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A patient with subcorneal pustular dermatosis was found to have a circulating monoclonal IgA kappa immunoglobulin. Direct immunofluorescence studies revealed IgA kappa deposits in the subcorneal zone of the epidermis. Circulating IgA kappa reacting with the subcorneal zone of normal human epidermis was demonstrated by indirect immunofluoresence. It is speculated that IgA deposition might be implicated in the pathogenesis of subcorneal pustular dermatosis. [ABSTRACT FROM AUTHOR]

In vitro proliferative response to Mycobacterium leprae and PPD of T cell subsets, isolated by selective depletion procedure from peripheral blood using OKT4 or OKT8 monoclonal antibodies plus complement, was investigated in leprosy patients. Whole peripheral blood mononuclear cells (PBMC) developed a strong proliferative response to both M. leprae and PPD in most tuberculoid patients. This proliferation was confined to T cells, and concerned predominantly OKT4+ cells. Both antigens, however, induced a smaller, but significant proliferation of OKT8+ cells. In lepromatous patients, proliferative response of whole PBMC incubated with M. leprae was in most cases unsignificant, at variance with PPD-induced proliferation, which was not significantly lower than that of PBMC from tuberculoid patients. In a majority of M. leprae non-responders, neither OKT4+ nor OKT8+ enriched PBMC developed a proliferative response to M. leprae. Unexpectedly in four M. leprae unreactive patients, control treatment of PBMC with complement alone restored a strong proliferative response to M. leprae. Taken together, these results suggest that in vitro unresponsiveness to M. leprae results at least in some patients, from an active suppressor mechanism but that the effector phase of such suppression does not directly involve OKT8+ T cells. [ABSTRACT FROM AUTHOR]

I cell subsets and T cell functions were explored in 31 leprosy patients with the following methods: determination of the percentages of the different T cell subpopulations defined by monoclonal antibodies directed at total T cells, helper T cells and suppressor cytotoxic T cells: measurement of the in vitro proliferative responses to mitogens: study of the concanavalin A-induced suppressive activity, assessed on MLC: measurement of delayed-type hypersensitivity by skin testing. The confrontation between immunological lepromatous patients without type-2 reaction (erythema nodosum leprosum). (2) lepromatous patients without INL (erytherm nodosum leprosum). (2) lepromatous patients with recent IENL and (3) tuberculoid patients. Unexpectedly. groups 1 and 3. although differing strongly in their clinical status and their sensitivity to lepromin (absent in group 1 and strong in group 3), showed a similar immunological profile with a normal percentage of T cells and a normal distribution of T cells among the major T cell subset contrasting with a moderate decrease of proliferative responses to mitogens and impaired delayed-type hypersensitivity reactions. Concanavalin A-induced suppressive activity was type-2 reaction) strongly differed from both other groups. showing striking abnormalities other groups. showing striking abnormalities of the repartition oldie T cell subsets, with increased percentages of helper T cells and decreased percentages of suppressor T cells. and elevated proliferative responses to mitogens. Concanavalin A-induced suppressive activity was reduced in most patients of this group. It is suggested that this imbalance between I cell subsets contributes to the occurrence of ENL reactions in lepromatous patients. [ABSTRACT FROM AUTHOR]

We report 2 new cases of immuno-allergic side-effects of rifampicin (RMP), occurred in leprosy patients treated by multidrug therapy. These cases illustrate the various features of this type of complication. In one case, the patient exhibited few days after restarting of RMP (600 mg daily), a typical flu syndrome associated to a thrombopenia. Previously, the patient had received discontinued RMP (300 mg, 3/5 days) that had to be stopped after 11 months for "general malaise" that in fact corresponded to a flu syndrome. The second patient developed a flu syndrome associated with a diffuse eczematous eruption one year after the onset of daily RMP (600 mg). Anti-RMP antibodies were detected only in the first case. The pathogenic mechanisms and the clinico-biologic features are discussed.

Between 1980 and 1994, 67 new or relapsing leprosy patients were treated by daily administered multidrug regimens. Tuberculoid patients (23 TT/BT) received either bitherapy [rifampin + dapsone or clofazimine (RMP + DDS or CLO)] or tritherapy [RMP + DDS and/or CLO and/or ethionamide (ETH)] until clinical cure. Lepromatous patients (44 BB/BL/LL) received tritherapy (RMP + DDS and/or CLO and/or ETH) at least until bacteriological negativity. Of the 23 tuberculoid patients only one patient (5%) was cured at 6 months and about 70% needed between 6 and 24 months of treatment to obtain clinical cure (mean 19.5 months). In the 44 lepromatous patients, the achievement of bacteriological negativity was significantly linked to the initial bacterial index (BI), and it occurred after 2 to 7 years (mean 66.5 months) of multidrug therapy (MDT). The average BI decrease per year was 1.1+ during the first year, 0.9+ the second year, and then < 0.5+ per year. Reactional states significantly (p < 0.01) influenced the BI course: reversal reactions (RR) accelerated while erythema nodosum leprosum (ENL) delayed the BI decrease. Three of the 23 (13%) tuberculoid and 19 of the 44 (43%) lepromatous patients (p < 0.02) exhibited a RR and 18 of 44 (41%) lepromatous patients had ENL during MDT. A late RR (LRR) was observed in 1 (5%) and 6 (17%) of our tuberculoid and lepromatous patients, respectively, and 3 (8%) of our lepromatous patients suffered post-MDT ENL. No confirmed relapse has been observed within a follow-up period of 6 months to 7 years and 3 months [59 person-years at risk (PYR)] for TT/BT patients and of 4 months to 5 years and 10 months (100 PYR) for BB/BL/LL patients. When compared to the recommended WHO/MDT, it appears that daily MDT does not increase the clinical or the bacteriological cure rates either at 6 months in paucibacillary tuberculoid patients or at 2d years in multibacillary lepromatous patients. Moreover, as does the WHO/MDT, our regimens show a high frequency of reactional states both during and after treatment. This fact constitutes the main new problem of the actual treatment of leprosy.

