Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to assess the prevalence of eosinophilia in 358 consecutive samples of pleural fluid (all cases corresponded to first thoracentesis), to review the cause of eosinophilic pleural effusions, and to determine whether the presence of eosinophils increases the likelihood of nonmalignant underlying disorders. Eosinophilic pleural effusions were identified in 45 patients (12.6%): malignant underlying conditions were diagnosed in 11 patients (24.4% with eosinophilic effusions) and benign aetiologies were found in 27 patients. Benign aetiologies included uncomplicated paraneumonic effusion in 10 patients, tuberculosis in seven, complicated paraneumonic in five, liver cirrhosis in three, hydronephrosis in one and pulmonary thromboembolism in one. Seven pleural effusions were idiopathic. There was no difference in the prevalence between eosinophilic and noneosinophilic effusions according to the different diagnoses. With parameters of sensitivity, specificity, pretest and post-test probability and positive and negative predictive values for any prevalence figure using the Bayes' theorem and for any value of eosinophils (both in percentage or absolute numbers) in the pleural fluid (receiver operating characteristic curve) an adequate predictor of benign disease was not found. It is concluded that pleural eosinophilia at the initial thoracentesis cannot be considered as a predictor of an underlying benign disorder.
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PMID:Diagnostic utility of eosinophils in the pleural fluid. 1096 19

To assess epidemiological and clinical significance of drug hepatotoxicity in the setting of liver diseases consultation, ten thousand and three hundred forty two prospectively designed clinical records from patient cared for in our Liver Unit in the period 1988-1998 were incorporated into the study; 58 out of 10,342 (prevalence = 5.6%) fulfilled at least the first three of the following causality requirements: 1.--Liver injury associated in time to drug exposition; 2.--Negative evaluation of more common other etiologies; (alcohol, viruses, immunologic, metabolic, etc) 3.--Favourable response to drug withdrawal (ALT < 50% of baseline in 8 to 30 days in acute hepatitis type, and alkaline phosphatase and/or total bilirubin < 50% of baseline up to 6 months, in acute cholestasis) 4.--Inadverted or rarely prescribed positive challenge. Acute hepatitis type of injury were considered when serum ALT rise 8 times or more above normal superior level with alkaline phosphatase (APh) below 3 times; "pure" cholestasis when APh rise 3 times or more above normal with ALT below 8 times; mixed acute injury or cholestatic hepatitis when both ALT and APh were elevated above 8 and 3 times respectively, and indeterminate type when both enzymes were below the referred levels. Chronic injury were considered when six or more month of evolution and compatible liver histology happens. Clinical severity were expressed as mild (absence of major clinical complications, serum bilirubin < 5 mg/dl and prothrombin concentration > 75%), moderate (presence of clinical complications, bilirubin > 5 mg/dl and prothrombin concentration between 50-75%), and severe (major clinical complications with bilirubin > 5 mg/dl and prothrombin concentration < 50%). Female/male ratio was 1.4:1, with age average 39 years (R = 15-77) and major concentration of cases above 40. More than 50% of cases received 2 or more drugs. Jaundice was present in 60.4%, and systemic manifestations of hypersensibility (fever, adenomegalies, rush, mononucleosis like syndrome, eosinophilia) in 29.3%. Acute injury represented 91.4% of the cases: 41.4% acute hepatitis, 15.5% "pure" cholestasis, 24.1% cholestatic hepatitis, and 10.3% indeterminate type. Four patients (4.5% of acute injury cases) were presented as severe acute liver failure, leading to liver transplant in one of them, drug association (INH-rifampicin and carbamazepine-phenobarbital) and inadverted challenge (sulphonamides and pemoline) were associated to clinical severity. Chronic injury were found in five patient (8.6%), four of them associated to chronic hepatitis and the other one to a ductopenic syndrome. Six drugs represented 53.4% of our cases; oral contraceptives (7 cases), INH alone or combined with rifampicin (6 cases), sulfonamides and clorpropamida (5 cases each), carbamazepine and amiodarone (4 cases each). Normalization of liver enzymes after drug suppression took 2 to 8 weeks in acute hepatitis type (X = 4 weeks), 4 to 20 in "pure" cholestasis (X = 12 weeks) and 8 to 24 weeks in cholestatic hepatitis or mixed type (X = 16 weeks). Two cases of chronic hepatitis normalize the histological activity index in 20 and 18 month respectively, one case remains as chronic hepatitis at 10 month and the other one progress to cirrhosis; the ductopenic syndrome normalize histology in 19 months receiving urso-deoxicolic acid, 10 mg/k/day.
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PMID:[Clinic-epidemiological significance of drug hepatotoxicity in liver disease consultation]. 1092 31

