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)

Leishmaniasis is a parasitic disease caused by a protozoon (Leishmania), with different clinical forms that are endemic in certain countries. The association of this disease in patients who are seropositive to human immunodeficiency virus (HIV) has recently been described. Leishmaniasis can develop in any stage of HIV infection, although the clinical manifestations - and hence the diagnosis - tend to coincide with the periods of maximum immune depression. We present the case of a HIV-positive, ex-intravenous drug abuser (in stage B2 of the CDC, 1992) with concomitant hepatitis C infection who presented with palatinal pain and bleeding for the past 2 months. Exploration revealed a vegetating tumoration of the hard palate. Hematoxylin-eosin and Giemsa staining of the biopsy confirmed the diagnosis of leishmaniasis. The definitive diagnosis was mucocutaneous leishmaniasis (MCL), for a bone marrow aspirate proved negative, and no further lesions could be established. The patient was treated with meglumine antimoniate (Glucantime), followed by improvement of the lesions.
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PMID:Oral leishmaniasis in a HIV-positive patient. Report of a case involving the palate. 1193 58

Cutaneous leishmaniasis is an endemic protozoan infection in Sardinia, one of the major islands of the Mediterranean Basin. The main causative strain in this country is Leishmania infantum, which rarely involves mucocutaneous areas, but has the potential to cause visceral leishmaniasis. An atypical leishmaniasis involving the inferior lip of a 57-year-old female with Down's syndrome was observed at the Dermatology Department of Cagliari (italy). The diagnosis was mainly based upon histopathological examination, revealing intra- and extra-cellular leishmania amastigotes. The leishmania infantum zymodeme MON-111 was identified by isoenzymatic characterization. Laboratory investigations revealed a normal complete blood count and biochemistry profile, except for an inverted CD4/CD8 ratio. Treatment with meglumine antimoniate 60 mg/kg/day (Glucantime) intramuscularly for 15 days, followed by intralesional administration 1 ml weekly for 4 weeks led to complete recovery. No relapses were observed at 6-month follow-up. The unusual localization is likely to be a reflection of the uncommon site of inoculation of the protozoa, transmitted by bites from flying vectors. Nevertheless, the presence of Down's syndrome in our patient may have contributed to the atypical presentation by traumatic exacerbation of the lesion, due to repeated auto-induced microtraumas of the inferior lip accompanied by subclinical immunodeficiency. In fact, the specific immune response to Leishmania infection depends on a host-cell-mediated immune response, reported as defective in Down's syndrome patients. Differential diagnosis and early detection of the infection are necessary in order to start effective treatment and prevent more serious complications.
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PMID:Leishmaniasis of the lip in a patient with Down's syndrome. 1532 5

We report in this study the in vivo efficacy of nine 2-substituted quinolines on the Leishmania amazonensis cutaneous infection murine model and on the Leishmania infantum and Leishmania donovani visceral infection murine models. In the case of the L. amazonensis model, quinolines were administered orally at 25 mg/kg twice daily for 15 days. Quinolines 1, 2, 3, and 7 reduced by 80 to 90% the parasite burdens in the lesion, whereas N-methylglucamine antimoniate (Glucantime), administered by subcutaneous injections at 100 mg [28 mg Sb(V)] per kg of body weight daily, reduced the parasite burdens by 98%. In visceral leishmaniasis due to L. infantum, mice treated orally at 25 mg/kg daily for 10 days with quinolines 1, 4, 5, and 6 showed a significant reduction of parasite burdens in the liver and spleen. These quinolines were significantly more effective than meglumine antimoniate to reduce the parasite burden in both the liver and spleen. Also, the oral in vivo activity of three quinolines (quinolines 4, 5, and 2-n-propylquinoline) were determined against L. donovani (LV 9) at 12.5 and 25 mg/kg for 10 days. Their activity was compared with that of miltefosine at 7.5 mg/kg. Miltefosine, 2-n-propylquinoline, and quinoline 5 at 12.5 mg/kg significantly reduced the parasite burdens in the liver by 72, 66, and 61%, respectively. From the present study, quinoline 5 is the most promising compound against both cutaneous and visceral leishmaniasis. The double antileishmanial and antiviral activities of these compounds suggest that this series could be a potential treatment for coinfection of Leishmania-human immunodeficiency virus.
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PMID:Efficacy of orally administered 2-substituted quinolines in experimental murine cutaneous and visceral leishmaniases. 1630 57