Cases reported "Leprosy"

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1/5. Post-kala-azar dermal leishmaniasis simulating leprosy. (A case report).

    The case of a 40 years male suffering from post-kala-azar dermal leishmaniasis simulating nodular lepromatous leprosy is reported. In countries where leprosy is endemic, other diseases are not infrequently taken to be leprosy (Schaller, 1971). Dermal leishmaniasis is a common cause of confusion in countries where the condition is endemic (Browne, 1964). Dharmendra and Chatterji (1940) discussed in detail the question of differential diagnosis between leprosy and Dermal leishmaniasis. The present communication is concerned with a patient suffering from post-kala-azar dermal leishmaniasis whose skin lesions simulated nodular lepromatous leprosy.
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ranking = 1
keywords = leishmaniasis
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2/5. Cutaneous leishmaniasis and leprosy.

    Eight patients who had concomitant leprosy and leishmaniasis are described. Two patients with lepromatous leprosy had high resistance leishmaniasis, implying that the immune deficiency in lepromatous leprosy is specific to mycobacterium leprae.
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ranking = 0.85714285714286
keywords = leishmaniasis
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3/5. Post-kala-azar dermal leishmaniasis mimicking leprosy: experience with 4 patients, with some unusual features in 1.

    We report on 4 cases of post-kala-azar dermal leishmaniasis (PKDL). history of kala-azar was available in all 4 patients. Slit-skin smears (SSS) for leishmania donovani (LD) bodies were negative in all 4. In 3 patients hypopigmented lesions were present over the face. Papules and nodules over his lips, tongue, scrotum and dactylitis were some unusual features observed in 1 patient. Histopathological examination showed LD bodies in 2 patients; histopathology was nonspecific in the other 2. All the patients were treated with sodium stibogluconate, 20 mg/kg/day. Infiltrated papules and nodules had subsided by 3 months, while hypopigmented macules took longer to improve. In 3 patients there had previously been a misdiagnosis as leprosy sufferers and they had been treated with antileprosy drugs. Clinical and histopathological differences between PKDL and leprosy are discussed.
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ranking = 0.71428571428571
keywords = leishmaniasis
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4/5. Distinguishing post-kala-azar dermal leishmaniasis from leprosy: experience in the sudan.

    In this study 4 patients were post-kala-azar dermal leishmaniasis (PKDL), whose lesions were similar to those of lepromatous and borderline leprosy, are described. In 2 patients there was no previous history of kala-azar but they were residents of an area of known endemic kala-azar. Lack of proper clinical and laboratory assessment was behind the failure to diagnose PKDL. Consequently the patients were treated with antileprosy drugs without proof of leprosy. The 3rd and 4th patients, though suspected clinically of leprosy, were correctly diagnosed as PKDL with adequate history, clinical assessment and appropriate laboratory investigations. The salient points in distinguishing PKDL from leprosy are described and discussed.
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ranking = 0.71428571428571
keywords = leishmaniasis
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5/5. genetics of host resistance and susceptibility to intramacrophage pathogens: a study of multicase families of tuberculosis, leprosy and leishmaniasis in north-eastern brazil.

    Genetic analysis of disease phenotypes segregating in recombinant inbred, congenic and recombinant haplotype mouse strains permitted us to effectively "scan" the murine genome for genes controlling resistance and susceptibility to leishmanial infections. Five major regions were implicated which, because they show conserved synteny with regions of the human genome, immediately provide candidate gene regions for human disease susceptibility genes. A common intramacrophage niche for leishmanial and mycobacterial pathogens, and a similar spectrum of immune response and disease phenotypes, also led to the prediction that the same genes/candidate gene regions might be responsible for genetic susceptibility to mycobacterial infections such as leprosy and tuberculosis. Indeed, one of the murine genes (Nramp1) was identified for its role in controlling a range of intramacrophage pathogens, including leishmanial, salmonella and mycobacterial infections. In recent studies, multicase families of visceral leishmaniasis, tuberculosis and leprosy, from north-eastern brazil have been analysed to determine the role of these candidate genes/regions in humans. Complex segregation analysis provides evidence for one or two major genes controlling susceptibility to these diseases in this population. family-based linkage analyses (e.g., combined segregation and linkage analysis; sib-pair analyses) and transmission disequilibrium testing have been used to examine the role of four regions in disease susceptibility and/or immune response phenotypes. Results to date demonstrate: (1) the major histocompatibility complex (MHC:H-2 in mouse, HLA in humans: mouse chromosome 17/human 6p; candidates class II and class III including tumour necrosis factor alpha/beta genes) shows both linkage to, and allelic association with, leprosy per se, but is only weakly associated with visceral leishmaniasis and shows neither linkage to, nor allelic association with, tuberculosis; (2) no evidence for linkage between NRAMP1, the positionally cloned candidate for the murine macrophage resistance gene Ity/Lsh/Bcg (mouse chromosome 1/human 2q35), and susceptibility to tuberculosis or visceral leishmaniasis; (3) the region of human chromosome 17q (candidates NOS2A, SCYA2-5) homologous with distal mouse chromosome 11 is linked to tuberculosis susceptibility; and (4) the "T helper 2" cytokine gene cluster (proximal murine chromosome 11/human 5p; candidates IL4, IL5, IL9, IRF1, CD14) is not linked to human disease susceptibility for any of the three infections, but shows linkage to and highly significant allelic association with ability to mount an immune response to mycobacterial antigens. The demonstration of an allelic association between IL4 and immune response to mycobacterial antigen may provide a genetic explanation for the inverse association recently demonstrated between delayed hypersensitivity T helper 1 responses to mycobacterial antigen and atopic disorder in Japanese children. These studies demonstrate that the "mouse-to-human" strategy, refined by our knowledge of the human immune response to infection, can lead to the identification of important candidate gene regions in humans.
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ranking = 1
keywords = leishmaniasis
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