We report a case of a 72-year-old woman with Churg-Strauss syndrome, who presented with intestinal perforation. She has had bronchial asthma with peripheral blood eosinophilia for 30 years. Gross findings of a resected colon showed multiple ulcers with perforation. Histologic findings demonstrated transmural inflammation infiltrated with large numbers of eosionophils, neutrophils and lymphoplasma cells, and characteristic extravascular granuloma in the subserosa. There were multifocally-distributed transmural vasculitis showing all stages of activity in medium and small-sized arteries and veins located in the submucosa, and proper muscle and subserosal layers of the colon, some of which revealed granulomatous inflammation. Histologic finding of liver showed chronic viral hepatitis B with mild inflammatory activity and macronodular cirrhosis. Immunohistochemical findings, acid fuschin orange G staining and electromicroscope found no evidence of hepatitis B virus infection contributing to the pathogenesis of this lesion.
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PMID:Churg-Strauss syndrome with perforating ulcers of the colon. 1106 98

The diagnosis and management of strongyloidiasis present a continuous challenge in developing countries including Taiwan. In this study, the clinical characteristics and microbiological findings of 27 patients with Strongyloides stercoralis infection were retrospectively analyzed. Intestinal infection was identified in 17 patients and hyperinfection syndrome or disseminated disease in 10 (including 2 autopsy cases). The most frequent clinical findings were diarrhea (74%), fever (70%), abdominal pain (59%), cough (37%), dyspnea (33%), and constipation (26%). The common initial laboratory abnormalities were leukocytosis (81%), anemia (67%), liver function impairment (52%), and eosinophilia (44%). Most of the 27 patients had comorbid conditions, including malnutrition in 20 (74%), corticosteroid dependence in 15 (55%), chronic obstructive pulmonary disease in 9 (33%), chronic liver disease or cirrhosis in 8 (30%), and peptic ulcer disease in 7 (26%). There was no difference in the time interval from symptom onset to diagnosis between the intestinal infection group and the hyperinfection/disseminated group (22 +/- 15 vs 17 +/- 9 days). Larvae of S. stercoralis were identified in the stool of 24 patients, in the sputum smear of 5, in the gastric biopsy of one, and on histology of autopsy specimens in 2. Twenty-six patients received antiparasitic drug therapy of variable duration (mebendazole in 24, albendazole in 2, combined therapy in one). The overall cure rate was 52% (14/27). Relapse occurred in 4 patients. The overall mortality was 26% (7/27). There was a high mortality (up to 50%) in the hyperinfection/disseminated disease group. In conclusion, diagnosis of strongyloidiasis is often delayed and overlooked because of nonspecific symptoms. Physicians in endemic regions should include strongyloidiasis in the differential diagnosis when patients present with gastrointestinal and/or pulmonary symptoms with peripheral eosinophilia.
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PMID:Clinical manifestations of strongyloidiasis in southern Taiwan. 1195 Jan 17

