Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nodular regenerative hyperplasia (NRH) of the liver is a local hyperplastic response of hepatocytes, probably due to vascular abnormalities. Since it was shown in a few case reports that NRH may be associated with antiphospholipid antibodies (APA) we wanted to analyze the relevance of APA in patients with this disease. Sera from 13 patients with histologically defined NRH were tested for APA by an in-house ELISA using as antigens cardiolipin (CL), beta2-glycoprotein I (beta2-gp I), phosphatidylserine (PS), and thromboplastin (TP), a mixture of different phospholipids and phospholipid-binding proteins. As controls, sera from patients with serologically and histologically defined autoimmune liver diseases (primary biliary cirrhosis n = 14; autoimmune hepatitis n = 14) without histological evidence for NRH as well as from 14 healthy blood donors were analyzed. 77% of the NRH patients had APA. In 46% they were directed against CL. In contrast, only 14% of the patients with autoimmune liver diseases and 14% of the healthy controls had anti-CL antibodies (p < 0,05). Antibodies to beta2-gp I and TP did not discriminate between NRH and autoimmune liver diseases. Anti-PS antibodies were not observed. These data indicate that determination of anti-CL antibodies in NRH may help to identify a subgroup of patients in whom an 'organ-specific antiphosholipid syndrome' of the liver may be involved in the pathogenesis.
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PMID:Nodular regenerative hyperplasia (NRH) of the liver--a manifestation of 'organ-specific antiphospholipid syndrome'? 1263 4

During the period from July 1, 1999 to September 30, 2000, 9 children with severe adenovirus infection were treated at Chang Gung Children's Hospital. The mean age was 22 months (range, 5-50 months). All of them had lower respiratory tract infections, which manifested as lobar or segmental pneumonia and pleural effusion. Eight (88.9%) of the 9 patients required intensive care and 4 of them required mechanical ventilation. Abnormal laboratory findings included leukocytosis, elevated C-reactive protein, anemia, and prolonged prothrombin time and partial thromboplastin time. Extrapulmonary complications included hepatitis (6 cases), encephalitis (3), conjunctivitis (3), periorbital ecchymosis (1), and coagulopathy (2). One patient died, resulting in a mortality rate of 12.5%. Follow-up at 3 months postdischarge, 5 patients (62.5% of survivors) had bronchiolitis obliterans and/or organizing pneumonia. Seven patients were infected by serotype 3 adenovirus, 1 patient by serotype 2, and another by serotype 11. In conclusion, the clinical, laboratory, and radiographic features of severe adenovirus infection may mimic bacterial infection. Rapid progression of the clinical course despite antibiotic therapy and the presence of unusual extrapulmonary symptoms are important clinical clues in the diagnosis of severe adenoviral infection.
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PMID:Severe adenovirus infection in children. 1274 31

The aim of this study was to estimate the risk of mouse hepatitis virus (MHV) transmission by the in vitro fertilization and embryo transfer (IVF-ET) procedure. In addition, resistance to infection of zona-intact and laser-microdissected oocytes was compared. For this purpose, infectious mouse hepatitis virus, a common viral pathogen in mouse facilities, was used. Oocytes having an intact or laser-microdissected zona pellucida were incubated for fertilization in media containing MHV-A59 and resulting embryos were transferred to the oviduct of specific pathogen-free (SPF) Swiss recipients. The oocytes were divided into three experimental groups: 1) zona-intact oocytes continuously exposed to MHV in fertilization (HTF), culture (KSOM), and embryo transfer (M2) media; 2) zona-intact oocytes exposed to MHV in HTF medium and transferred after a standard washing procedure with virus-free KSOM and M2; and 3) laser-microdissected oocytes exposed to MHV in HTF medium and transferred after a standard washing procedure with virus-free KSOM and M2. Respective serum samples of embryo recipients and their offspring were tested for MHV antibodies using ELISA. In experiment 1, 10 out of 14 embryo recipients seroconverted to MHV and only their offspring (8 of 19) received maternal antibodies. In experiments 2 and 3, MHV antibodies were detected neither in the recipients nor in the offspring. These results indicate, for the first time, that even if the zona pellucida is partially disrupted by laser microdissection, the transmission of MHV-A59 can be avoided by correctly performed washing steps in the IVF-ET procedure.
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PMID:Risk assessment of mouse hepatitis virus infection via in vitro fertilization and embryo transfer by the use of zona-intact and laser-microdissected oocytes. 1622 89

