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)

Disseminated histoplasmosis (DH) is recognized as an opportunistic infection in patients with the human immunodeficiency virus (HIV), especially in regions where histoplasmosis is endemic. At the Kansas University Medical Center 148 patients were hospitalized with the diagnosis of AIDS from December 1983 to March 1991; 23 of these patients (16%) had disseminated histoplasmosis. The charts of these 23 patients were reviewed. Clinical signs and symptoms included fever (91%), cough (65%), and weight loss (48%). Splenomegaly, hepatomegaly, or lymphadenopathy was present in 52% of all patients. Anemia (39%), leukopenia (65%), and thrombocytopenia (52%) were common, and 22% had pancytopenia. Diagnosis was made by peripheral smear examinations (organisms visualized on 7 of 22 smears [32%]), blood cultures (positive for H capsulatum in 16 of 20 patients, [80%]), bone marrow cultures (positive in 14 of 15 patients, [93%]), and bone marrow aspirate and biopsy examinations (organisms seen on 18 of 21 stains, [86%]). The combination of these four tests revealed the diagnosis of DH in 23 of 23 patients (100%). Induction and maintenance amphotericin B therapy was given to all but 2 patients, and currently 8 of the 23 are alive. DH is a common opportunistic infection in AIDS patients from regions endemic for histoplasmosis. When DH is suspected, a peripheral smear examination, blood cultures, bone marrow cultures and bone marrow aspirate and biopsy should be done to make the diagnosis, since suppression of the disease is possible with appropriate therapy.
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PMID:Disseminated histoplasmosis in patients with AIDS. 147 Sep 57

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

Scurfy (sf) is a spontaneous, sex-linked, recessive mutation that maps to the extreme proximal portion of the X chromosome, about 2 centimorgans from sparse fur (spf). Hemizygotes for sf manifest several clinical disorders, evident at 14 days of age, including scaliness and crusting of the eyelids, ears, and tail, runting, reddening and swelling of the genital papilla, anemia, cachexia, and early death (average, 24 days). Our studies indicate that the phenotype of hemizygous scurfy is not, as has been suggested, a model for human X-linked ichthyosis, but appears to be a disease primarily affecting the lymphoreticular, and possibly the hematopoietic, systems. Gross lesions include marked splenomegaly, hepatomegaly, enlarged lymph nodes, and variable thickening of the ears. The characteristic histologic lesion is a lymphohistiocytic proliferation and infiltration of peripheral lymph nodes, spleen, liver, and skin. In routine hematoxylin and eosin-stained sections, these lesions efface lymph node architecture, thicken the dermis, and form nodular portal infiltrates in the liver. Scurfy lesions characteristically contain a population of large blastlike cells with round to oval nuclei, a vesicular chromatin pattern, and prominent single nucleoli. Mixed perivascular infiltrates of lymphocytes, macrophages, and granulocytes sometimes are found in kidney, heart, pancreas, lung, and mesenteries. There is excessive hematopoiesis in the liver and spleen. Cells expressing B220 or Thy-1 antigens localize to appropriate areas in the lymph nodes and spleen, but are rare in the portal infiltrates and are absent from the skin. There is a marked, polyclonal increase in serum IgG, severe Coombs'-positive anemia, and leukocytosis with atypical mononuclear cells. Scurfy mice are negative for antinuclear antibodies. Despite their morphologically aberrant lymphoreticular system, scurfy mice can exist in a conventional environment without evidence of opportunistic infection. Raising scurfy mice in a specific-pathogen-free environment does not alter disease expression. Thus, while our findings indicate that scurfy disease may be the result of immune dysfunction, it is not a classic immunodeficiency.
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PMID:X-linked lymphoreticular disease in the scurfy (sf) mutant mouse. 205 95

Although the clinical and epidemiologic features of progressive disseminated histoplasmosis (PDH) in the acquired immunodeficiency syndrome (AIDS) have been well described, the pathologic and pulmonary aspects remain to be fully defined. A retrospective review of three patients and a prospective study of four more with PDH and AIDS recently admitted to an inner city hospital in a non-endemic area were used to elucidate these features more fully. All patients were men aged 23 to 46 years, born in endemic areas, who had immigrated to the US seven to 15 years before the onset of their illnesses. Five had been exposed to human immunodeficiency virus (HIV) through intravenous drug use (one was also a homosexual), and two through heterosexual contacts. Respiratory symptoms were evident in five of the seven patients, fever in seven, weight loss in seven, hepatomegaly in four, splenomegaly in three, peripheral adenopathy in three, and gastrointestinal symptoms in three. PDH was the initial or only opportunistic infection in five patients. Bilateral nodular infiltrates (4/7), bilateral interstitial infiltrates (2/7), and mediastinal adenopathy associated with pleural effusion (1/7) were the chest roentgenographic findings. Histoplasma capsulatum was isolated from five of five bronchoalveolar lavages, four of four transbronchial biopsies, one of one endobronchial biopsy, one of one brushing, one of one pleural biopsy, three of three lymph node biopsies, two of two bone marrow biopsies, one of one liver biopsy, and three of four peripheral blood smears. Granuloma formation was seen in only three of 12 biopsies. There were ten or more fungi per monocyte in almost all tissues, some with extracellular forms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disseminated histoplasmosis in AIDS. Clinicopathologic features in seven patients from a non-endemic area. 234 42

