Nerve and skin damage in leprosy is associated with increased intralesional heat shock protein.

Leprosy is frequently complicated by the development of reversal reactions in which peripheral nerve and skin lesions become inflamed and irreversible nerve damage may ensue. Increased expression of proteins belonging to the 70-kD heat shock family (hsp 70) occurs in cells of the central nervous system exposed to hyperthermia, physical damage or drug-induced trauma. In the present study we have used immunocytochemical staining to monitor hsp70 levels in peripheral nerves infected by Mycobacterium leprae. Hsp70 was detected in skin and nerve lesions from all leprosy patients, but was particularly prominent in lesions from patients undergoing reversal reactions. Hsp70 immunocytochemistry can thus be used as a marker of neural injury in the peripheral as well as in the central nervous system. The cellular dynamics of nerve damage in leprosy are currently poorly understood, and we postulate that the immunopathology of leprosy may be partly due to an autoimmune response to heat shock proteins.

Ocular manifestations of Hansen's disease.

A detailed ophthalmic evaluation including slitlamp biomicroscopy, measurement of corneal sensitivity using Cochet and Bonnet aesthesiometer, Schirmer's test and Goldmann applanation tonometry was carried out in 89 patients of Hansen's disease attending the leprosy clinic with or without ocular symptoms and willing to undergo eye evaluation. Thirty-one patients had lepromatous leprosy (8 with erythema nodosum leprosum), 56 patients had borderline disease (13 with reversal reactions) and 2 had tuberculoid disease. In addition to the well documented changes of lagophthalmos (6.7%), uveitis (7.3%) and cataracts (19%), we noted prominent corneal nerves in 133 eyes (74.7%), beaded corneal nerves in 19 eyes (10.7%), corneal scarring in 10 eyes (5.6%), corneal hypoaesthesia in 51 eyes (28%) and dry eye in 18 eyes (13%). Beaded corneal nerves and/or stomal infiltrates occurred mainly in the lepromatous group (75%). Ocular hypotony (IOP less than 12 mm Hg) was not seen more frequently in Hansen's as compared to age and sex matched controls with refractive errors or cataracts (33.7%, vs. 37.8%, p = 0.33). Our study highlights the primary corneal involvement with corneal neuropathy as the predominant feature of Hansen's disease.

Clinical features and outcome of reversal (type 1) reactions in Hyderabad, India.

A retrospective survey of the notes on all patients attending Dhoolpet Leprosy Research Center, India, during 1985 was done to establish the frequency, timing, and clinical features of reversal (type 1) reactions; 494 case notes were examined and clinical evidence of a reversal reaction was found in 44 cases (10.9%). Reactions were most common in borderline patients, with 11.4% and 14.8% of borderline tuberculoid (BT) and borderline lepromatous (BL) patients developing reactions, respectively. Presentation in reaction was frequent with 47.5% of reactional patients having signs of a reversal reaction at the time of their first visit to the Dhoolpet clinic; 50% of skin reactions developing in patients on antileprosy treatment occur within the first month of treatment. Neurological reactions occur later and over a longer time course. Late reactions may occur up to 6 1/2 years after the start of treatment. Further reactional episodes occurred in 31.8% of the patients, and may be repeated. Steroid treatment produced improvement of both skin lesions and neuritis, but improvement in clinical signs and symptoms occurred in only 50% of the neuritic episodes.

Episodic edema in type 2 lepra reaction can be caused by transient lymphatic obstruction in the lymph node.

Fourteen patients with lepromatous leprosy developed attacks of edema of the hands and/or feet associated with attacks of type 2 lepra reaction (erythema nodosum leprosum). The regional lymph nodes were enlarged and often tender when edema was present. Lymph node biopsies in five cases showed compression of the subcapsular sinus against the thickened fibrotic capsule of the inflamed node. It is suggested that this obstructs the inflow of lymph into the regional nodes, thereby causing the edema.