Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visceral leishmaniasis (VL) infections in patients with human immunodeficiency virus (HIV) infection are dramatically increasing in Mediterranean countries such as Spain, France and Italy. A study has been carried out to characterize biochemically the agents of typical or unusual VL in subjects with HIV infection and to compare results with those obtained so far from VL and cutaneous leishmaniasis (CL) infections in HIV negative subjects. Twelve Leishmania stocks were isolated from 8 HIV patients and typed through the electrophoretic analysis of 14 isoenzymes. All the stocks were identified as L. infantum s.l. According to zymodeme classification, the results can be summarized as follows: (i) only half of the subjects were infected with the expected commonest viscerotropic zymodeme in the Mediterranean area, MON 1; (ii) 2 patients were infected with the most widespread agent of CL in Italy, L. infantum MON 24; (iii) one subject was found infected with a zymodeme (MON 78) which, so far, has been found only in Malta as an agent of CL; (iv) one subject was infected with a new zymodeme, MON 136, which shares biochemical characteristics with 2 dermotropic L. infantum zymodemes, MON 78 and MON 111. Thus, half of the HIV patients surveyed displayed severe visceralization of parasites usually showing low virulence in HIV negative subjects.
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PMID:HIV-Leishmania co-infections in Italy. Isoenzyme characterization of Leishmania causing visceral leishmaniasis in HIV patients. 144 Jul 76

In an area endemic for visceral leishmaniasis, 16 patients with human immunodeficiency virus (HIV) infection developed the disease. All belonged to populations at risk for AIDS (15 were intravenous drug abusers). Five patients fulfilled the criteria for full-blown AIDS, and two more fulfilled them after diagnosis of leishmaniasis. All presented with the classic manifestations of visceral leishmaniasis, but leishmania serology was negative in 15 patients (93%). Leishmania donovani amastigotes were identified in the bone marrow in all cases. Most patients responded initially to treatment with pentavalent antimonial drugs, but seven (43%) followed a chronic course, with multiple relapses in five, despite alternative treatments. Visceral leishmaniasis occurred in patients with different levels of depression of the CD4 to CD8 lymphocyte ratio. Mortality was 37% (six patients) and was independent of the chronic-relapsing course of the disease. In no case was leishmaniasis the primary cause of death. Our data establish that visceral leishmaniasis is an opportunistic infection in HIV-infected patients, and we suggest that in endemic areas it should be considered an indicator disease for the diagnosis of AIDS.
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PMID:Visceral leishmaniasis (kala-azar) as an opportunistic infection in patients infected with the human immunodeficiency virus in Spain. 210 72

In an 8-month period nine patients with human immunodeficiency virus (HIV) infection were diagnosed as having visceral leishmaniasis; all diagnoses were based on cultures (eight from bone marrow and one from the skin). Visceral leishmaniasis developed before full-blown acquired immunodeficiency syndrome (AIDS) in seven patients and at the same time as or after AIDS in the other two patients. Three patients had a history of leishmaniasis. Clinical manifestations and laboratory findings were atypical. Leishmania species were cultured from samples taken from all patients; however, six patients had an insignificant antileishmanial antibody titer and Leishmania amastigotes were not seen in their bone marrow smears. Four isolates were identified by isoenzyme analysis as Leishmania donovani infantum. Five patients died, including two patients who had completed at least one 3-week course of therapy with N-methylglucamine antimoniate. Screening should be done for visceral leishmaniasis in patients with HIV infection who live or travel in areas where the disease is endemic. The diagnosis of visceral leishmaniasis may frequently be missed if cultures are not done.
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PMID:Visceral leishmaniasis in patients infected with human immunodeficiency virus (HIV). 274 48

Visceral leishmaniasis is infrequently reported in immunocompromised hosts; hence, the clinical manifestations and outcome of the disease in these patients are unknown. In a series of 10 patients with visceral leishmaniasis complicating renal transplantation (three), hematologic neoplasms (two), systemic lupus erythematosus (two), or infection with human immunodeficiency virus (three), typical hallmarks of kalaazar such as enlargement of spleen or hyperglobulinemia were absent in three and six patients, respectively. Extensive visceral involvement was noted by biopsies or autopsies in four patients. Diagnosis was made during evaluation for fever of unknown origin. Myriads of amastigotes were seen in bone marrow smears. Measurement of antibodies against Leishmania donovani was positive in each patient tested. Ultimately, three patients died, and chronic infections refractory to treatment developed in two other patients. Visceral leishmaniasis is a potentially fatal infection in immunocompromised hosts. Current antiparasitic therapy frequently fails to eradicate L. donovani from infected tissues.
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PMID:Visceral leishmaniasis in immunocompromised hosts. 333 67

The cutaneous affection in visceral leishmaniasis (VL) or Kala-azar, is well known although poorly documented. The coinfection by the human immunodeficiency virus (HIV) has resulted in the development of frequent atypical forms of VL, increasing the descriptions of cutaneous affection in its evolution. We present two cases of VL-HIV, stressing the location of Leishmania in cutaneous lesions and in apparently normal skin. We suggest the cutaneous biopsy as diagnostic procedure and criteria for the definition of VL-HIV as indicative of AIDS.
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PMID:[Visceral leishmaniasis and AIDS. Report of 2 cases with cutaneous dissemination]. 777 89

