Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a non alcoholic, Chinese, 65 years old male that presented in august, 1992 with painful hepatomegaly of rapid installation and malaise. Ultrasound examination revealed multiple substitution images, diagnosed histologically as hepatoma. Serum alpha fetoprotein was 6600 U/ml. Malaise increased and the patient died two months later. This patient had a porphyria cutanea tarda and a chronic hepatitis diagnosed 6 years before. He also had positive titers for hepatitis C virus antibodies. In patients with porphyria cutanea tarda, hepatoma frequency is 400 fold higher and hepatitis C virus infection is highly prevalent. Thus, the surveillance of these patients with periodic alpha feto protein determinations and abdominal ultrasound examinations is recommended, specially in those infected by hepatitis C virus.
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PMID:[Porphyria cutanea tarda, chronic liver disease caused by the C virus and hepatocarcinoma. Clinical case]. 791 41

The aim of this work was to offer a description of the clinical manifestations developed by patients under 1 year who had dengue virus infection and dengue hemorrhagic fever during the epidemic which broke out in 1981, and to determine if the passive transfer of maternal dengue antibodies to the fetuses influenced the occurrence of a severe development of the disease, through a retrospective study. In 20 cases, type 2 dengue virus infection was confirmed. Eight patients showed the clinical manifestations of dengue hemorrhagic fever of dengue shock syndrome (DHF/DSS), and the other 12 had the typical dengue virus infection. The former were of the white racial phenotype, aged under 6 months. There was a predominance of type 1 dengue antibodies in the mothers of children with DHF/DSS. Fever, rash, vomiting and diarrheas (not frequent) appeared in the two clinical manifestations of the infection; blood leukocytes were predominantly lymphocytic; and erythrocyte sedimentation was always normal. Patients with DHF/DSS presented with some bleeding (87.5%); cyanosis and ascites (37.5%); and shock (25%), as well as hepatomegaly. All these infants with DHF/DSS had thrombocytopenia and most of them showed hemoconcentration. No deaths occurred.
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PMID:[Dengue fever and hemorrhagic dengue in infants with a primary infection]. 798 23

A 16-year old woman with LGL leukemia developed peripheral neuropathy. She showed virus-associated hemophagocytic syndrome (VAHS)-like signs including high fever, liver dysfunction, huge splenomegaly, hepatomegaly and pancytopenia. The presence of chronic active EB virus infection was proved by marked high titers for IgG and IgA antibodies to the Epstein-Barr viral capsid and early antigens and low titers of antibody to Epstein-Barr nuclear antigens. She showed dysesthesia and paresthesia of bilateral lower extremities with marked swelling and tenderness, and later developed muscular weakness and atrophy with areflexia of lower extremities. Findings of the central nervous system dysfunction were not observed except for the acceleration of jaw jerk. Pleocytosis and increased protein levels in the cerebrospinal fluid were found. Pulse therapy of methyl-prednisolone and high dose intravenous immunoglobulin therapy (20 g/day for 3 days) were effective for neurological findings. The increased neopterin in the cerebrospinal fluid suggested that peripheral neuropathy was caused by activated macrophages.
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PMID:[Peripheral neuropathy in large granular lymphocytic leukemia]. 821 4

We studied 57 infants < or = 14 days of age referred for possible enterovirus (EV) infection to assess the accuracy of that clinical diagnosis and describe the natural history of neonatal EV infection. Twenty-nine neonates proved to have EV infection, 23 had illnesses compatible with (but not proven to be) EV infection, and 5 had alternative diagnoses: bacterial infections (2); herpes simplex virus infection (1); and metabolic disorders (2). Neonates with proved EV infection were generally full term and had uncomplicated immediate postnatal periods but high percentages of ill contacts. Neonatal symptoms and signs included fever, irritability, anorexia, lethargy, hypoperfusion, rash, jaundice and respiratory findings. Laboratory abnormalities included cerebrospinal fluid (CSF) pleocytosis, chest radiograph infiltrates, abnormal urinalyses and elevated transaminases. EVs were most commonly isolated from CSF and rectum/stool but also frequently from serum and urine. Five EV-infected patients had severe multisystem disease (pneumonitis, hepatitis, thrombocytopenia, bleeding and meningitis), requiring supportive care and lengthy hospitalizations. All survived, 2 with residual hepatic dysfunction. Markers of severe disease included: early age of illness onset (especially Day 1 of life); maternal viral symptoms at delivery; absence of fever and irritability; tachypnea; lethargy; abdominal distension; hepatomegaly; and positive serum viral culture. These data support conservative management of ill infants < or = 2 weeks of age and suggest that antiviral therapy for neonatal EV infection would be optimally targeted at infants with early onset illness, multisystem disease and/or viremia.
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PMID:Profile of enterovirus disease in the first two weeks of life. 828 18

