The osteoporosis is frequently observed in the patients with the inflammatory arthritis and painful rheumatism. The treatment of the osteoporosis for them is different from that for the patients without the arthritis or rheumatism. The recently developed biologic agents blocking tumor necrosis factor, interleukin(IL)-1, IL-6, or receptor activator of nuclear factor-kappaB ligand (RANKL) which are designed to treat the inflammatory arthritis are also expected to heal the osteoporosis in the inflammatory arthritis. The early use of the bisphosphonate is useful to prevent the glucocorticoid induced bone loss and to treat the spondyloarthropathy including the SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome. The clacitonin is useful for the painful rheumatism and osteoporotic fracture. The estrogen replacement is disputed because the stroke is known to occur more commonly in chronic inflammatory rheumatism than in general population. Moreover the pathogenesis of the most rheumatism may be partly related to the hormone. The parathyroid hormone therapy needs caution in the patients with calcium deposition disease and the hyperuricemia. We are reviewing the recent trend and development in the management of the primary, secondary and inflammatory osteoporosis in the patients with arthritis.
Acne Vulgaris ; Arthritis* ; Biological Factors ; Calcium ; Estrogen Replacement Therapy ; Female ; Humans ; Hyperostosis ; Hyperuricemia ; Interleukin-6 ; Osteoporosis* ; Osteoporotic Fractures ; Parathyroid Hormone ; RANK Ligand ; Rheumatic Diseases ; Rheumatic Fever ; Spondylarthropathies ; Stroke ; Tumor Necrosis Factor-alpha

The clinical spectrum of spondyloarthritis is included various diagnostic entities that share clinical, genetic and pathological characteristics. As human tissue specimens of the sacroiliac joints are very difficult to obtain, most of the new concepts have emerged from different animal models of disease. Animal models are available for the study of several different aspects of spondyloarthritis. The models include human leukocyte antigen (HLA) B-27 based on transgenic rat and mouse models, inflammation-driven models, and models of ankylosing enthesitis. Areas of investigation to which these models contribute include the role of HLA B-27, process of spinal and peripheral joint inflammation and calcification, immune responses to candidate antigens and the role of tumor necrosis factor.
Animals ; Humans ; Inflammation ; Joints ; Leukocytes ; Mice ; Models, Animal ; Rats, Transgenic ; Sacroiliac Joint ; Tumor Necrosis Factor-alpha

Kawasaki disease or mucocutaneous lymph node syndrome is an acute inflammatory illness of childhood characterized by systemic panvasculitis. It presents with high fever, dramatic changes of the skin and mucous membranes, and lymphadenopathy. Adult-onset Kawasaki disease is rare and reports on coronary involvement in adult are even rarer. Herein, we report a case of adult-onset Kawasaki disease complicated by splenic infarction and development of coronary aneurysm even despite of treatment with intravenous gamma globulin. A 20-year-old man presented with fever, erytheatous rash, induration and desquamation of hands and feet, pulmonary edema and shock due to cardiomyopathy, splenic infarction, bilateral conjunctivitis, jaundice, and cervical lymphadenopathy. After Kawasaki disease was suspected, intravenous gamma globulin (2 g/kg once) and aspirin (6 g/day) were administered. On the 30th hospital day, transesophageal echocardiography showed one coronary aneurysm and coronary angiography showed three aneurysms. Eight months after the first admission, follow-up coronary angiography showed normalization of the previous coronary abnormalities.
Adult ; Aneurysm ; Aspirin ; Cardiomyopathies ; Conjunctivitis ; Coronary Aneurysm* ; Coronary Angiography ; Echocardiography, Transesophageal ; Exanthema ; Fever ; Follow-Up Studies ; Foot ; gamma-Globulins ; Hand ; Humans ; Jaundice ; Lymphatic Diseases ; Mucocutaneous Lymph Node Syndrome ; Mucous Membrane ; Pulmonary Edema ; Shock ; Skin ; Splenic Infarction* ; Young Adult