A national prevalence survey of leprosy was made in june 1989 in Popular Republic of Congo: authors report results. The prevalence rate is 5.8% +/- 2.6% among people more than 15 years of age, and 10.5% of all forms are multibacillary. All patients are under DDS monotherapy. One overwhelming risk factor is leprosy antecedents in the family history; active case-finding and surveillance of contacts are recommended.

The authors report the results of a national prevalence survey of leprosy made in 1989 in Popular Republic of Congo. Leprosy is essentially found in rural areas and frequently causes disabilities. The prevalence rate is 5.8 +/- 2.6% among people more than 15 years of age, and 10.5% of all forms are multibacillary. All patients are under DDS monotherapy. One overwhelming risk factor is leprosy cases in the family history; active case-finding and surveillance of contact cases are recommended. Generally, leprosy is poorly understood by the general population; an educational effort is necessary.

Since the application of short duration multidrug therapy (MDT) in leprosy, it has been reported that reversal reactions (RR) may occur after withdrawal of treatment. Surprisingly, such "late reversal reactions" have quite never been described after monosulphonotherapy. Such RR, especially in endemic areas, may represent diagnostic and therapeutic difficult problems. We report 5 cases of late RR. In 4 cases (1 BT patient and 3 BL-LLs patients), the RR occurred 1 month 1/2 to 3 years after cessation of MDT. In the last case (form LLs), the RR happened 6 months after that a 14 years monosulphonotherapy has been stopped. These observations strengthen the need of a complete clinical, bacteriological and immunological evaluation at the time of the diagnostic, more useful than a single bacteriological study, to differentiate late RR from relapses. Moreover, the last case confirms that late RR may occur after monosulphonotherapy.

In a retrospective study of 95 patients seen between 1950 and 1978, the outcome of malignant melanoma levels III, IV and V of Clark's classification was reviewed. Patients with lentigo malignant melanoma were excluded. The overall survival rate was 63% at 5 years and 48% at 10 years. For the whole population of patients significant differences in survival rate were associated with level (p = 0,00002), thickness (less than 2 mm or greater than or equal to 2 mm; p less than 0.0,0001) and histological type (p = 0,02). The significance of prognostic variables taken separately was calculated by the Breslow method and was found to be: p = 0,0005 for thickness, p = 0,0009 for patient's age and p = 0,02 for histological type. In analysis with two variables, including level, thickness was the variable that added most to the information on prognosis supplied by level. For the population of patients with melanoma levels III and IV significant differences in survival rate were associated with thickness (less than 2 mm or greater than or equal to 2 mm; p less than 0,001), though not with level. When the variables were studied separately, thickness and patient's age were significant (p = 0,02 and p = 0,03 respectively). Analysis with two variables, including thickness, showed that age was the variable that added most to the information on prognosis supplied by thickness.

The authors submit a simplified sample survey methodology designed to evaluate prevalence rates of leprosy. The system proposed uses a cluster sampling technique. A cluster is a randomly selected group of households. In each household visited by the epidemiological teams all the inhabitants of the target-group are interviewed and examined. Various samples sizes are used (from 6500 to 12,000 peoples) according to the expected prevalence rate of the studied area. All the new cases detected through these surveys are notified to the National Departments in charge of leprosy programmes. Two surveys are already achieved (Equatorial Guinea, Cameroon), a third one in on the way.

We analysed the mechanisms of T-cell unresponsiveness to Mycobacterium leprae antigens and to unrelated antigens or T-cell mitogens in human leprosy and in an experimental model of murine infection by M. lepraemurium (MLM). In human leprosy, monoclonal antibodies OKT3, OKT4 and OKT8 were used to enumerate T-cell subpopulations within peripheral blood. Increased percentages of OKT8+ cytotoxic/suppressor cells were observed in untreated, non-reactional lepromatous patients. Conversely, lepromatous patients suffering from erythema nodosum leprosum, an Arthus-like phenomenon, exhibited a transient drop in the percentage of OKT8+ cells with a correlative increase in the proliferative response to T-cell mitogens. We studied the proliferative response to M. leprae of OKT4+ and OKT8+ cells isolated by a negative selection procedure using antibody-induced cytotoxicity plus complement. None of these subpopulations proliferated when incubated with M. leprae. In some patients, control treatment of mononuclear cells with complement alone induced the reappearance of a strong proliferative response to M. leprae, suggesting the existence of an active suppressor mechanism through soluble factors of an unknown nature. In MLM-induced murine leprosy, a progressive decrease was observed in the proliferative response to concanavalin A (ConA), and an early decrease in interleukin 2 activity in supernatants from ConA-stimulated spleen cells. Splenic T cells from MLM-infected mice transferred into naive recipients accelerated the local MLM growth in these recipients, suggesting that suppressor T cells may play a pathogenic role in the progression of MLM infection.

The authors report on a 76-year-old woman presenting with malignant thymoma associated with myasthenia, erythroblastopenia, myositis and giant cell myocarditis. Blood examination showed antinuclear antibodies, anti-platelet antibodies and LE cells. Only one similar case and 22 cases of thymoma associated with giant cell myocarditis have been published. It seems probable that thymomas plays a part in the pathogenesis of giant cell myocarditis.