From Oct 1, 1982, to Oct 1, 1983, the Centers for Disease Control (CDC) received reports of 35 children whose illness met the CDC definition of acquired immune deficiency syndrome (AIDS). All of the children had serious opportunistic infections without a known underlying illness to explain susceptibility to the infections. The 35 children were residents of ten different states; cases clustered in five major metropolitan areas. Three of the children had a parent with AIDS, and one child who had been previously reported had received a blood transfusion from a person in whom AIDS later developed. Most of the children had at least one parent in a population group in which adult AIDS cases have occurred. Many of the children had histories of prodromal symptoms, including pneumonitis, lymphadenopathy, hepatomegaly, and oral thrush. The mean age at onset of illness was 5 months, and the mean age at diagnosis was 12 months. To determine whether opportunistic infection in children without underlying immunodeficiency was truly a new phenomenon, a review of requests to the CDC for the drug pentamidine isethionate was undertaken. This revealed an apparent increase from 1979 to 1983 in Pneumocystis carinii pneumonia in children without known underlying immunodeficiency.
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PMID:Unexplained immunodeficiency in children. A surveillance report. 661 Jul 74

Between 1986 and 1993 visceral leishmaniasis (VL) was diagnosed in 50 adult patients with human immunodeficiency virus type 1 (HIV-1) infection (8 females, 42 males: 31 intravenous drug users, 11 homosexual or bisexual men, 6 heterosexual individuals, 2 blood recipients) from 5 hospital centres in southern France. Diagnosis of VL was by demonstration of Leishmania and isolation of promastigotes by culture in Novy-McNeal-Nicolle medium. Leishmania isolates were identified by their isoenzyme profile in 28 patients. All the patients were immunocompromised when VL was diagnosed. Their median CD4 cell count was 25 x 10(6) (0-200). However, only 21 patients (42%) fulfilled the 1987 CDC criteria for the acquired immune deficiency syndrome before VL developed. Fever (84%), splenomegaly (56%), hepatomegaly (34%), and pancytopenia (62%) were the most common presenting features. Clinical signs were lacking in 10% of patients. Anti-leishmanial antibodies were detected by indirect immunofluorescence or enzyme-linked immunosorbent assay in 26/47 cases (55%). Combining these techniques with Western blotting (WB) gave a positivity rate of 95%. Amastigotes were demonstrated in bone marrow aspirates in 47 cases (94%). Unusual sites for parasites were found in 17 patients (34%), mainly in the digestive tract but also skin and lung. Viscerotropic L. infantum zymodeme MON-1 was characterized in 86% of cases. Dermotropic zymodemes MON-24, MON-29, MON-33, and a previously undescribed zymodeme MON-183, were isolated from 4 patients. The response rate to pentavalent antimony was 50% and to amphotericin B 100%, but clinical relapses were noted in both groups. In endemic areas, VL should be considered as a possible opportunistic infection in HIV-infected patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Visceral leishmaniasis and HIV-1 co-infection in southern France. 777 40