BACKGROUND/AIMS: Our aim was to assess whether short-term treatment with soluble tumor necrosis factor (TNF) receptor affects circulating markers of bone metabolism in rheumatoid arthritis (RA) patients. METHODS: Thirty-three active RA patients, treated with oral disease-modifying antirheumatic drugs (DMARDs) and glucocorticoids for > 6 months, were administered etanercept for 12 weeks. Serum levels of bone metabolism markers were compared among patients treated with DMARDs at baseline and after etanercept treatment, normal controls and naive RA patients not previously treated with DMARDs (both age- and gender-matched). RESULTS: Bone-specific alkaline phosphatase (BSALP) and serum c-telopeptide (CTX)-1 levels were lower in RA patients treated with DMARDs than in DMARD-naive RA patients. After 12 weeks of etanercept treatment, serum CTX-1 and sclerostin levels increased. In patients whose DAS28 improved, the sclerostin level increased from 1.67 +/- 2.12 pg/mL at baseline to 2.51 +/- 3.03 pg/mL, which was statistically significant (p = 0.021). Increases in sclerostin levels after etanercept treatment were positively correlated with those of serum CTX-1 (r = 0.775), as were those of BSALP (r = 0.755). CONCLUSIONS: RA patients treated with DMARDs showed depressed bone metabolism compared to naive RA patients. Increases in serum CTX-1 and sclerostin levels after short-term etanercept treatment suggest reconstitution of bone metabolism homeostasis.
Adult ; Alkaline Phosphatase/blood ; Arthritis, Rheumatoid/blood/diagnosis/*drug therapy ; Biological Markers/blood ; Bone Morphogenetic Proteins/blood ; Bone Remodeling/*drug effects ; Collagen Type I/blood ; Female ; Genetic Markers ; Homeostasis ; Humans ; Immunoglobulin G/*administration & dosage ; Immunosuppressive Agents/*administration & dosage ; Inflammation Mediators/blood ; Male ; Middle Aged ; Peptides/blood ; Receptors, Tumor Necrosis Factor/*administration & dosage ; Time Factors ; Treatment Outcome ; Tumor Necrosis Factor-alpha/antagonists & inhibitors

BACKGROUND/AIMS: This study sought to evaluate the diagnostic value of salivary gland ultrasonography in primary Sjogren's syndrome with anti-Ro/SS-A antibody. The secondary goal was to assess the relationship between the grade of parenchymal inhomogeneity and the anti-Ro/SS-A antibody titer or clinical manifestations. METHODS: The parotid and submandibular glands were examined ultrasonographically in 30 patients having primary Sjogren's syndrome with anti-Ro/SS-A antibody and 30 control subjects with no evidence of Sjogren's syndrome. The ultrasonographic definition of parenchymal inhomogeneity of the salivary glands was blurred glandular borders, multiple hyperechoic bands, and hypoechoic areas. The parenchymal inhomogeneity of the glands was categorized into four grades. RESULTS: Parenchymal inhomogeneity of the parotid gland was seen in 25 (83.3%) patients with primary Sjogren's syndrome and 2 (6.7%) control subjects. Of these cases, the submandibular gland showed parenchymal inhomogeneity in 24 (80%) patients with primary Sjogren's syndrome and 2 (6.7%) control subjects. The sensitivity and specificity of parenchymal inhomogeneity of the parotid gland were 83.3% and 93.3%, respectively, and 80% and 93.3% for the submandibular gland. The grade of ultrasonographic parenchymal inhomogeneity was related to a diagnosis of Sjogren's syndrome (p<0.001) and the time of dissolution of the wafer, but had no relationship with the anti-Ro/SS-A antibody titer. A high degree of interobserver agreement was found in the assessment of parenchymal abnormalities of the salivary gland (parotid gland: kappa=0.859; submandibular gland: kappa=0.837). CONCLUSIONS: Salivary gland ultrasonography is a useful method for visualizing glandular structural changes and making a diagnosis of primary Sjogren's syndrome.
Humans ; Parotid Gland ; Salivary Glands ; Sensitivity and Specificity ; Sjogren's Syndrome ; Submandibular Gland

