**Treatment**

**Chapter 12**

**Treatment with Methotrexate**

Additional information is available at the end of the chapter

Sarcoidosis is a systemic inflammatory disease of unknown etiology. The hallmark histological feature of the disease is epithelioid cell granuloma derived from activated T cells and macro‐ phages triggered by unknown immune stimuli such as bacterial protein or beryllium metal [1, 2]. Various inflammatory cytokines and growth factors can participate in the pathophysiolog‐

Sarcoidosis is fundamentally a chronic inflammatory disease. The pathological and clinical courses vary widely from spontaneous regression to fibrotic progression leading to various

Any of the following may be selected as therapeutic targets for sarcoidosis, depending on the pathophysiology and evolution of the disease: 1) delete the etiological agents, 2) attenuate the hyperimmune reactions directly underlying the epithelioid cell granuloma formation, 3) arrest any pathophysiological processes that tend to persist, 4) relieve functional disturbances caused

It is critical to grasp or predict the whole clinical course of sarcoidosis when considering

Corticosteroids, the established standard therapy for sarcoidosis, have drawbacks. While corticosteroids are reliably therapeutic, some patients manifest adverse effects during treat‐ ment or functional declines in spite of treatment [4]. Corticosteroids may also disturb the defensive function of granulomas surrounding etiological antigens or disturb healing proc‐

and reproduction in any medium, provided the original work is properly cited.

© 2013 Nagai and Izumi; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

by fibrotic lesions, 5) replace disabled organs by transplantation.

esses by attenuating various inflammatory processes homogeneously.

**in Patients with Sarcoidosis**

Sonoko Nagai and Takateru Izumi

http://dx.doi.org/10.5772/55042

ical processes of sarcoidosis [1].

patterns of organ dysfunction [3].

**1. Introduction**

therapies.

**Chapter 12**