Chronic hepatitis B is a widespread viral illness with the serious sequelae of cirrhosis and hepatocellular carcinoma. Current therapy with interferon is not universally efficacious, and this has led to the evaluation of other antiviral agents. A recent Phase II trial of the nucleoside analogue, fluoroiodoarabinofuranosyluracil (fialuridine, FIAU) was halted because of the sudden development of severe multisystem toxicity characterized by hepatic failure, lactic acidosis, and pancreatitis, which resulted in the deaths of five patients. We systematically evaluated pre- and post-therapy biopsy, explant, and autopsy specimens from the 15 patients involved in this trial to define the hepatic changes of fialuridine toxicity and to determine whether the degree of pre-existing hepatitis contributed to the severity of toxicity. Severe hepatotoxicity from fialuridine was characterized by hepatomegaly with diffuse, predominantly microvesicular steatosis, hepatocellular glycogen depletion, marked bile ductular proliferation, and cholestasis. Ultrastructural examination revealed intracytoplasmic lipid droplets and marked mitochondrial injury. Patients in whom severe toxicity did not develop mainly showed changes caused by the underlying chronic hepatitis B alone. There was a subtle increase in the amount of microvesicular steatosis in two of six patients with mild or no symptoms of toxicity. The microscopic and ultrastructural pattern of injury and systemic symptoms in patients with fialuridine toxicity are consistent with severe mitochondrial and metabolic derangements. Similar hepatic pathologic findings have been reported rarely for other antiviral nucleoside analogues, which suggests that the mechanisms of toxicity might be related.
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PMID:Histopathologic changes associated with fialuridine hepatotoxicity. 907 26

Sarcoidosis is a chronic multisystem disorder of unknown cause characterized by the presence of noncaseating epitheloid granulomas and derangement of the normal skin architecture. Though an array of organs may be affected by the disease the most common site of affection is the lung. An extrathoratic manifestation is rare. We describe a 66-year-old patient who was admitted to our hospital because of weight loss and hepatomegaly. A thorough examination revealed the diagnosis of a granulomatous hepatitis characterized by a markedly elevated alkaline phosphatase concentration of 1,490 U/I. A drug-induced hepatitis could be excluded and no evidence was found for the existence of a bacterial or viral infection or an autoimmune disorder. An ERCP revealed a normal common bile duct and normally branching small intrahepatic ducts. The patient was discharged with the diagnosis of a biliary cirrhosis. Half a year later the patient was readmitted to the hospital because of severe intestinal bleeding due to pancytopenia. A bone marrow biopsy showed infiltration of the marrow by granulomas. A histiocytosis X could be ruled out. The diagnosis of an extrathoracic sarcoidosis was assumed and a therapy with prednisone was started. Within six weeks the blood count normalized. After 18 months the serum alkaline phospatase concentration also normalized and no granulomas were found in the bone marrow. The case demonstrates that pancytopenia in sarcoidosis is not due to bone marrow failure.
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PMID:[Granulomatous hepatitis and myelitis: an unusual manifestation of extrapulmonary sarcoidosis]. 1019 Feb 49

During cardiac surgery for transposition of the great arteries at age 7 weeks, a female infant received blood, fresh frozen plasma and platelet transfusions. Eleven days postoperatively, she developed bloody diarrhoea, fever, an erythematous macular rash, hepatomegaly, seizures and pancytopaenia. A clinical diagnosis of transfusion related graft-versus-host disease (GVHD) was supported by skin histopathology. DNA polymorphism studies confirmed that circulating lymphocytes in peripheral blood and infiltrating cells in the skin were foreign in origin and were derived from transfused blood cells. No underlying immunodeficiency was identified. Treatment with steroids cyclosporin and antithymocyte globulin was unsuccessful and death occurred 2 months after surgery. The features of fever, rash, diarrhoea, liver dysfunction and pancytopaenia which characterize GVHD may mimic drug reactions or viral infection. In addition to histological features on skin biopsy. DNA polymorphism studies on skin and blood samples provide a unique and sensitive method to confirm GVHD. Irradiation of blood products should be considered for acutely compromised infants requiring urgent cardiac surgery.
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PMID:DNA polymorphism analysis in transfusion-associated graft-versus-host disease. 1023 46