The study included 200 patients with pleural effusion. Pleural effusions were transudative in 48 (24%) and exudative in 152 (76%) of cases. Congestive cardiac failure (14.5%), nephrotic syndrome (5.5%), and liver cirrhosis (2.5%) were the most common etiological diagnoses of transudate cases. Malignant effusion (16.5%), pneumonia (13%), pleural empyema (9%), tuberculosis (6%), and pulmonary embolism (5.5%) were the most common etiological diagnoses of exudative cases. Thirty-two (16%) cases of exudative pleural effusions were of undertermined etiology. Polymorphonuclear leucocytes predominated in 48 patients with exudative pleural effusions. The most common etiological diagnoses were pneumonia (41.67%), pleural empyema (39.59%) and pulmonary embolism (10.42%). Lymphocytes in pleural fluid were predominant in 63 patients, with malignant (6.34%), tuberculous pleurisy (19.02%), pulmonary embolism (6.34%), trauma (6.34%), and (46.11%) cases in patients with pleural exudate undertermined etiology. Eosinophyls were predominant in 16 (8%) patients with exudative pleural effusions. The most common etiology of eosinophilic pleural fluid were pneumonia (37.5%), malignant pleural effusion (25%), pulmonary embolism (12.5%), pyopneumothorax (6.25%) and trauma 6.25%. From 16 patients with eosinophilic pleural exudate, in 31% cases air, in 12.5% blood in pleural fluid were determined and in 12.5% cases previous pleural puncture was performed. Pleural fluid eosinophilia is most commonly associated with the presence of air or blood in the pleural fluid (correalation index 0.82). Malignant pleural effusions were determined in 33 patients. Malignant cells in pleural fluid were identified in 25 cases. The diagnostic sensitivity of pleural fluid cytology for malignant pleural effusions were 76%. Hemoragic pleuritis was determined in 18 and hemothorax in 4 patients. Etiology of hemothorax were trauma (75%) and coaguliopathia (25%). Most common etiological diagnoses of hemoragic pleuritis were neoplasia (33.3%), pulmonary embolism (16.65%), trauma (16.65%), pneumonia (11.11%), and congestive cardiac failure (11.11%). Diagnostic sensitivity and specifity of hemoragic pleuritis is low, 58% and 45% respectively.
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PMID:[Diagnostic value of pleural fluid cytologic examination]. 1255 57

There is some portion of patients with clinically manifested acute viral hepatitis, which are seronegative to hepatitis A markers. They have to be differentiated with other patients with B, C, D hepatitis, mechanical jaundice, etc. Such clinical cases make physician to recall the parasitic diseases, such as fascioliasis, which affects hepatobiliary system, causes prolongation of cholestasis and dystrophic changes in the biliary tract and likely to cause liver cirrhosis. In the presented case the initial diagnosis was severe acute Hepatitis A (anti-HAV IgM+), though the peripheral blood examination showed moderate eosinophilia, ultrasound investigation revealed multiple sites of damage in the liver, which made us to consider fascioliasis, the latter was confirmed by the serological analysis. Appropriate medical treatment was effective and the state of the patient has improved.
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PMID:[Fascioliasis case in the patient with hepatitis A]. 1585

A characterization of the humoral immune response of alpacas to Fasciola hepatica Fas1 and Fas2 antigens, two abundant cysteine proteinases in the excretory/secretory (E/S) products, was performed over the course of 6 months of experimental infection. Six adult alpacas aged 1-2 years old received a single dose of 200 F. hepatica metacercariae; two non-infected alpacas were kept as control group. All infected animals shed eggs 8 weeks post-infection (PI) and the number of flukes recovered at necropsy averaged 41+/-4. The livers of infected animals showed regions with chronic inflammation, granuloma containing parasite eggs, necrosis and cirrhosis. Peripheral eosinophilia in infected animals was greatly enhanced 6 weeks post-infection and later. A single peak of serum glutamic piruvic transaminase (SGPT) was observed 4 weeks PI and serum glutamic oxalacetic transaminase (SGOT) elevated 3 weeks PI and later. Circulating IgG Abs against Fas1 and Fas2 were measured by enzyme-linked immunosorbent assay (ELISA). Fas2-ELISA detected the infection 10 days PI reaching to highest titer on 7-8 weeks PI and kept elevated, until the end of infection. Fas1-ELISA detected the infection 2 weeks PI and followed the same pattern as Fas2-ELISA. Anti Fas2 IgG Abs were in higher titers and showed stronger avidity than anti Fas1 IgG Abs. In addition, rabbit IgG antibodies raised against cysteine proteinase Fas2 showed infiltration of this parasite antigen associated to the degradation of bile ducts and liver parenchyma of infected alpacas. In the present study we have established a F. hepatica experimental infection of alpacas, Fas2 appears to have a role in the pathogenesis of the liver damage in alpacas caused by the liver fluke. Infected alpacas elicited a strong humoral immune response against fluke cysteine proteinases Fas1 and Fas2, which might be considered as candidates for immunodiagnosis and vaccine development against fasciolosis in alpacas.
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PMID:Characterization of the humoral immune response in alpacas (Lama pacos) experimentally infected with Fasciola hepatica against cysteine proteinases Fas1 and Fas2 and histopathological findings. 1591 Sep 94

