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)

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.
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PMID:[Fever and liver cirrhosis]. 22 38

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

Four infants with Lues connata, three with the early stage of the disease (patients 1-3), are reported. Diagnosis was made after exclusion of other diseases. Initially an infectious disease was expected, since anemia, leucocytosis, thrombocytopenia, hepatomegaly and/or splenomegaly and a bad condition were found. In two patients bone structure was abnormal. Elevated serum concentrations of liver enzymes (ALAT, ASAT) were the indication for liver biopsy in one patient, in whom an accompanying hepatitis was diagnosed. Treatment was performed with penicillin, no JARISCH-HERXHEIMER reaction was observed. The Lues tests were negative during pregnancy but a displacental transfer of pathogenic agents could be assumed. Patient 4 was diagnosed at 9 months of age. Infection of the mother probably occurred in the last 6 weeks of pregnancy. It can not be decided if the baby has a connatal or acquired Lues. The titer decrease of the CMT-test after the end of the penicillin therapy is a marker for a successful treatment. If treatment was started at 2 years of age a total clinical recovery can be expected. The case reports demonstrate that negative Lues test during pregnancy do not exclude Lues connata in newborns. The Lues diagnosis should be considered if an infectious disease in a newborn can not be diagnosed. A general Lues serodiagnostic test is recommended in all newborns before they leave the obstetrics department.
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PMID:[Congenital syphilis]. 130 79

Patients with the acquired immune deficiency syndrome (AIDS) frequently develop hepatic dysfunction. Although hepatic injury may indirectly result from malnutrition, hypotension, administered medications, sepsis, or other conditions, the hepatic injury is frequently due to opportunistic hepatic infection, directly related to AIDS. Infection with Mycobacterium avium intracellulare typically occurs in patients with advanced immunocompromise and with systemic symptoms due to widely disseminated infection. In contrast, hepatic tuberculosis often occurs with less advanced immunocompromise. Cytomegaloviral infection may produce a hepatitis. Cytomegaloviral and cryptosporidial infections have been implicated as causes of acalculous cholecystitis and of a secondary sclerosing cholangitis. About 10-20% of patients with AIDS have chronic hepatitis B infection. These patients tend to develop minimal hepatic inflammation and necrosis. The clinical findings in patients with hepatic cryptococcal infection are usually due to concomitant extrahepatic infection. Hepatic histoplasmosis usually develops as part of a widely disseminated infection with systemic symptoms. Hepatic involvement by Kaposi's sarcoma is rarely documented ante mortem because an unguided liver biopsy is an insensitive diagnostic procedure. Patients with non-Hodgkin's lymphoma of the liver typically have lymphadenopathy, hepatomegaly, and systemic symptoms. As a pragmatic approach, patients with liver dysfunction and HIV-related disease should have a sonographic or computerized tomographic examination of the liver. Patients with dilated bile ducts should undergo endoscopic retrograde cholangiopancreatography because opportunistic infection may produce biliary obstruction. Patients with a focal hepatic lesion should be considered for a guided liver biopsy. Patients with a significantly elevated serum alkaline phosphatase level should be considered for a percutaneous liver biopsy. When performed for these indications, liver biopsy will demonstrate a significant disease involving the liver in about 50% of patients with AIDS and in about 25% of patients who are HIV seropositive but who are not known to have AIDS. The clinical impact of a diagnostic biopsy is blunted by a lack of efficacious therapy for many opportunistic infections.
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PMID:Hepatobiliary manifestations of the acquired immune deficiency syndrome. 198 33

There is an increased frequency of disseminated tuberculosis in patients with acquired immunodeficiency syndrome (AIDS). The authors reviewed 6 thoracic and 10 abdominal computed tomography scans from 11 patients who had AIDS and disseminated tuberculosis. All scans demonstrated multiple, large, mediastinal or retroperitoneal lymph nodes, or both; low-density centers within enlarged nodes were identified in seven patients (63%). The scans also showed a diffuse miliary pattern (three patients), pericardial effusion (three patients), mild hepatomegaly (six patients), moderate splenomegaly (seven patients), hypodense splenic lesions (one patient), peritoneal fluid (four patients), bowel involvement (two patients) and dilatation of the biliary tract (two patients). Infection with Mycobacterium tuberculosis was demonstrated in all cases. The findings of this study show that lymph-node enlargement and nodes with low-density centers in patients who have AIDS are suggestive of disseminated tuberculous infection.
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PMID:Disseminated lymphatic tuberculosis in acquired immunodeficiency syndrome: computed tomography findings. 225 9

We report a series of seven patients with reactive hemophagocytic syndrome, which was quite characteristic of its etiological spectrum. Infections were the leading cause, among them a case associated with HIV and another one with Salmonella enteritidis (a hitherto unreported association). The clinical findings consisted of fever, hepatomegaly, splenomegaly, lymphadenopathy, rash and pancytopenia. The diagnosis was carried out by bone marrow aspiration-biopsy except in two patients who were diagnosed at autopsy. The difficulty of the differentiation from malignant histiocytosis is discussed: one case of hemophagocytic syndrome due to diphenylhydantoin toxicity (the second reported one in the literature) was histologically undistinguishable from it. We think that, in any etiology, hemophagocytic syndrome is a reactive syndrome with variable intensity. The need for extensive microbiological investigation even in cases of histiocytosis of neoplastic appearance is emphasized.
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PMID:[Reactive hemophagocytic syndrome: analysis of a series of 7 cases]. 232 64