Fulminant herpes simplex viral hepatitis is uncommon in immunocompetent subjects. A 24-year-old woman presenting hepatomegaly with fever was hospitalized after returning from a trip to southern Africa. The patient was neither pregnant nor immunocompromised. Because of recent tropical travel, differential diagnosis included alphabetic hepatotropic virus infection, yellow fever, African hemorrhagic fever, and arbovirus infection. After ruling out other common viral etiologies, a definitive diagnosis of herpes simplex viral infection was made on the basis of clinical and laboratory findings showing high fever, leukopenia, and thrombopenia; of histological examination of the native liver after transplantation showing non-inflammatory confluent focal hemorrhagic necrosis; and on serologic tests demonstrating seroconversion for herpes simplex virus type 2. Outcome after transplantation was rapidly fatal but the death was not directly related to infection. The most likely etiology of fulminant hepatitis in a young woman returning from travel in a tropical area is hepatitis virus B or hepatitis virus E in cases involving pregnancy. However herpes simplex virus should be included in differential diagnosis even in immunocompetent subjects.
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PMID:[Fatal fulminating hepatitis due to Herpes simplex virus type 2 in a young immunocompetent female]. 1047 85

Sera were collected from a total of 122 children, comprising 117 cases with undifferentiated fever and 5 cases with dengue hemorrhagic fever (DHF), during June to September 1994 in Karachi, Pakistan. Sera were tested by the IgM-capture ELISA using dengue type 1 (D1), dengue type 2 (D2), West Nile (WN), and Japanese encephalitis (JE) viral antigens. Among 92 single sera from undifferentiated fever cases, IgM antibodies were detected in 5 cases by D1, 8 cases by D2, and 5 cases by WN antigens, respectively. Corresponding number of positives among 25 paired sera from undifferentiated fever cases were 3 by D1, 6 by D2, and 1 by WN antigen. Four out of 5 DHF cases possessed anti-D1 as well as anti-D2 IgM antibodies. Only a single DHF case was positive for anti-WN IgM antibodies. Anti-JE IgM antibodies were not detected in any of the tested serum specimens. Clinical manifestations of undifferentiated fever patients were generally non specific, but the percentage of children with anemia, hepatomegaly and splenomegaly was higher in patients possessing anti-dengue IgM antibodies than those without. Among the groups with anti-dengue IgM antibodies, those possessing only anti-D2 but not anti-D1 IgM antibodies showed higher percentages with cough, edema, and splenomegaly. The results indicated that up to 26% of the undifferentiated fever cases were caused by dengue virus infection in Karachi, Pakistan.
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PMID:Dengue virus infection among children with undifferentiated fever in Karachi. 1077 30

Dengue virus infection may remain asymptomatic or manifest as nonspecific viral infection to life threatening dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). Patients with DHF/DSS have fever, hemorrhagic manifestations along with thrombocytopenia and hemoconcentration. Thrombocytopenia and hemoconcentration are distinguishing features between DHF/DSS and dengue fever (DF). Some patients with dengue fever may have significant bleed and mild thrombocytopenia but no hemoconcentration. These patients are labelled to have dengue fever with unusual bleeds. Laboratory findings in DHF/DSS include rising hematocrit, thrombocytopenia and transformed lymphocytes on peripheral smear. There may be increased transaminases, hyponatremia, transient increase in blood urea nitrogen and creatinine. In severe disease there may be lab evidence of dissemination intravascular coagulation. X-ray film of the chest may show pleural-effusion. Ultrasonogram of abdomen may detect thickened gall bladder wall with hepatomegaly and ascitis. In some patients there may be abnormality in electrocardiogram and echocardiogram. The diagnosis of DHF/DSS is based on typical clinical findings. For confirmation of dengue virus infection viral culture can be done on blood obtained from patients during early phase of illness. In later part of illness antibodies against dengue virus can be demonstrated by various techniques. The treatment of DF is symptomatic. For control of fever nonsteroidal anti-inflammatory drugs should be avoided. DHF/DSS are managed by intravenous fluid infusion with repeated monitoring of vital parameters and packed cell volume (PCV).
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PMID:Dengue hemorrhagic fever: clinical manifestations and management. 1079 41


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