Sarcoidosis is predominantly seen in young and middle-aged patients and may involve multiple organs [7]. Although the cause of sarcoidosis remains uncertain, much is known about the immunology of this disease. The immunological hallmark is an accumulation of activated CD4+ T lymphocytes at the sites of inflammation. Interaction between the CD4+ cells and alveolar macrophages leads to a Th1-skewed cytokine profile that orchestrates the ensuing granulomatous inflammatory process [8].
The diagnosis of sarcoidosis is commonly established on the basis of compatible clinical and/or radiological features, supported by the histological findings of noncaseating granulomas and the exclusion of other diseases with a similar clinical or histological picture [7]. The recommended diagnostic procedure is fiber-optic bronchoscopy combined with various biopsy techniques (endobronchial biopsy, transbronchial lung biopsy, transbronchial needle aspiration and biopsy) as well as BAL. Studies of the lymphocyte subpopulations in the BAL fluid may be diagnostically important. A CD4+/CD8+ ratio of >3.5 in a patient with a typical clinical and radiological picture is very specific for sarcoidosis and may obviate the need for further invasive diagnostic procedures [8]. If bronchoscopy fails to confirm the diagnosis, labial biopsy is a fairly useful method for providing histological confirmation of the disease [9]. In the case presented here, the compatible radiographic findings, the results of BAL fluid analysis and the characteristic histological findings from the lip biopsy were considered sufficient to support the diagnosis of sarcoidosis.
Psoriasis is a common inflammatory skin disorder characterized by erythematous, sharply demarcated papules and rounded plaques, covered by silvery micaceous scales which most commonly appear on the elbows, knees, scalp, umbilicus and lumbar area [10]. Skin biopsy may show a variable histological picture but is usually diagnostic in early lesions or at the advancing edge of a well-established plaque. The characteristic histological features in psoriasis include proliferation of epidermal keratinocytes and hyperkeratosis as well as infiltration of immunocytes along with angiogenesis, and subsequent typical thickening and scaling of the erythematous skin. More specifically, the epidermis in psoriatic skin is characterized by dramatic pathological alterations, such as profound acanthosis with elongation of epidermal rete ridges. Likewise, neutrophils migrate through the epidermis and form Munro microabscesses beneath the stratum corneum; this is one of the most salient features of the disease [10]. The findings from skin lesions in our patient were identical to those mentioned above.
Compelling circumstantial and experimental evidence suggests that the primary immunopathogenesis of psoriasis is T-lymphocyte based, so least in part it resembles sarcoidosis. The immigrant immunocytes interact with resident epithelial and mesenchymal cells to generate the psoriatic lesion. Once activated, the T-lymphocytes excrete a panel of Th1-type proinflammatory cytokines, which are thought to explain many of the histopathological changes seen in psoriatic skin. It is likely that the inflammation of psoriasis is a balance between the adaptive (T-cell mediated) immune response and innate immune responses [11].
Sarcoidosis is rarely associated with other diseases, and most of these are characterized by a Th1/Th2 imbalance (common variable immunodeficiency, autoimmune diseases etc.) [12]. Moreover, the skin manifestations in sarcoidosis are not always granulomatous (e.g. erythema nodosum) and may result from a systemic immunological reaction. Such a reaction might explain the presence of psoriatic lesions in a patient with sarcoidosis. Thus the coexistence of sarcoidosis and psoriasis might not be coincidental. Both diseases share common pathogenic pathways and the occurrence of psoriasis in a sarcoidosis patient might result from a variable response to a common antigenic stimulus. Enhancement of the Th1 immune response is well recognized in both diseases. Moreover, the promising results obtained in both sarcoidosis and psoriasis patients after application of anti-TNF alpha agents (e.g. infliximab, adalimumab, etanercept) further support this hypothesis, since these therapeutic agents may alter pathogenic mechanisms common to both disorders [11, 13–15]. It has also been reported that the expression of pso p27, a psoriatic scale antigen linked to the pathogenesis of psoriasis, is markedly increased in the lungs of patients with pulmonary sarcoidosis [16].
