[Cutaneous lesions at the beginning of leprosy; tuberculoid leprosy, neuritis].
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Scalp hair and blood sera of three groups of individuals were studied for mineral contents by flame photometric and colorimetric procedures. Patients in one of the three groups were suffering from lepromatous leprosy, the second group comprised patients with tuberculoid leprosy and the third group consisted of normal controls. The results obtained revealed changes in the mineral content of the scalp hair of those suffering from lepromatous leprosy and tuberculoid leprosy. A possible relationship may exist between hair and serum minerals.
Tuberculoid and lepromatous leprosy (TL and LL) manifest exaggerated Th1 and Th2 type immunity, respectively. Serum soluble CD23, which is regulated by the stimulatory action of IL4 and inhibitory action of IFNgamma, was significantly elevated in LL relative to TL and healthy controls. These results confirm the state of cellular and humoral immunity in TL and LL.
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Radial or superficial peroneal nerve biopsies of 6 patients with tuberculoid or borderline-tuberculoid leprosy and 6 control nerve biopsies were examined by electron microscopy. Endoneurial blood vessels showed histopathology in all the leprosy patients. Changes, in particular, involved the basement membrane in postcapillary venules and venules. Multilayered parellel basement membranes, with collagen and ground substance, formed a thick coat ("hyaline zone") around the vessels. It is suggested that the zone inhibits passage of nutrients and metabolites and, thus, contributes to or is the main cause of the local destruction of (unmyelinated) nerve fibres and the lack of nerve fibre regeneration observed in this type of leprosy. The perivascular zone, presumably, is produced by pericytes in response to defects in the "blood-nerve barrier" of endoneurial vessels. In granulomata of leprosy skin lesions, a perivascular zone was not present. The endothelium of endoneurial vessels, in affected nerves, generally was normal. Occasionally, however, gaps and fenestrations were seen and there were histological indications that leakage of blood plasma had occurred through the gaps and through the basement membrane of the endothelium. Occlusion of endoneurial vessels was found only in the oldest patient and the degeneration of nerve fibres generally observed thus is considered not to be caused by ischaemia. Histopathology in epi-and perineurial vessels was definitely less pronounced than in endoneurial vessels.
Nodular leprosy of childhood (NL) is a benign clinical variant of tuberculoid leprosy that affects breast-feeding infants and children that remained in a highly infected environment. The lesions resolve with complete healing and NL has been considered a manifestation of allergy and congenital immunity to Mycobacteria leprae. We studied the tissue reaction, Mycobacterial antigen frequency, and the lymphocyte subsets (CD45RO+, CD4+, CD8+, B, NK), dendritic cells (epidermal CD1a+ cells and S100+ dermal dendrocytes), and macrophages in skin lesions of a clinically well characterized NL group (N = 11). Results were compared to children (N = 23) and adults (N = 24) with classical tuberculoid leprosy. NL lesion histopathology was characterized by dense granulomatous inflammatory reaction, with a greater number of confluent tubercles when compared to the other groups. Neural compromise was seen in all biopsies. The frequency of Mycobacterium antigen was similar in all groups. The population of CD45RO+, CD4+ and CD8+ T lymphocytes, natural killer cells, B lymphocytes, CD1a+ epidermal cells, and macrophages of NL lesions did not differ from the other groups. The number of S100+ dermal dendritic cells of the NL group was smaller than that of the adult group, although it did not differ from the other group of children. Except for the confluent tubercules, our data could not disclose any other difference in the tissue reaction of NL, in spite of its peculiar clinical features and evolution when compared with the classical tuberculoid leprosy. The localization of NL lesions may be the result of the intimate skin contact with lepromatous parents or relatives, in areas such as cheeks, arms, buttocks, and limbs, and the innoculation of M. leprae into skin may strongly stimulate cell mediated immunity (CMI) against the bacilli. These circumstances might explain the good CMI response leading to high resistance, stability, and auto-resolution of nodular leprosy of childhood.
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Leprosy is rarely diagnosed in our part of the world. In our 26-year-old patient, borderline lepromatous leprosy was first diagnosed in 1992 and was treated with Rifoldin, Lemprene and Dapson according to the standard WHO scheme of treatment. Ophthalmic examination showed minor epithelial lesions of the cornea in both eyes, a reduced corneal reflex in the left eye and a scleral leproma nasally and close to the limbus, also in the left eye. In 1995, the patient was examined again and was treated as above for lepromata of the left eyebrow nasally and of both lower legs. Ophthalmic examination revealed conjunctival irritation, anterior uveitis with leprosy pearls on the pupillary margin and secondary glaucoma. The glaucoma was treated with hypotonics, the uveitis was treated with topical cortisone. The intra-ocular pressure normalised and the uveitis improved. Of the two main types of leprosy, lepromatous leprosy and tuberculoid leprosy, our patient had the second, milder form.
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Existence of subpolar tuberculoid leprosy was postulated by a few leprologists to explain clinical variations near the tuberculoid pole but failed to precisely identify the same. An attempt has been made to describe the clinical and histological features of subpolar tuberculoid leprosy. 76 cases of the TT-BT range according to Ridley-Jopling classification were examined by detailed clinical, histological and immunological methods. Definite clinical and histological discrepancies from either BT or TTp were seen in 30 (39.4%) cases, confirming the existence of subpolar tuberculoid leprosy (TTs) and thus clarifying the immunological spectrum of leprosy.
