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Intra-Abdominal Complications of Sarcoidosis Quality of Life After Breast-Conserving Therapy in Taiwan Self-Efficacy in Type 1 Diabetic Adolescents

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Intra-Abdominal Complications of Sarcoidosis Quality of Life After Breast-Conserving Therapy in Taiwan Self-Efficacy in Type 1 Diabetic Adolescents CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector J Formos Med Assoc 2010;109(6):484–492 Contents lists available at ScienceDirect Volume 109 Number 7 July 2010 ISSN 0929 6646 Journal of the Journal of the Formosan Medical Association Formosan Medical Association Human papillomavirus vaccines Intra-abdominal complications of sarcoidosis Quality of life after breast-conserving therapy in Taiwan Self-efficacy in type 1 diabetic adolescents Formosan Medical Association Journal homepage: http://www.jfma-online.com Taipei, Taiwan Review Article Intra-abdominal Complications of Sarcoidosis Kristin Loening MacArthur,1 Faripour Forouhar,2 George Yung-Hsing Wu1 Sarcoidosis is an inflammatory disease characterized by non-caseating granulomas in the absence of other autoimmune processes, infectious diseases, or foreign agents. The etiology of sarcoidosis is not completely understood. Several organ systems can be affected, of which the most frequently involved include the lungs and lymph nodes. Intra-abdominal sarcoidosis is less common, but can be found in the absence of pulmonary or lymphatic disease. Intra-abdominal sarcoidosis is most often asymptomatic. However, long-standing unrecognized disease can result in life-threatening complications. The identification, mon- itoring and prevention of these complications will be discussed, with emphasis on both clinical and his- tological presentations of intra-abdominal sarcoidosis. Key Words: gastrointestinal, hepatic, pancreatic, peritoneal, splenic Introduction age-adjusted incidence of 35.5/100,000 versus Caucasian Americans at 10.9/100,000.3 The dis- Sarcoidosis is a systemic inflammatory disease ease affects women more frequently than men marked by diversity of clinical presentation, organ and is usually diagnosed in young adults between involvement and disease progression. Sarcoidosis 20–40 years of age.4 A second incidence peak after affects individuals worldwide, occurring most age fifty has been found in females in Japan and commonly in young middle-aged adults. Epi- Scandinavia.5 Compared to patients in Western demiological reports of sarcoidosis vary among countries, Chinese patients in Taiwan have been racial groups, but the worldwide prevalence varies reported to present later in life, more commonly between 2–60 per 100,000 people, with higher have intrathoracic involvement, and less fre- rates seen in patients of Irish and Scandinavian quently have hypercalcemia and hyperglobuline- descent.1 Sarcoidosis in Chinese patients in Taiwan mia.6 In a report from Singapore, the calculated has been reported to be relatively rare, although annual incidence of sarcoidosis was 0.23/100,000 incidence has increased from 0.4/100,000 in the for Chinese, 4.57/100,000 for Indians and 1980s to 2.7/100,000 in the 1990s.2 In the United 1.30/100,000 for Malays. The overall annual inci- States, African Americans have a three-fold higher dence of sarcoidosis was 0.56/100,000.7 Overall, ©2010 Elsevier & Formosan Medical Association ................................................... Departments of 1Medicine and 2Anatomical Pathology, University of Connecticut Health Center, Farmington, USA. *Correspondence to: Dr George Y. Wu, Department of Medicine, Division of Gastroenterology Hepatology, University of Connecticut Health Center, Rm. AM-044, 263 Farmington Ave, Farmington, CT 06030, USA. E-mail: [email protected] 484 J Formos Med Assoc | 2010 • Vol 109 • No 7 Gastrointestinal sarcoidosis the mortality of sarcoidosis has been reported to be 1–5%, and is usually attributed to progressive respiratory insufficiency, central nervous system involvement, or myocardial compromise.5,8 This multisystem disorder usually involves the lungs (> 90%) and the lymphoid system (30%) (Figure 1), and classically presents as intratho- racic hilar lymphadenopathy. Other sites include the heart (5%), skin (25%), and eyes (11–83%), and less commonly the nervous system, muscles, bones, and salivary glands.5 The hepatobiliary and gastrointestinal tracts can also be affected even in patients without intrathoracic disease. Liver in- Figure 1. Lymph node showing tight non-necrotizing epithelioid granulomata, typical of sarcoidosis. (Hematoxylin volvement follows lung and lymph nodes in fre- and eosin; original magnification, 100×). quency, although it is usually asymptomatic, and does not often cause significant organ dysfunction. Approximately 50–80% of autopsy and biopsy specimens of patients with systemic sarcoidosis have been shown to have detectable hepatic sar- coidosis.9 In contrast, sarcoidosis of the gut is