Here we report a familial cluster of 3 cases of coxsackievirus B3 infection: a recent history of illness in a woman's 3-year-old son with a coxsackievirus B3-positive stool culture indicated that he probably infected his mother at home during her last week of pregnancy. Consequently, she delivered an infected neonate who developed severe hepatitis, disseminated intravascular coagulation, and bilateral intracranial hemorrhage. The neonate remained well for the first 2 days of life. On the third day, he developed fever (39 degrees C) and poor peripheral circulation. On the fourth day, he developed petechiae and bruises over his chest wall and extremities, and prolonged bleeding was observed over venipuncture sites. Investigations revealed severe thrombocytopenia (platelets: 41 x 10(9)/L) and a markedly deranged coagulation profile (prothrombin time: 19 seconds [reference: < 10 seconds]; activated partial thromboplastin time: > 120 seconds [reference: 24.2-37.0 seconds], serum D-dimers: 6722 ng/mL [reference: < 500 ng/mL]), suggestive of disseminated intravascular coagulopathy. Clinical examination revealed yellow sclera, hepatomegaly (5 cm), and splenomegaly (2 cm), consistent with hepatitis. Serial chest radiographs showed bilateral pleural effusions, and an ultrasound of the abdomen demonstrated ascites. An echocardiogram showed normal cardiac structure and good contractility of both ventricles. However, a cranial ultrasound revealed bilateral grade 2 intraventricular hemorrhages. Serum C-reactive protein increased to 33.9 mg/L. Liver-function tests were also markedly deranged at this time, with maximum values for serum alanine transferase, bilirubin, alkaline phosphatase, and ammonia concentration of 1354 IU/L, 258 micromol/L, 189 IU/L, and 147 micromol/L, respectively. Serum glucose levels were normal. Over the next 3 days, his fever subsided, and his liver function and clotting profile normalized by day 13 after onset of illness. A stool sample from the older brother, collected 14 days after his onset of illness at home, was positive for coxsackievirus B3 by both virus culture and enterovirus reverse-transcription polymerase chain reaction. He had neutralizing coxsackievirus B3 antibody titers of 1:2560 and 1:1280 on days 14 and 28 after his onset of illness, respectively. No virus was cultured from the mother's stool sample, collected 5 days after her onset of illness, but the enterovirus polymerase chain reaction was positive and maternal sera neutralized the coxsackievirus B3 isolated from the neonate. The maternal sera also showed a more than fourfold rise in antibody titer from 1:80 to 1:640 on days 5 and 16 after her onset of illness, respectively. Neonatal antibody titers also showed a more than fourfold rise from < 1:80 to 1:2560 on days 1 and 21 after his onset of illness, respectively. This demonstrates that both the mother and the neonate had had recent coxsackievirus B3 infections. Serially collected neonatal throat swab and stool samples were culture negative for enterovirus by 4 and 8 days after his onset of illness, respectively. However, enterovirus RNA remained detectable by reverse-transcription polymerase chain reaction in these samples for considerably longer, only becoming undetectable by 16, 23, and 41 days after his onset of illness. We show that even mild household infections may have potentially serious consequences for pregnant women and their infants.
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PMID:Probable intrafamilial transmission of coxsackievirus b3 with vertical transmission, severe early-onset neonatal hepatitis, and prolonged viral RNA shedding. 1690 22

The clinical information of acute Q fever in Taiwan was limited. A clinical study of 109 adults with serologically documented acute Q fever in the past decade (1994-2005) at 3 referral hospitals in southern Taiwan was reported. Their clinical manifestations, laboratory findings, and clinical outcomes were analyzed. Males predominated (98, 90%). There is a significant correlation between monthly average temperature and case numbers of acute Q fever (r = 0.74, P = 0.006). Fever (99%), chills (69%), and headache (45%) were the common symptoms, and relative bradycardia (44/60, 73 %) was often noted. Acute hepatitis, defined as either serum aspartate aminotransferase >or=60 IU/L or alanine aminotransferase >or=78 IU/L, was found in 88 (85%) cases, and more than one-third (31/87, 36%) had hyperbilirubinemia (serum total bilirubin >or=1.4 mg/dL) at initial presentation. The intervals between initiation of appropriate therapy to defervescence were longer in patients with hyperbilirubinemia than those without hyperbilirubinemia, irrespective of tetracycline or fluoroquinolone therapy. Of note, 8 (7.3%) cases experienced a prolonged period of fever (>28 days). In southern Taiwan, the predominant presentation of acute Q fever is acute febrile illness with hepatitis with or without jaundice. Acute Q fever should be added to the list of differential diagnoses of patients with fever, headache, relative bradycardia, elevated serum aminotransferase levels, or prolongation of activated partial thromboplastin time, irrespective of jaundice.
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PMID:Acute Q fever in southern Taiwan: atypical manifestations of hyperbilirubinemia and prolonged fever. 1794 35

We report a case of acute severe hepatitis with Mycoplasma pneumoniae (M. pneumoniae) infection and transient depression of multiple coagulation factors. A 5-year-old boy, previously healthy, was admitted with pneumonia. M. pneumoniae infection was confirmed by serology testing. Liver enzymes were elevated on admission without any past medical history. After treatment with azithromycin for 3 days, pneumonia improved, but the hepatitis was acutely aggravated. Partial thromboplastin time (PTT) was prolonged and depression of multiple coagulation factors developed. Liver biopsy revealed features consistent with acute hepatitis. A week later, liver enzymes were nearly normalized spontaneously. Normalization of prolonged PTT and coagulation factors were also observed several months later. This may be the first case of transient depression of multiple coagulation factors associated with M. pneumoniae infection.
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PMID:A case of acute hepatitis with Mycoplasma pneumoniae infection and transient depression of multiple coagulation factors. 1910 34