The pattern of illness in 60 consecutive children with homozygous sickle cell disease who attended the Paediatric Emergency Room of a busy Lagos hospital with acute illness was studied prospectively. Their ages ranged from 3 months to 13 years with a peak in the 2nd year. There were twice as many boys as girls. The commonest symptoms were fever, limb or abdominal pain and cough, and the commonest signs were pallor and hepatomegaly. Painful crises occurred in 27, anaemic crises in 11, and a combination of these in 12 children. Infection was detected in 76% of subjects in crises. Infection was found in 82% of all the children and was mainly bacterial. The commonest infections were pneumonia (35%), bacteraemia (32%), tonsillitis/pharyngitis (17%) and osteomyelitis (8%). The predominant bacteria isolated were Klebsiella spp (38%), E. coli (23%), Staph. aureus (23%), Staph. albus (23%) and Pseudomonas spp (23%). Some children had multiple isolates. Bacterial infection was a major cause of morbidity in very young children and merits appropriate control and preventive measures in this age group. The spectrum of bacteria isolated makes it unlikely that the specific anti-pneumococcal measures widely advocated in Europe and America for young children with SCA would be appropriate in Nigeria.
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PMID:Acute illness in Nigerian children with sickle cell anaemia. 244 66

We have analysed 139 consecutive cases (71 males and 68 females) of nutritional megaloblastic anaemia over a period of four and a half years. The majority of these patients belonged to the low socio-economic class and many of them were strict vegetarians. Sixty one percent were in the second and third decades of life. At the time of presentation, 46% had mild hepatomegaly, 42% fever, 34% mild splenomegaly and 20% bleeding manifestations. Of 102 cases in whom the biochemical parameters were available, vitamin B12 deficiency was detected in 76%, folate deficiency in 6.8%, combined B12 and folate deficiency in 8.8%; the remaining 7.8% had normal vitamin levels at presentation. All 139 patients had severe anaemia, 80.5% had thrombocytopenia and 43.8% had neutropenia as well as thrombocytopenia. It appears that during progression (in terms of duration) of megaloblastosis, anaemia is followed by thrombocytopenia and then neutropenia. Infection and bleeding in these patients may be aggravated by impaired functions of neutrophils and platelets, respectively.
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PMID:Pancytopenia in nutritional megaloblastic anaemia. A study from north-west India. 263 48

In Lesotho's central hospital 55 (25%) of 218 admissions for severe PEM died during 1981 and 1982. Most deaths (62%) occurred in the first week. The most important causes of death were acute GE and pneumonia in marasmus and kwashiorkor, respectively. The cause of death remained obscure in 16 children, however. In marasmus a poor prognosis was significantly associated with the finding on admission of a temperature less than 36.5 degrees C (P less than 0.05), apathy (P less than 0.01) and a depigmented skin (P less than 0.05), while in marasmic kwashiorkor only the finding of the latter was significantly (P less than 0.05) associated with death. In non-survivors with kwashiorkor the following characteristics were observed significantly more often: complaints of diarrhoea and/or vomiting on admission (P less than 0.05), the finding of apathy, pallor, skin defects and hepatomegaly on admission (P less than 0.01), and the finding of a low serum albumen, Na+ and K+ in the first days (P less than 0.05). Irritability was significantly (P less than 0.05) more common in survivors with kwashiorkor. Xerophthalmia was observed only once. Infections were diagnosed in 86% of all and giardiasis in 28% of 146 children. Twenty-eight children contracted measles of whom 5 died. Severe PEM still carries a high mortality despite hospitalisation. The findings confirm the need for intensive management of severe PEM.
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PMID:Severe protein energy malnutrition in Lesotho, death and survival in hospital, clinical findings. 310 Dec 51

Infection with the human immunodeficiency virus (HIV) is characteristically associated with hypergammaglobulinemia in both adult and pediatric cases. We report herein four infants who had an HIV infection in association with severe hypogammaglobulinemia and did not exhibit antibodies against HIV. HIV was isolated antemortem or postmortem in all four infants from either peripheral blood, cerebrospinal fluid, or body tissues. HIV infection could be presumed to be acquired transplacentally in two infants and by way of infected blood transfusions during the neonatal period in the other two. Each infant became symptomatic within the first year of life and developed rapidly progressive manifestations of the disease. Features that were common to all four infants include premature birth, failure to thrive, hepatomegaly, and progressive neurological abnormalities that were associated with intracranial calcifications. We concluded that, when infection occurs early in development either by transplacental exposure to the virus or from blood transfusion in small premature infants, hypogammaglobulinemia and deficiency of antibody production leading to the absence of antibody responses on which diagnosis is usually based can occur. Furthermore, progressive central nervous system disease may be a frequent finding in such infants, and this may lead to cerebral calcifications that must be attributed to the HIV infection itself and not to complicating infections--e.g., toxoplasmosis. It is suggested that patients with hypogammaglobulinemia, antibody deficiency syndrome, and central nervous system disease have an extremely bad prognosis.
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PMID:Prematurity, hypogammaglobulinemia, and neuropathology with human immunodeficiency virus (HIV) infection. 347 85


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