed severe and prolonged cholestasis after treatment with sulbactam/ampicillin 750 mg twice daily for 7 days. All other etiologies, including Hodgkin's disease, were appropriately ruled out and the cholestasis was ascribed to sulbactam/ampicillin treatment. The patient improved gradually and became asymptomatic 7 months after the last dose of sulbactam/ampicillin. According to the Naranjo probability scale, sulbactam/ampicillin was the probable cause of the cholestasis. DISCUSSION: Ampicillin, a semisynthetic penicillin, has rarely been associated with hepatic injury when used alone. Hepatocellular and acute cholestatic injury due to ampicillin have been described. Cholestasis secondary to sulbactam/ampicillin use has not been previously reported. CONCLUSIONS: Sulbactam/ampicillin, one of the most widely used antibiotics, may cause chronic cholestatic hepatitis. Clinicians should be aware of this adverse affect and consider it during diagnostic workup of liver injury.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.