A case of fatal visceral leishmaniasis associated with immunodeficiency syndrome in a 32 year-old male patient is reported. The protozoonosis was responsible for the patient's death. Visceral leishmaniasis showed itself in an atypical form, at necropsy, with an intense parasitation of the mononuclear phagocitic system and damaging organs not usually affected by the disease, such as the adrenals, the kidneys, the lungs and the brain. Parasitised cells were observed within small vessels in several tissues. An immunohistochemical study was done on samples from the spleen, lymph nodes and brain, showing strong reactivity with antibody directed against leishmania.
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PMID:[Fatal visceral leishmaniasis associated with acquired immunodeficiency syndrome: report of a case with necropsy findings and immunohistochemical study]. 785 68

Visceral leishmaniasis is an anthropozoonosis endemic in the south of France. Its occurrence among patients infected with human immunodeficiency virus (HIV), in whom it presents with uncommon clinical, biological, and evolutionary signs, is being reported more and more often. We describe a case of leishmaniasis in an HIV-seropositive man that we believe is unique with respect to the cutaneous and then visceral location of the disease and the discovery at necropsy of an adrenal and myocardial leishmanial infiltrate.
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PMID:Atypical leishmaniasis in a patient infected with human immunodeficiency virus. 852 63

Visceral leishmaniasis has been reported as a complication in patients infected with human immunodeficiency virus (HIV) who live in areas where leishmaniasis is endemic or in patients who have traveled to these areas. Kaposi's sarcoma has been found frequently in patients with acquired immunodeficiency syndrome (AIDS). We report a HIV-infected patient having visceral leishmaniasis associated with Kaposi's sarcoma in which a biopsy specimen obtained from a pigmented cutaneous lesion revealed the coexistence of a Kaposi's sarcoma pattern with Leishmania parasitic colonization.
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PMID:Kaposi's sarcoma with an intense parasitization by Leishmania. 864 53

Visceral leishmaniasis (VL) in patients coinfected with human immunodeficiency virus (HIV) is often atypical, and characteristically relapses after treatment. We treated 10 HIV infected patients (9 men) with parasitologically confirmed VL with liposomal amphotericin B ("AmBisome': L-AMB) at a dose of 4 mg/kg/day on days 1, 2, 3, 4, 5, 10, 17, 24, 31, and 38. Patients were hospitalized for the first 5 days, and were monitored during, and 1 week and 1, 3 and 6 months after, L-AMB therapy. There were no serious adverse events, and L-AMB was well tolerated. 9/10 patients completed therapy, one patient defaulted at day 24. Clinical improvement was seen in all nine patients and the bone marrow aspirate was cleared of visible/culturable parasites in 8/9 patients. During follow-up, one patient defaulted. The seven remaining patients relapsed at 2, 3, 3, 5, 5, 6 and 7 months. Re-treatment with a variety of antileishmanial drugs was unsatisfactory. The time from first diagnosis of VL to death in six patients was 5-40 months (mean 18.8 months). Only one patient remained alive 26 months after treatment. L-AMB is safe and provides a good initial clinical response. Intermittent dosing enables a short period of hospitalization. However, relapse is probably inevitable.
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PMID:Visceral leishmaniasis in HIV infected patients: treatment with high dose liposomal amphotericin B (AmBisome). 870 70

Over 850 Leishmania-human immunodeficiency virus (HIV) coinfection cases have been recorded, the majority in Europe, where 7 to 17% of HIV-positive individuals with fever have amastigotes, suggesting that Leishmania-infected individuals without symptoms will express symptoms of leishmaniasis if they become immunosuppressed. However, there are indirect reasons and statistical data demonstrating that intravenous drug addiction plays a specific role in Leishmania infantum transmission: an anthroponotic cycle complementary to the zoonotic one has been suggested. Due to anergy in patients with coinfection, L. infantum dermotropic zymodemes are isolated from patient viscera and a higher L. infantum phenotypic variability is seen. Moreover, insect trypanosomatids that are currently considered nonpathogenic have been isolated from coinfected patients. HIV infection and Leishmania infection each induce important analogous immunological changes whose effects are multiplied if they occur concomitantly, such as a Th1-to-Th2 response switch; however, the consequences of the viral infection predominate. In fact, a large proportion of coinfected patients have no detectable anti-Leishmania antibodies. The microorganisms share target cells, and it has been demonstrated in vitro how L. infantum induces the expression of latent HIV-1. Bone marrow culture is the most useful diagnostic technique, but it is invasive. Blood smears and culture are good alternatives. PCR, xenodiagnosis, and circulating-antigen detection are available only in specialized laboratories. The relationship with low levels of CD4+ cells conditions the clinical presentation and evolution of disease. Most patients have visceral leishmaniasis, but asymptomatic, cutaneous, mucocutaneous, diffuse cutaneous, and post-kala-azar dermal leishmaniasis can be produced by L. infantum. The digestive and respiratory tracts are frequently parasitized. The course of coinfection is marked by a high relapse rate. There is a lack of randomized prospective treatment trials; therefore, coinfected patients are treated by conventional regimens. Prophylactic therapy is suggested to be helpful in preventing relapses.
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PMID:Leishmania and human immunodeficiency virus coinfection: the first 10 years. 910 56


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