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TEXTBOOK : SARCOIDOSIS

SARCOIDOSIS

Edited by Yoshinobu Eishi .

298 pages . 
Open Access . 

Sarcoidosis is one of the best-known systemic granulomatous diseases. Despite intensive investigation, however, the etiology of sarcoidosis has remained unresolved for more than 100 years [1]. Sarcoidosis seems to result from the exposure of a genetically susceptible subject to an environmental agent, and microbial etiologies of sarcoidosis have long been considered based on the clinical similarities to infectious granulomatous diseases [2]. Several epidemiologic mechanisms may underlie the association of an infective agent or agents with the etiology of sarcoidosis, including spatial, seasonal, and occupational clustering [3]. The results of the ACCESS (A Case Control Etiologic Study of Sarcoidosis) study support an association between selected microbially-rich environments and sarcoidosis [4].
Mycobacterial and propionibacterial organisms are the most commonly implicated etiologic agents based on studies indicating the detection by polymerase chain reaction (PCR) of microbial DNA from these organisms in tissues from sarcoid patients around the world [5-7].
Different studies have produced considerably varying results, however, with microbial DNA detected in 0% to 80% of sarcoidosis tissues and in 0% to more than 30% of control tissues [8, 9]. The failure to detect microbial DNA from these organisms in samples from some sarcoid patients suggests other causes of sarcoidosis in those patients, whereas detection of the microbial DNA in some control samples suggests latent infection of the bacterium. Immune responses against microbial antigens from these organisms, such as ESAT-6 and KatG peptides from Mycobacterium tuberculosis and a recombinant trigger-factor protein from Propionibacterium acnes, have been examined in sarcoid patients and control subjects [10, 11]. 
Immune responses are frequently detected in sarcoid patients as well as in some non-sarcoid patients and healthy subjects. Latent infection by these organisms complicates the interpretation of the results of these immunologic studies. Unless microbial antigens that cause a specific immune response found only in sarcoid patients can be used to stimulate an immune response, immunologic approaches will not be sufficient to unequivocally confirm that these organisms are causative.
Granuloma formation results from the persistence of a nondegradable product or a hypersensitivity response [12]. The two mechanisms overlap in most infectious diseases because microorganisms act as both foreign bodies and antigens to induce immunologic responses.
Granulomas serve as protective mechanism to sequester and degrade the invading agent. The pathologic hallmark of sarcoidosis is an epithelioid cell granuloma, thus some etiologic agent of sarcoidosis must be present or have been present within the sarcoid granuloma. Histopathologic studies are therefore essential to demonstrate mycobacterial or propionibacterial organisms or antigens within sarcoid granulomas to demonstrate an etiologic link between sarcoidosis and these organisms. 
P. acnes is so far the only microorganism isolated from sarcoid lesions by bacterial culture [13, 14]. P. acnes is an anaerobic, non-spore-forming, gram-positive rod bacterium indigenous to the skin and mucosal surfaces. A series of Japanese studies has provided accumulating evidence for a role of P. acnes in sarcoidosis. In this review, we propose mechanisms of granuloma formation in response to this indigenous bacterium in subjects with sarcoidosis based on our results obtained using histopathological and experimental approaches, and introduce a new concept of infectious disease in which endogenous infection is caused by indigenous bacteria.


Yoshinobu Eishi
Assistant Professor Department Of Dermatology,
Kinki University School Of Medicine, 
Osaka-Sayama,
Japan
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CONTENTS :


Section 1 of the textbook : Pathogenesis .


1 Propionibacterium acnes as a Cause of Sarcoidosis 3 
Yoshinobu Eishi

2 The Role of Type I IFN and TNF-α in the Pathogenesis of 
Sarcoidosis 35 Mitsuteru Akahoshi


Section 2 of the textbook : Genetic Factors .


3 Genetic Factors Involved in Sarcoidosis 53 
Birendra P. Sah and Michael C. Iannuzzi

4 Genetics of Sarcoidosis 79 
Nabeel Y. Hamzeh and Lisa A. Maier

Section 3 of the textbook : Clinical Features .


5 Clinical Manifestations of Sarcoidosis 109 
Luis Jara-Palomares, Candela Caballero-Eraso, Cesar Gutiérrez, Alvaro Donate and Jose Antonio Rodríguez-Portal

6 Airways Disease in Sarcoidosis 145 
Adam S. Morgenthau

7 Physiological Manifestation in Pulmonary Sarcoidosis 165 
Kentaro Watanabe

8 Neurosarcoidosis 183 
Mohankumar Kurukumbi, Preema Mehta, Isha Misra and Jayam- Trouth Annapurni

Section 4 of the textbook : Diagnosis .


9 Laboratory Investigations and Immunological Testing in 
Sarcoidosis 201 Hasib Ahmadzai, Paul S. Thomas and Denis Wakefield

10 Endobronchial Ultrasound in the Diagnostic Evaluation of 
Sarcoidosis 239 Abiramy Jeyabalan and Andrew RL Medford

11 Pathological Diagnosis with Endobronchial Ultrasonography 
— Guided Transbronchial Needle Aspiration (EBUS-TBNA) 257 Atsushi Kitamura and Yuichi Takiguchi

Section 5 of the textbook : Treatment .


12 Treatment with Methotrexate in Patients with 
Sarcoidosis 275 Sonoko Nagai and Takateru Izumi .


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