19 research outputs found
Dermatological preparations for the tropics. A formulary of dermatological preparations and background information on choices, production and dispensing.
Dermatological preparations for the tropics. A formulary of dermatological preparations and background information on choices, production and dispensing.
Dermatological preparations for the tropics. A formulary of dermatological preparations and background information on choices, production and dispensing.
Dermatological preparations for the tropics. A formulary of dermatological preparations and background information on choices, production and dispensing.
Advances in leprosy immunology and the field application: a gap to bridge
Advances concerning the hosts' immune response to Mycobacterium leprae infection have focused on elucidating the immune pathomechanisms involved, with the hope that predictive diagnostic and prognostic parameters (biomarkers) for field use would emerge; however, improvements in our understanding of the immunologic responses to this complex disease have, to date, somewhat failed to provide the effective and robust methods for improving its predictive diagnosis in the field situation, particularly in those patients suffering from paucibacillary disease. In this contribution we have attempted to review some of the advances both in the immunology and immunopathology of leprosy, and also highlight the limited clusters of immune parameters that are now available. Most importantly, we point out the limitations that still prevail in the provision of effective biomarkers in the field situation for either: (1) the diagnosis of indeterminate disease, (2) predictive diagnosis of individuals developing reactional states, (3) monitoring efficacy of treatment, or (4) monitoring treatment of reactional state
Granulomatous Reactivation during the Course of a Leprosy Infection: Reaction or Relapse
Leprosy is a serious infectious disease whose treatment still poses some challenges. Patients are usually treated with a combination of antimicrobial drugs called multidrug therapy. Although this treatment is effective against Mycobacterium leprae, the bacillus that causes leprosy, patients may develop severe inflammatory reactions during treatment. These reactions may be either attributed to an improvement in the immunological reactivity of the patient along with the treatment, or to relapse of the disease due to the proliferation of remaining bacilli. In certain patients these two conditions may be difficult to differentiate. The present study addresses the histopathology picture of and the M. leprae bacilli in sequential biopsies taken from lesions of patients who presented such reactions aiming to improve the differentiation of the two conditions. This is important because these reactions are one of the major causes of the disabilities of the patients with leprosy, and should be treated early and appropriately. Our results show that the histopathology picture alone is not sufficient, and that bacilli's counting is necessary
Immunohistological Analysis of In Situ Expression of Mycobacterial Antigens in Skin Lesions of Leprosy Patients Across the Histopathological Spectrum : Association of Mycobacterial Lipoarabinomannan (LAM) and Mycobacterium leprae Phenolic Glycolipid-I (PGL-I) with Leprosy Reactions
The presence of mycobacterial antigens in leprosy skin
lesions was studied by immunohistological methods using monoclonal
antibodies (MAbs) to Mycobacterium leprae-specific
phenolic glycolipid I (PGL-I) and to cross-reactive mycobacterial
antigens of 36 kd, 65 kd, and lipoarabinomannan (LAM).
The staining patterns with MAb to 36 kd and 65 kd were heterogeneous
and were also seen in the lesions of other skin diseases. The in
situ staining of PGL-I and LAM was seen only in leprosy. Both
antigens were abundantly present in infiltrating macrophages in the
lesions of untreated multibacillary (MB) patients, whereas only
PGL-I was occasionally seen in scattered macrophages in untreated
paucibacillary lesions. During treatment, clearance of PGL-I
from granulomas in MB lesions occurred before that of LAM,
although the former persisted in scattered macrophages in some
treated patients. This persistence of PGL-I in the lesions paralleled
high serum anti-PGL-I antibody titers but was not indicative for the
presence of viable bacilli in the lesions. Interestingly, we
also observed a differential expression pattern of PGL-I and LAM in the
lesions of MB patients with reactions during the course of the disease
as compared with those without reactions. In conclusion, the
in situ expression pattern of PGL-I and LAM in MB patients
may assist in early diagnosis of reactions versus
relapse