Не в курсе ли Вы, доктор, чем характерен саркоидоз легких? А то в сети описания разные, и меня смутило высказывание про "неясную этиологию" и еще славный оборот: "...учитывая возможность спонтанного выздоровления..." Собственно, интересна как раз неясная этиология. Должны же быть хоть какие-то гипотезы?
Background: Sarcoidosis is characterized by noncaseating epithelioid granulomas that may affect any organ system. Although Jonathan Hutchinson described the first case in 1869, the etiology of the disease is still unknown. The disease most commonly involves granuloma formation in the lungs. Other commonly involved organ systems include the lymph nodes (especially the intrathoracic nodes); the skin; the eyes; the liver; the heart; and the nervous, musculoskeletal, renal, and endocrine systems.
Pathophysiology: The etiology of sarcoidosis is unknown, but several immune aberrations have been noted and are thought to play a role in its pathogenesis. Studies have shown an increase in B-cell activity with hypergammaglobulinemia noted in about one half of patients and in nonspecific immune-complex formation. Reduced delayed-type hypersensitivity responses are also found in many patients with sarcoidosis. Cutaneous anergy to tuberculin intradermal testing occurs in two thirds of patients. Immune dysregulation has been theorized to be due to a persistent antigen of low virulence that is poorly cleared by the immune system, leading to a chronic T cell of the Th1 subtype response, which results in granuloma formation.
Proposed antigens fall into 3 categories that include infectious, environmental, and autoantigens. The most common infectious agents implicated are Mycobacterium tuberculosis, Mycoplasma species, Corynebacteria species, spirochetes, atypical mycobacteria, Propionibacterium acnes, Borrelia burgdorferi, herpes simplex virus, Epstein-Barr virus, cytomegalovirus, coxsackievirus, rubella virus, Histoplasma species, Cryptococcus species, coccidioidomycosis, and sporotrichosis. Environmental antigens implicated include metals (eg, zirconium, aluminum, beryllium), organic dusts (eg, pine, pollen), and inorganic dusts (eg, clay, soil, talc). Heat shock protein has also been implicated http://www.emedicine.com/DERM/topic381.htm
Limited but encouraging progress has been made over the last several years in our understanding of the etiology of sarcoidosis as a result of recent investments in epidemiologic, immunologic, and molecular biologic studies. A recent US multicenter study of sarcoidosis found few environmental or occupational exposures associated with a two-fold or higher risk of development of sarcoidosis, suggesting noninfectious exposures play a small, if any, role in causing systemic sarcoidosis. In contrast, recent studies have linked infectious agents including mycobacterial and propionibacterial organisms with sarcoidosis. The association of sarcoidosis with the use of Th1-promoting biologic response modifiers is consistent with a central role for enhanced Th1 immune responses in the pathogenesis of sarcoidosis. Given evidence for a genetic predisposition to sarcoidosis, these findings suggest that the etiology of systemic sarcoidosis is linked to genetically determined enhanced Th1 immune responses to a limited number of microbial pathogens.
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Date: 2005-01-25 02:05 pm (UTC)no subject
Date: 2005-01-25 03:18 pm (UTC)no subject
Date: 2005-01-25 10:20 pm (UTC)Пока ждете, не подскажете ли?..
Date: 2005-01-25 02:07 pm (UTC)А то в сети описания разные, и меня смутило высказывание про "неясную этиологию" и еще славный оборот: "...учитывая возможность спонтанного выздоровления..."
Собственно, интересна как раз неясная этиология. Должны же быть хоть какие-то гипотезы?
Re: Пока ждете, не подскажете ли?..
Date: 2005-01-25 03:19 pm (UTC)Re: Пока ждете, не подскажете ли?..
Date: 2005-01-25 03:22 pm (UTC)Pathophysiology: The etiology of sarcoidosis is unknown, but several immune aberrations have been noted and are thought to play a role in its pathogenesis. Studies have shown an increase in B-cell activity with hypergammaglobulinemia noted in about one half of patients and in nonspecific immune-complex formation. Reduced delayed-type hypersensitivity responses are also found in many patients with sarcoidosis. Cutaneous anergy to tuberculin intradermal testing occurs in two thirds of patients. Immune dysregulation has been theorized to be due to a persistent antigen of low virulence that is poorly cleared by the immune system, leading to a chronic T cell of the Th1 subtype response, which results in granuloma formation.
Proposed antigens fall into 3 categories that include infectious, environmental, and autoantigens. The most common infectious agents implicated are Mycobacterium tuberculosis, Mycoplasma species, Corynebacteria species, spirochetes, atypical mycobacteria, Propionibacterium acnes, Borrelia burgdorferi, herpes simplex virus, Epstein-Barr virus, cytomegalovirus, coxsackievirus, rubella virus, Histoplasma species, Cryptococcus species, coccidioidomycosis, and sporotrichosis. Environmental antigens implicated include metals (eg, zirconium, aluminum, beryllium), organic dusts (eg, pine, pollen), and inorganic dusts (eg, clay, soil, talc). Heat shock protein has also been implicated
http://www.emedicine.com/DERM/topic381.htm
Re: Пока ждете, не подскажете ли?..
Date: 2005-01-25 03:23 pm (UTC)no subject
Date: 2005-01-25 03:08 pm (UTC)no subject
Date: 2005-01-26 07:52 am (UTC)no subject
Date: 2005-01-26 09:26 am (UTC)не настолько важное
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