ex- tremely rare with clinical symptoms present in < 1% of patients.10,11 Autopsy reports are variable, with gut involvement anywhere from 0% to 10% of patients with proven systemic sarcoidosis.9,12,13 Gut involvement is usually associated with con- comitant pulmonary disease, and is most com- Figure 2. Liver biopsy with necrotizing sarcoidal granuloma. monly asymptomatic. Clinical complications of Fibrinoid necrosis in the center of necrotizing type sarcoidal hepatobiliary and gut sarcoidosis are rare, but granulomata (asterisk). This is quite different from caseation are important to recognize as they may cause sig- necrosis of tuberculosis and suppurative necrosis in Yersinia. Multinucleated giant cell (arrow). (Hematoxylin and eosin; nificant morbidity and mortality. original magnification, 100×). The sine qua non for the diagnosis of sarcoido- sis is the histological demonstration of epithe- for sarcoidosis, but clinical and radiographic fea- lioid granulomatous reactions in the absence of tures can aid in making the diagnosis. other granulomatous diseases such as tuberculo- The etiology of sarcoidosis is still not com- sis, fungal infections, inflammatory bowel dis- pletely understood although it has been suggested ease, malignancy, and delayed-type hypersensitivity that the disease arises in genetically susceptible to foreign antigens.14 The granulomata are typi- individuals who are exposed to deleterious envi- cally non-necrotizing (Figure 1). However, central ronmental agents. Certain familial clusters and fibrinoid necrosis may occur (Figure 2) and rarely, common human leukocyte antigens have sug- it can be significant. Caseation necrosis never gested a polyclonal inheritance pattern, with his- occurs. Typically, there is a sparse population of tocompatibility leukocyte antigens (HLA-A1, B8, lymphocytes in the mantle zone around the DRB1, DQB1, DRB3) correlating with suscepti- granulomata (Figures 3 and 4). This is in contrast bility in different populations.15 No particular in- to the granulomatous reaction formed in response citing environmental agent has been proven, but to infectious diseases. Biopsies showing histologi- several examples have been proposed. These in- cal features in two or more organs is most specific clude viruses such as herpesviruses, retroviruses, J Formos Med Assoc | 2010 • Vol 109 • No 7 485 K.L. MacArthur, et al A B Figure 3. (A and B) Liver biopsy showing a conglomerate of sarcoidal granulomata. Note prominence of fibrosis and scarcity of lymphocytic infiltration (portal location). Note also the advantage of reticulin stain in exhibiting the architec- ture of granulomatous reaction. Portal area showing granulomatous reaction and extreme fibrosis (asterisk). Reticulin outlining granulomatous complex (arrow). (Hematoxylin and eosin; original magnification, 40×). A B Figure 4. Sarcoidosis involving a portal area of the liver. (A) Sarcoid granuloma (arrow; hematoxylin and eosin; original magnification, 400×). (B) The granulomatous complex (asterisk) surrounded by extent of fibrosis (blue) and bile duct in- jury by trichrome stain (arrow). (Trichrome, original magnification, 400×). and cytomegalovirus, as well as bacteria including disease.1,16 The clinical presentation of hepatic Borrelia burgdorferi, mycobacteria and mycoplasma. sarcoidosis is usually asymptomatic, and despite The immunologic abnormalities demonstrated in the presence of granulomas on biopsy or on ra- sarcoidosis usually encompass an antigen-triggered diologic studies, there is rarely organ dysfunction. abnormal Th-1 response accompanied by cytokine However, there are some clinical signs that may production. This inflammatory pattern results in suggest hepatic sarcoidosis, and may suggest need local macrophage recruitment, granuloma forma- for a liver biopsy. Fever and arthralgias, although tion, injury and eventual fibrosis.1 not specific, are present in the majority of indi- The following will outline both clinical man- viduals with active hepatic sarcoidosis.17,18 More ifestations, and complications of intra-abdominal specific symptoms include jaundice, pruritis, right sarcoidosis. upper quadrant abdominal pain and hepato- megaly.10,19 These symptoms most likely result from chronic cholestasis due to intrahepatic gran- Sarcoidosis of the Liver ulomas in the portal space (Figure 4B) or through external compression of bile ducts from granulo- Although more than half of patients with sar- mas in extrahepatic lymph nodes. Chronic in- coidosis have hepatic involvement on biopsy, flammation and fibrosis can result in long-term only 10–30% have laboratory evidence of liver complications including portal hypertension,20 486 J Formos Med Assoc | 2010 • Vol 109 • No 7 Gastrointestinal sarcoidosis Budd-Chiari syndrome,21 and cirrhosis,19,22,23 Mild nonspecific lobular hepatitis often accom- although the prevalence of these complications panies the granulomatous reaction
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