Celiac Disease and Metabolic Bone Disease

Celiac disease is a common autoimmune gastrointestinal disorder affecting multiple organs, precipitated in genetically vulnerable persons by the ingestion of gluten. Gluten is poorly digested and is presented to the intestinal mucosa as a large polypeptide. Binding to human leukocyte antigen-DQ2 and human leukocyte antigen-DQ8 molecules on antigen-presenting cells stimulates cellular and humeral immune reactions. Although common serological tests are available to diagnose celiac disease, the diagnosis of celiac disease is often delayed or missed because of lack of recognition as the disease presentation in adults is highly variable and may be asymptomatic. Celiac disease is a common secondary cause of metabolic bone disease and delayed treatment with gluten-free diet affects bone mineral density and fracture risk, so it is crucial to diagnose and treat celiac disease promptly. In this article, we will review recent studies of celiac disease in adults and provide practical, easily accessible information for busy clinicians.     

Joint Disease in End-Stage Renal Disease

The joint diseases that are encountered in chronic dialysis have been reviewed. There are two general categories: de novo disease and arthropathy anteceding ESRD. The de novo joint diseases include categories that are probably the direct result of ESRD. Microcrystalline CaOHapatite and CaPPD arthritis is associated with hyperparathyroidism and a high Ca X P. Aluminum phosphate joint disease is the result of aluminum toxicity. Both types have severe disease of the adjacent bone: osteitis fibrosa with CaOHapatite-CaPPD arthropathy and osteomalacia with aluminum phosphate. Calcium oxalate joint disease probably results from renal oxalate retention in ESRD and conversion of ascorbate to oxalate. The evidence for uric acid arthropathy in the absence of primary gout or lead toxicity is not convincing. Amyloid is the most frequent cause of the carpal tunnel syndrome and is related to retention of β-2 microglobulin. Infective arthritis may be Seen, often occumng as a result of bacteremia from an infected fistula site. A degenerative arthritis different from osteoarthritis has also been described. Pathologic fractures can occur with both amyloid deposition in bone and aluminum osteomalacia. Long-term steroid therapy can lead to avascular necrosis of femoral or humeral heads. Diabetes mellitus with neuropathy can give rise to a very destructive Charcot joint. Tendon ruptures occur, but the mechanism is obscure.
It is most important that the nephrologist work closely with the rheumatologist. Carefbl and sophis ticated examination of synovial fluid and tissue is mandatory in the microcrystalling diseases. Immunohistochemical methods may be required, particularly for tissue removed during decompression of the median nerve. Together the subspecialists can establish the diagnosis and determine the appropriate therapy for the iarge number of joint disorders to which the dialysis patient is subject.     

Joint Disease in End-Stage Renal Disease

The joint diseases that are encountered in chronic dialysis have been reviewed. There are two general categories: de novo disease and arthropathy anteceding ESRD. The de novo joint diseases include categories that are probably the direct result of ESRD. Microcrystalline CaOHapatite and CaPPD arthritis is associated with hyperparathyroidism and a high Ca X P. Aluminum phosphate joint disease is the result of aluminum toxicity. Both types have severe disease of the adjacent bone: osteitis fibrosa with CaOHapatite-CaPPD arthropathy and osteomalacia with aluminum phosphate. Calcium oxalate joint disease probably results from renal oxalate retention in ESRD and conversion of ascorbate to oxalate. The evidence for uric acid arthropathy in the absence of primary gout or lead toxicity is not convincing. Amyloid is the most frequent cause of the carpal tunnel syndrome and is related to retention of β-2 microglobulin. Infective arthritis may be Seen, often occumng as a result of bacteremia from an infected fistula site. A degenerative arthritis different from osteoarthritis has also been described. Pathologic fractures can occur with both amyloid deposition in bone and aluminum osteomalacia. Long-term steroid therapy can lead to avascular necrosis of femoral or humeral heads. Diabetes mellitus with neuropathy can give rise to a very destructive Charcot joint. Tendon ruptures occur, but the mechanism is obscure. It is most important that the nephrologist work closely with the rheumatologist. Carefbl and sophis ticated examination of synovial fluid and tissue is mandatory in the microcrystalling diseases. Immunohistochemical methods may be required, particularly for tissue removed during decompression of the median nerve. Together the subspecialists can establish the diagnosis and determine the appropriate therapy for the iarge number of joint disorders to which the dialysis patient is subject.     

Simultaneous Development of Dieterich Disease and Freiberg Disease

Dieterich disease is an uncommon arthropathy of the hand, with few studies published. This lesion shares a similar etiopathogenesis with Freiberg disease, although the association of both conditions has only been described once. We report a 65-year-old man consulting for inflammatory pain in his right hand of 1 month's duration and also in his right foot of 4 months' duration. The rheumatology department was consulted to rule out systemic disease because the synovitis had occurred simultaneously in 2 different locations. The plain radiography and magnetic resonance imaging findings supported the diagnosis of Dieterich disease and Freiberg disease, although only increased uptake was found on scintigraphy in the affected zones. Few studies have been published about Dieterich disease, most in case report form. To our knowledge, only 1 study has described the association of Dieterich disease and Freiberg disease. Surgical treatment has been described when conservative management is unsuccessful, with multiple techniques used. The present case is the first in which Dieterich disease and Freiberg disease manifested simultaneously in the initial painful inflammatory phase.     

Castleman病

Castleman病（Castleman disease,CD）亦称巨大淋巴结增生症,是一种少见的淋巴组织增生性疾病。由Castleman等在1954年首次以病理现象报道,1956年定义。1972年Keller等首次描述其浆细胞分型,1978年Gaba等报道了首例多中心型CD。临床上分为局灶型（localize Castleman disease,LCD）与多中心型（multicentric Castleman disease,MCD）。CD临床表现复杂,影像学亦无特异性表现,若临床医生缺乏对CD的认识,很难早期发现并诊断,甚至漏诊、误诊。治疗亦需根据临床及病理分型区别对待。     

Castleman病

Castleman病（Castleman disease,CD）亦称巨大淋巴结增生症,是一种少见的淋巴组织增生性疾病。由Castleman等在1954年首次以病理现象报道,1956年定义。1972年Keller等首次描述其浆细胞分型,1978年Gaba等报道了首例多中心型CD。临床上分为局灶型（localize Castleman disease,LCD）与多中心型（multicentric Castleman disease,MCD）。CD临床表现复杂,影像学亦无特异性表现,若临床医生缺乏对CD的认识,很难早期发现并诊断,甚至漏诊、误诊。治疗亦需根据临床及病理分型区别对待。