Microsporidia cause opportunistic infections in AIDS patients and commonly infect laboratory animals, as well. Euthymic C57B1/6 mice experimentally infected with intraperitoneal injections of 1 x 10(6) Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923, Encephalitozoon hellem Didier et al., 1991, or Nosema corneum Shadduck et al., 1990 displayed no clinical signs of disease. Athymic mice, however, developed ascites and died 8-16 days after inoculation with N. corneum, 21-25 days after inoculation with E. cuniculi, and 34-37 days after inoculation with E. hellem. All athymic mice displayed hepatomegaly, dilated intestine and accumulation of ascites fluid. Granulomatous lesions are primarily located in the liver, lung, pancreas, spleen, and on serosal surfaces of abdominal organs. The murine microsporidiosis model also was used to examine immune response that inhibit microsporidia growth in vitro. Recombinant murine interferon-gamma (mIFN-gamma, 100 mu/ml) alone or in combination with lipopolysaccharide (LPS; 10 ng/ml) could activate thioglycollate-induced peritoneal murine macrophages to destroy E. cuniculi. The production of the nitrogen intermediate, NO2-, correlated with parasite destruction. Inhibition of NO2- generation by addition of the L-arginine analogue, NG-monomethyl L-arginine (NMMA), inhibited microsporidia killing, as well. Since microsporidiosis is becoming an important opportunistic infection in AIDS patients, a microsporidiosis model is being developed using SIV/DeltaB670-infected rhesus macaque monkeys (Macaca mulatta). SIV-infected immunocompetent monkeys given E. cuniculi or E. hellem per os developed specific antibodies, and microsporidia could be detected sporadically by calcofluor or antibody fluorescence staining of stool and urine sediment smears. As immunodeficiency progressed, monkeys developed diarrhoea, cachexia, and anorexia, and organisms were detected in urine and stool with greater frequency. Immunodeficient SIV-infected monkeys died approximately 27 days after receiving E. hellem by intravenous inoculation, and approximately 110 days after receiving E. hellem per os. Lesions typical for SIV-infection were observed in both groups of monkeys and microsporidia were detected in kidney and liver of the intravenously-injected monkeys. The murine microsporidiosis model provides an efficient means for studying protective immune responses to microsporidiosis, and may prove useful for screening immunological and chemotherapeutic agents. The pathogenesis of Encephalitozoon microsporidiosis in SIV-infected monkeys appears to parallel encephalitozoonosis in AIDS patients, suggesting that simian microsporidiosis may provide a useful model for evaluating diagnostic methods and therapeutic strategies during various stages of progressing immunodeficiency.
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PMID:Experimental microsporidiosis in immunocompetent and immunodeficient mice and monkeys. 805 Jul 48

The authors report two cases of peliosis hepatis, occurring in patients with AIDS, who presented a persistent fever and an hepatomegaly. The liver biopsies showed areas of peliosis, where bacilli were observed by Warthin-Starry stain. In one case, techniques of molecular biology allowed the identification of Rochalimaea henselae, pathogen involved in bacillary angiomatosis. This rickettsia has been newly recognized in the United-States, where 17 cases of bacillary peliosis have been published in immunocompromised hosts and mainly in patients with AIDS. These observations illustrate the clinical and histological features of this new opportunistic infection, as it is described in the literature. The clinical signs include an unexplained fever, an hepatomegaly, and in 75% of the cases, a splenomegaly. The cutaneous lesions of bacillary angiomatosis are associated in 40% of the cases. An antibiotic treatment by erythromycin ensures a complete recovery.
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PMID:[Bacillary peliosis in AIDS. Anatomo-clinical study of 2 cases]. 831 62

Clinical characteristics associated with bacillary angiomatosis and bacillary peliosis (BAP) in patients with human immunodeficiency virus (HIV) infection were evaluated in a case-control study; 42 case-patients and 84 controls were matched by clinical care institution. Case-patients presented with fever (temperature, > 37.8 degrees C; 93%), a median CD4 lymphocyte count of 21/mm3, cutaneous or subcutaneous vascular lesions (55%), lymphadenopathy (21%), and/or abdominal symptoms (24%). Many case-patients experienced long delays between medical evaluation and diagnosis of BAP (median, 4 weeks; range, 1 day to 24 months). Case-patients were more likely than controls to have fever, lymphadenopathy, hepatomegaly, splenomegaly, a low CD4 lymphocyte count, anemia, or an elevated serum level of alkaline phosphatase (AP) (P < .001). In multivariate analysis, a CD4 lymphocyte count of < 200/mm3 (matched odds ratio [OR], 9.9; P < .09), anemia reflected by a hematocrit value of < 0.36 (OR, 19.7; P < .04), and an elevated AP level of > or = 2.6 mukat/L (OR, 23.9; P < .05) remained associated with disease after therapy with zidovudine was controlled for. BAP should be considered an AIDS-defining opportunistic infection and should be included in the differential diagnosis for febrile, HIV-infected patients with cutaneous or osteolytic lesions, lymphadenopathy, abdominal symptoms, anemia, or an elevated serum level of AP.
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PMID:Bacillary angiomatosis and bacillary peliosis in patients infected with human immunodeficiency virus: clinical characteristics in a case-control study. 872 33

Opportunistic infections are major causes of morbidity in patients with human immunodeficiency virus (HIV) infection. Penicillium marneffei infection is very common in HIV-infected individuals in northern Thailand. The patients usually present with fever, anemia, weight loss, skin lesions, generalized lymphadenopathy, and hepatomegaly. The average number of CD4+ T-lymphocytes at presentation was 63.8 cells/mm3. Diagnosis depends on familiarity with the clinical syndromes and support from the mycology laboratory. The response to antifungal treatment of the patients is generally good, but depends on the ability of the physician to make the diagnosis and start the treatment early. New approaches to the laboratory diagnosis of P. marneffei infection have been reported. Further study of these approaches may help physicians in taking better care of the patients.
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PMID:Penicillium marneffei infection in patients infected with human immunodeficiency virus. 950 65


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