We conducted a cross-sectional study to investigate the clinical factors associated with mortality in patients with dengue viral infection at a tertiary care center over a 3 year period. Six hundred ninety-nine patients with a clinical diagnosis of dengue fever (DF), dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) during the study period were included in the study. Data were collected with a predesigned form comprised of demographics, duration of fever, associated symptoms, diagnosis of DF, DHF and DSS, and laboratory parameters [complete blood count, coagulation tests, creatinine, serum glutamic pyruvic transaminase (SGPT)]; dengue IgM was checked in all patients by ELISA. Outcomes (survival/mortality) and complications were recorded. Mortality was the primary outcome measure. DF constituted 86.4% (604), DHF constituted 11.6% (81) and DSS constituted 2% (14) of patients. The mortality rate was 2.7% (19). The mean white blood cell count in those who died was 13.3, in those who survived was 5.3, the difference was significant (p = 0.02). The mean BUN in those who died was 33.2, those who survived was 13.8, (p = 0.007). The mean bicarbonate level in those who died was 17.1, those who survived was 18.5 (p < 0.001). Mean activated partial thromboplastin time in those who died was 56.8, those who survived was 36.8 (p = 0.01). The mean SGPT in those who died was 802, those who survived was 176 (p = 0.01). Those who died were significantly (p < 0.001) more likely to have severe hepatitis (63%) than those who survived (13.8%). On multivariate logistic regression analysis, having an SGPT >300 mg/dl, bleeding, an altered mental status and shock at presentation were all significantly associated with mortality in patients with dengue virus infection (p = 0.008, p < 0.001, p < 0.001, p < 0.001, respectively).
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PMID:Clinical factors associated with mortality in dengue infection at a tertiary care center. 2057 16

Acquired haemophilia A, secondary to systemic lupus erythematosus (SLE), is a rare bleeding diathesis. Here we report a 37-year-old woman with autoimmune hepatitis who developed SLE and acquired haemophilia caused by factor VIII (fVIII) inhibitors. She presented with spontaneous ecchymosis and haematuria. There were a prolongation of the activated partial thromboplastin time, reduced fVIII activity and a high titre of fVIII inhibitors. Therapeutic regimen was started with intravenous methylprednisolone pulse, continued with prednisolone, intravenous pulse cyclophosphamide and fresh frozen plasma. After 8 weeks, fVIII inhibitor assay was negative.
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PMID:Acquired haemophilia A in a woman with autoimmune hepatitis and systemic lupus erythematosus: review of literature. 2188 54

Acquired haemophilia A, secondary to systemic lupus erythematosus (SLE) is a rare bleeding diathesis. Here we report a 37-year-old woman with autoimmune hepatitis who developed SLE and acquired haemophilia caused by factor VIII inhibitors. She presented with spontaneous ecchymosis and haematuria. There were a prolongation of the activated partial thromboplastin time, reduced factor VIII activity and a high titer of FVIII inhibitors. Therapeutic regimen was started with intravenous methylprednisolone pulse, continued with prednisolone, intravenous pulse cyclophosphamide and fresh frozen plasma. After 8 weeks, factor VIII inhibitor assay was negative.
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PMID:Acquired haemophilia A in a woman with autoimmune hepatitis and systemic lupus erythematosus; review of literature. 2202 58

Acquired haemophilia A is a very rare (1-2 cases per million people) but often life-threatening haemorrhagic disorder characterized by antibodies directed against coagulation factor VIII. We report the case of a 55-year old woman under treatment with Pegylated alpha 2a interferon (IFN) and Ribavirin for chronic viral C hepatitis, who developed a progressive severe haemorrhagic syndrome diagnosed as acquired haemophilia based on supplementary laboratory data (prolonged activated partial thromboplastin time, extremely low factor VIII level - 1%, high titre of factor VIII inhibitor - 30 Bethesda U/ml).The onset was insidious, about three months before presenting to our unit. Antiviral therapy had been stopped three weeks before current admission. Emergency intensive treatment included: haemostatic agents - rFVII (Novoseven), FEIBA (Factor VIII Inhibitor Bypassing Activity), vitamin K, adrenostazin, cryoprecipitate, fresh frozen plasma, as well as immunosuppressive therapy (high dose corticotherapy and cyclophoshamide), immunoglobulins (Humaglobin), prophylactic PPI and antibiotics. The evolution was slowly favourable with the remission of the haemorrhagic syndrome and regression of the iliopsoas muscle haematoma. Clinicians should be aware that acquired forms of haemophilia do exist, representing a rare diagnosis and a therapeutic challenge. To our knowledge, this is the first reported case of acquired haemophilia in Romania, in a patient with chronic viral C hepatitis under antiviral treatment.
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PMID:Acquired haemophilia complicated with gastrointestinal bleeding and spontaneous iliopsoas muscle haematoma in a woman with chronic C hepatitis under treatment with pegylated IFN alpha 2a and ribavirin. 2245 65


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