[10] Antigens which might be selleck compound involved include infectious agents Mycobacterium tuberculosis and other atypical species, Propionibacterium acnes and Chlamydia species. Mineral dust such as silica and titanium are also implicated. Firefighters are at a great risk of developing sarcoidosis. Genetic factors are also important in defining the pattern of disease presentation, severity, and prognosis of the disease. There is association between class I HLA B 8 antigens and acute sarcoidosis. HLA�CDRB I and DQB I have been associated with sarcoidosis. Sarcoidosis susceptible genes are present on chromosome 3 p and 5q 11.2 and protective genes on region of 5p 15.2. The development and accumulation of granulomas is the main abnormality in sarcoidosis. Granulomas form to confine pathogens, restrict inflammation, and protect surrounding tissue.

Granulomas are compact centrally organized collections of macrophages and epitheloid cells encircled by lymphocytes. There is depression of cutaneous delayed type hypersensitivity and heightened helper T-cell type response at sites of disease. Circulating immune complexes along with signs of B-cell hyperactivity may be found. Most granuloma-associated lymphocytes produce high levels of tumor necrosis factor (TNF), Interleukin 12, IL-15, IL-18, MIP I, MCP I, GM-CSF. The CD4+ lymphocytes and immune effector cells such as macrophages, mast cells, and natural killer cells perpetuate inflammatory response by release of cytokines. Skin lesions of sarcodosis can be psychologically devastating.

Most frequent presentation is soft red to yellowish brown or violaceous flat-topped papules or plaques most frequently on the face. Larger lesions may be found on the trunk, extremities, and buttocks. Erythema nodosum was noted in 31% of patients in a study. Other cutaneous manifestations include lupus pernio which is indurated lumpy violaceous lesions on nose, cheeks, lips, and ears. Other cutaneous lesions include angiolupoid form, scar sarcoidosis, scarring alopecia, lichenoid form, nodular form, mannular form, and subcutaneous sarcoidosis also occur. No lab test is diagnostic of sarcoidosis. Laboratory evaluation may reveal elevated ESR, anemia, leucopenia, hypercalcemia, or hypercalciuria. The serum level of ACE is elevated in over 50% of children with late-onset sarcoidosis. Chest radiograph may reveal bilateral hilar adenopathy.

Bronchoalveolar lavage (BAL) demonstrates the increased number of lymphocytes which are activated helper inducer T-cells. However in children, BAL lymphocytosis does not correlate with disease activity, treatment response, or prognosis so it is not recommended GSK-3 in children.[11] The diagnosis of sarcoidosis is confirmed by demonstrating a typical noncaseating epitheloid cell granuloma on biopsy.[12] The therapy of choice for cutaneous sarcoidosis with multisystem involvement is topical or systemic corticosteroids. Oral prednisolone is usually initiated at 1�C2 mg/kg/day for 4�C8 weeks.