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Sarcoidosis is a multisystem disease characterized by the presence of noncaseating granulomas in multiple organs. The trigger factor is presumed to be the inhalation of a yet unidentified antigen (1). Antigen-presenting cells release IL-1, IL-15, IFN-c, and TFN-a. They recruit activated TH1 CD4 T cells, which leads to an oligoclonal T-cell alveolitis. Further release of monocyte chemoattractant protein-1 (MCP-1), monocyte inflammatory protein 1a (MIP-1a), CXCL10, and IL-16 induces migration of monocytes and T-cell proliferation. The monocytes produce fibrin, fibronectin, TGF-b, IL-3, IFN-c, and TNF-a and then transform into epithelioid cells. Some of them coalesce to form multinucleate giant cells and form noncaseating (nonnecrotic) epithelioid cell granulomas. IL-4 and IL-6 lead to polyclonal B cell stimulation, which is reflected as hypergammaglobulinemia. In many cases, the disease is incidentally discovered due to the presence of bilateral enlargement of the mediastinal lymph nodes (bilateral hilar lymphadenopathy) in chest radiograms (4). An acute form of the disease (Loefgren's syndrome) is characterized by bilateral hilar lymphadenopathy, fever, erythema nodosum, and acute arthritis, particularly of the knee and the ankle (2). Bronchoalveolar lavage (BAL) typically reveals the presence of CD4+ T-cell alveolitis (3). The BAL fluid often contains up to 10 times as many CD4+ T lymphocytes as the peripheral blood because lymphocytes are recruited from the peripheral blood and the skin (anergy to skin antigens) into the lung. In normal individuals, more than 90% of the cells in the BAL fluid are macrophages, and fewer than 1 106 lymphocytes are recovered; in sarcoidosis, ten or twenty times more lymphocytes are typically recovered. A decrease in the CD4/CD8 ratio in peripheral blood is also observed. Fever and malaise develop due to increased levels of TNF, IL-1, and IL-6 in serum. Erythema nodosum, a nongranulomatous inflammation of the subcutaneous tissue, is the most common skin lesion. Eye involvement is common and may range from a harmless conjunctival nodule to blindness as a complication of intermediate and posterior uveitis (see pp. 244, 246). Granulomatous meningitis is a possible manifestation of neurosarcoidosis. Increased intestinal absorption of calcium occurs because the macrophages in the granulomas convert 25-hydroxyvitamin D to 1,25-hydroxyvitamin D. Osteolytic bone lesions ravely contribute to hypercalcemia and hypercalciuria. Ventricular tachycardia may occur due to the presence of granulomas in myocardial tissue. Small periportal granulomas or T cell infiltrates exhibiting various degrees of fibrosis are often found in the liver (5). The development of splenic granulomas can cause splenomegaly. The concentration of angiotensin-converting enzyme (ACE) in the serum increases due to the synthesis by granuloma tissue.

annals of saudi medicine/annals of saudi medicine

Color Atlas of ImmunologyGerd-Rudiger Burmester, Antonio Pezzutto: <i>Color Atlas of Immunology</i> . 322 pages. Thieme, New York, 2003, ISBN 3-13-126741-0 (GTV). ISBN 0-86577-964-3 (TNY)

Color Atlas of ImmunologyGerd-Rudiger Burmester, Antonio Pezzutto: Color Atlas of Immunology . 322 pages. Thieme, New York, 2003, ISBN 3-13-126741-0 (GTV). ISBN 0-86577-964-3 (TNY)