Colin L. Crawford

Experimental leprosy: a model of epithelioid cell granuloma

An animal model of granulomatous hypersensitivity has been developed, which reproduces some features of the pathologies of important chronic granulomatous disorders, including tuberculosis, tuberculoid leprosy, sarcoidosis, berylliosis, Crohn’s disease, and sensitivity to zirconium. The lesions consist of focal collections of epithelioid cells surrounded by lymphocytes to form tubercles. The epithelioid cell has a secretory function and is not phagocytic. Plasmacytoid dendritic cells are precursors of epithelioid cells, which are therefore part of the innate immune system. Subplasmalemmal linear densities are also present in these cells. This autoimmune model has been induced in rabbits using a non‐myelin sensory peripheral antigen to reproduce the features of tuberculoid leprosy. The antigen is probably present only in human tissue. A granuloma antigen, which is tissue specific similar to that in peripheral nerves, could be present in sarcoidosis and Crohn’s disease. In multiple sclerosis, mononuclear cells in the brain parenchyma are not phagocytic and are therefore similar to epithelioid cells. The induction of tolerance leading to the development of a vaccine to prevent the lesions in multiple sclerosis, sarcoidosis, and Crohn’s disease is possible after purification of the granuloma antigen.

Comment on “DNA Sensing via TLR-9 Constitutes a Major Innate Immunity Pathway Activated during Erythema Nodosum Leprosum”

Dias et al. ([1][1]) conclude that erythema nodosum leprosum (ENL) is a major cause of peripheral nerve damage. They state that each patient was clinically assessed throughout treatment but do not provide any details of the results of clinical examination of the peripheral nervous system. Clinical

Comment on “TLR9 Provokes Inflammation in Response to Fetal DNA: Mechanism for Fetal Loss in Preterm Birth and Preeclampsia”

Scharfe-Nugent and colleagues ([1][1]) have suggested that the use of chloroquine may reduce the frequency of preterm births. The drug acts as a TLR9 inhibitor, reducing inflammation and the concentration of IL-6. Other TLR9 antagonists produce their effect by lowering the level of IFN-α ([2][2]),

Leprosy in Brazil1

erysipelas or cellulitis, keloids, and even scleroderma. To the best of our knowledge, there are only five documented cases of AL associated with tuberculosis infection. Four of them were located on the vulva secondary to genital tuberculosis. There is only one report of AL resulting from dermal and subcutaneous scarring caused by past involvement with tuberculous lymphadenitis involving the right axillary nodes, which resulted in scrofuloderma. Our case is the second report of AL secondary to scrofuloderma. The present case, together with the previous case, indicates that scrofuloderma scarring may cause damage to lymphatic vessels resulting in lymphostasis which leads to AL. Treatment of lymphangiectasia often includes surgical resection of involved tissue and closure with skin grafting. Other treatments include sclerotherapy, cryotherapy, electrodesiccation, and CO2 laser vaporization. Although preferred treatment of AL is complete surgical excision, recurrence may occur. Our patient was treated with cryosurgery and some of them were drained and treated with electrocautery. In conclusion, lymphangiectasias represent a rare cutaneous condition that result from lymphatic obstruction caused by a spectrum of scarring processes. Clinicians should evaluate patients with lymphatic drainage problems for neoplastic processes, radiotherapy, trauma, infection, and inflammation.

Leprosy in Brazil1: Correspondence

erysipelas or cellulitis, keloids, and even scleroderma. To the best of our knowledge, there are only five documented cases of AL associated with tuberculosis infection. Four of them were located on the vulva secondary to genital tuberculosis. There is only one report of AL resulting from dermal and subcutaneous scarring caused by past involvement with tuberculous lymphadenitis involving the right axillary nodes, which resulted in scrofuloderma. Our case is the second report of AL secondary to scrofuloderma. The present case, together with the previous case, indicates that scrofuloderma scarring may cause damage to lymphatic vessels resulting in lymphostasis which leads to AL. Treatment of lymphangiectasia often includes surgical resection of involved tissue and closure with skin grafting. Other treatments include sclerotherapy, cryotherapy, electrodesiccation, and CO2 laser vaporization. Although preferred treatment of AL is complete surgical excision, recurrence may occur. Our patient was treated with cryosurgery and some of them were drained and treated with electrocautery. In conclusion, lymphangiectasias represent a rare cutaneous condition that result from lymphatic obstruction caused by a spectrum of scarring processes. Clinicians should evaluate patients with lymphatic drainage problems for neoplastic processes, radiotherapy, trauma, infection, and inflammation.