OBJECTIVE: This study analyzes the major clinical characteristics of patients with active leprosy in relation to the in vitro immune response to the T-lymphocyte activator anti-CD3. METHODS: Thirty-eight patients with an established diagnosis of leprosy were classified according to the Ridley and Jopling table. Peripheral blood mononuclear cells from both lepromatous leprosy (LL) and tuberculoid leprosy (TL) patients and healthy controls were used to evaluate lymphocyte proliferation; immunoenzymatic assays were used to evaluate cytokine production (IL-1, IL-2, IL-4, IL-6, IL-10, IFN-gamma). RESULTS: Peripheral blood mononuclear cells from both LL and TL patients displayed blastogenic responses to anti-CD3. The cytokines IL-1 beta, IL-6, IL-10, and IFN-gamma were detected in culture supernatants. Endogenous production of IL-1 beta was significantly higher in cell cultures from patients with the lepromatous form of the disease compared to those with tuberculoid leprosy. Production of IL-6 in response to anti-CD3 was observed in a significantly higher proportion of LL than TL patients (P = 0.0025). Gamma-interferon production did not differ between TL and LL, but a direct correlation was observed between time of multidrug treatment and IFN production in vitro (P = 0.016). Interleukin-10 was detected in culture supernatants of lymphocytes activated by anti-CD3 from both patient groups, but not from healthy controls. CONCLUSIONS: The findings of this study suggest that patients with the two distinct forms of leprosy are capable of responding to a polyclonal T-lymphocyte stimulus such as anti-CD3 and provide evidence suggestive of alterations in the immune responses mediated by cytokines that may contribute to the spectrum of disease and response to treatment.
BACKGROUND: The diagnosis of tuberculoid leprosy is often difficult on hematoxylin and eosin (H&E) due to the absence of demonstrable nerve destruction. This study evaluates the utility of S-100 staining in identifying nerve fragmentation and differentiation of tuberculoid leprosy from other cutaneous granulomatous diseases. METHODS: Fifty cases of leprosy including 38 borderline tuberculoid (BT), two tuberculoid (TT), and 10 indeterminate leprosy (IL) were studied. Eleven controls of non-lepromatous cutaneous granulomatous lesions were included. S-100 was used for identifying the following dermal nerve patterns: infiltrated (A), fragmented (B), absent (C), and intact (D) nerves. RESULTS: On H&E, only 18/38 (47.4%) BT cases and 1/2 (50%) TT cases revealed neural inflammation. On S-100 staining of BT cases, 28/38 (73.7%) showed pattern B followed by patterns C and A in 8/38 (21.1%) and 2/38 (5.3%) cases, respectively. Both the TT cases showed pattern B. Only intact nerves (D) were seen in all the control cases. S-100 identified nerve damage in 4/10 (40%) IL cases. The patterns A, B, and C had sensitivity, specificity, and positive and negative predictive values of 100% in diagnosing tuberculoid (BT + TT) leprosy. CONCLUSIONS: S-100 is superior to H&E in identifying nerve fragmentation (p < 0.01). It also aids the differential diagnosis of tuberculoid leprosy.
A 5-year-old contact of a lepromatous leprosy patient with a tuberculoid lesion on the anterior aspect of the shaft of the penis is reported. The child was clinically suspected to have borderline tuberculoid leprosy during a survey of contacts of leprosy patients, which on histopathology revealed features of subpolar tuberculoid leprosy. The father of the child was recently detected as a case of lepromatous leprosy and was started on multibacillary regime of WHO multidrug therapy. The reason for the localization of the lesion to the shaft of the penis is also suggested. Skin as a route of transmission of tuberculoid leprosy is also emphasized.
Two cases of tuberculoid leprosy with primary hyperpigmented anaesthetic lesions are reported and subject is reviewed.
Inoculation Tuberculoid Leprosy has been described by various leprologists off and on and this mode of onset has been established. A case of tuberculoid leprosy over thumb, appearing after trauma in an Army recruit is described with the review of the literature.
We have compared epidermal cell proliferation in skin biopsies from areas with lesions to contralateral areas without lesions in patients with indeterminate, tuberculoid and lepromatous leprosy. Cell proliferation was determined as the percentage of labeled cells in the basal and suprabasal epidermal layers, using autoradiographic preparations of skin biopsies taken 1 hr after a 3H-thymidine intradermal injection. We have found a significant reduction in epidermal cell proliferation in areas with lesions in the three groups of patients. The greatest reduction occurred in lepromatous patients. In lesions of patients with indeterminate or tuberculoid leprosy, the reduction was the same, and in both groups it was smaller than in lepromatous patients. In the areas without lesions, the index of labeled cells was similar to that of "normal" skin of nonleprosy patients. In the contralateral unaffected areas from leprosy patients and in "normal" skin from nonleprosy patients, as well as in affected areas from patients with indeterminate leprosy, epidermal cell labeling was greater in the suprabasal layer than in the basal layer. In lesions of lepromatous patients, cell labeling was greater in the basal layer than in the suprabasal layer. Our findings suggest that the reduction of epidermal cell proliferation in leprosy patients is restricted to the cell-mediated immune response, more intense in lepromatous leprosy. It does not seem to be related to denervation, which is greater in tuberculoid leprosy.