No abstract available.
Arthritis* ; Dermatitis* ; Humans ; Neutrophils*

Early differentiation between bacterial infections and disease flares in autoimmune disease patients is important due to different treatments. Seventy-nine autoimmune disease patients with symptoms suggestive of infections or disease flares were collected by retrospective chart review. The patients were later classified into two groups, disease flare and infection. C-reactive protein (CRP) and serum procalcitonin (PCT) levels were measured. The CRP and PCT levels were higher in the infection group than the disease flare group (CRP,11.96 mg/dL +/- 9.60 vs 6.42 mg/dL +/- 7.01, P = 0.003; PCT, 2.44 ng/mL +/- 6.55 vs 0.09 ng/mL +/- 0.09, P < 0.001). The area under the ROC curve (AUC; 95% confidence interval) for CRP and PCT was 0.70 (0.58-0.82) and 0.84 (0.75-0.93), which showed a significant difference (P < 0.05). The predicted AUC for the CRP and PCT levels combined was 0.83, which was not significantly different compared to the PCT level alone (P = 0.80). The best cut-off value for CRP was 7.18 mg/dL, with a sensitivity of 71.9% and a specificity of 68.1%. The best cut-off value for PCT was 0.09 ng/mL, with a sensitivity of 81.3% and a specificity of 78.7%. The PCT level had better sensitivity and specificity compared to the CRP level in distinguishing between bacterial infections and disease flares in autoimmune disease patients. The CRP level has no additive value when combined with the PCT level when differentiating bacterial infections from disease flares.
Adult ; Aged ; Area Under Curve ; Autoimmune Diseases/complications/*diagnosis ; Bacterial Infections/complications/*diagnosis ; C-Reactive Protein/analysis ; Calcitonin/*blood ; Female ; Humans ; Male ; Middle Aged ; Odds Ratio ; Protein Precursors/*blood ; ROC Curve ; Retrospective Studies ; Sensitivity and Specificity

This erratum is being published to correct of title.

OBJECTIVE: This study examines the effects of tumor necrosis factor (TNF) blockade on markers of bone metabolism in peripheral blood from active rheumatoid arthritis (RA) patients. METHODS: Eighteen patients (16 women, 2 men) aged 50 years (range 37-63 years), with persistently active RA (mean disease duration 7 years) were studied. Most took methotrexate (mean dose 12.5 mg) and all except one received corticosteroid (mean dose 5.7 mg). Four were treated with etanercept, eight received adalimumab and six received infliximab. Before and six months after taking TNF blockers, blood was sampled to obtain peripheral blood mononuclear cells (PBMCs), and serum bone turnover markers and acute phase reactants were measured. PBMCs were seeded and cultured to produce osteoblastic lineage cells and osteoclasts. RESULTS: The formation of calcified nodules by osteoblastic lineage cells from PBMC increased from 205.7±196.3 µmol/well at the baseline to 752.5±671.9 µmol/well after TNF blockade (p<0.024). The serum levels of bone formation markers, including bone specific alkaline phosphatase and osteocalcin also increased. The number of circulating osteoclasts and area of bone resorption pits made by osteoclasts were reduced after TNF blockade. CONCLUSION: The activity of circulating osteoblastic lineage cells increased after TNF blockade, whereas peripheral osteoclastogenesis tended to be suppressed. This is the first study of cultured human peripheral osteoblastic lineage cells in RA patients. Given that peripheral bone formation is difficult to study using radiologic methods, culture of these cells may provide a new modality for studying bone metabolism in RA.
Acute-Phase Proteins ; Adalimumab ; Alkaline Phosphatase ; Arthritis, Rheumatoid ; Biological Therapy ; Bone Remodeling ; Bone Resorption ; Etanercept ; Female ; Humans ; Infliximab ; Metabolism ; Methotrexate ; Osteoblasts* ; Osteocalcin ; Osteoclasts* ; Osteogenesis ; Tumor Necrosis Factor-alpha*