A rare case of well-differentiated minute hepatocellular carcinoma (HCC) with hepatitis C virus-related cirrhosis, with unusual radiologic features, is presented. A 10-mm hypoechoic nodule disclosed by ultrasound in segment six showed hypoattenuation on computed tomography hepatic arteriography and hyperattenuation on computed tomography during arterial portography, indicating that the portal vein may have been the dominant vascularity of the nodule. Contrast-enhanced ultrasound revealed hypovascularity in the early arterial phase, isovascularity in the late vascular phase, and the same perfusion as that surrounding the liver parenchyma in the post-vascular phase, with the same pattern observed on the two imaging techniques. These findings were considered not compatible with those of well-differentiated HCC. Ultrasound-guided biopsy showed histological features of well-differentiated HCC with over two-fold the cellularity of the non-tumorous area with a high nuclear/cytoplasmic ratio, increased cytoplasmic eosinophilia, slight atypia and fatty change with an irregular thin trabecular pattern. Further studies may provide insights into the correlation between tumor neovascularity in multistep hepatocarcinogenesis and dual hemodynamics, including the artery and the portal vein.
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PMID:Well-differentiated HCC manifesting hyperattenuation on CT during arterial portography. 1620 Nov 19

We describe a rare case of the transformation of a dysplastic nodule into well-differentiated hepato-cellular carcinoma (HCC) in a 56-year-old man with alcohol-related liver cirrhosis. Ultrasound (US) disclosed a 10 mm hypoechoic nodule and contrast enhanced US revealed a hypovascular nodule, both in segment seven. US-guided biopsy revealed a high-grade dysplastic nodule characterized by enhanced cellularity with a high N/C ratio, increased cytoplasmic eosinophilia, and slight cell atypia. One year later, the US pattern of the nodule changed from hypoechoic to hyperechoic without any change in size or hypovascularity. US-guided biopsy revealed well-differentiated HCC of the same features as shown in the first biopsy, but with additional pseudoglandular formation and moderate cell atypia. Moreover, immunohistochemical staining of cyclase-associated protein 2, a new molecular marker of well-differentiated HCC, turned positive. This is the first case of multistep hepatocarcinogenesis from a dysplastic nodule to well-differentiated HCC within one year in alcohol-related liver cirrhosis.
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PMID:Multistep hepatocarcinogenesis from a dysplastic nodule to well-differentiated hepatocellular carcinoma in a patient with alcohol-related liver cirrhosis. 1745 Dec 13

Idiopathic HES is characterlized by prolonged eosinophilia without an identifiable underlying cause and multiple-organ dysfunction. We report a case of a LDLT for a 12-yr-old Japanese girl with BA accompanied by HES. Histological examination of the resected liver showed biliary cirrhosis with dense eosinophilic infiltration of portal tracts and the lobules of the liver. She developed portal vein thrombosis on post-operative day 10 and the histopathological findings of the thrombus revealed dense eosinophilic deposition, suggesting that HES might have influenced the formation of this thrombus. Liver graft biopsies also demonstrated the presence of activated eosinophilils with biliary damage. Blood chemistry findings suggested liver dysfunction as a result of the eosinophilic infiltrations. Prednisolone treatment improved the liver dysfunction. Four years after LDLT, she remains clinically well on prednisolone at 0.3 mg/kg/day, with an eosinophil count ranging from 10 to 15%. A literature review has not shown any previous reports of HES with BA. This case demonstrates the possibility of an association between eosinophilic infiltration and liver dysfunction during follow-up for BA and after LDLT.
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PMID:Idiopathic hypereosinophilic syndrome in a case with ABO-incompatible liver transplantation for biliary atresia complicated by portal vein thrombosis. 2004 17


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