Subcutaneous edema on back detected by MRI in hospitalized patients with osteoporotic vertebral compression fracture.

OBJECTIVES: Almost all hospitalized patients with osteoporotic vertebral compression fracture are given an MRI. At that time, subcutaneous edema on their back is often identified. It is empirically known that patients with subcutaneous edema on their back have a history of compression fracture and vertebral kyphotic deformity. In this study, we examined whether there were any differences between patients who had subcutaneous edema on their back and those who did not; those with a history of compression fractures would be especially assessed. MATERIALS AND METHODS: The observation period was between January 1, 2009, and December 31, 2020. All patients were on the ward, and there were a total of 375 patients (male: 114; female: 261) aged 66-98 years old (mean: 81.1 years).Patients who had subcutaneous edema on their back and those who did not were compared in terms of sex, age, osteoporosis diagnosis by DEXA and X-ray imaging, body mass index (BMI), serum total protein and albumin, Japanese senile independence score, presence of decubitus, history of vertebral compression fracture and incidents of compression fracture during the observation period. RESULTS: Significant differences were not observed for sex, osteoporosis diagnosis by DEXA, BMI, blood serum total protein and albumin, or the presence of decubitus. However, age, osteoporosis diagnosis by X-ray imaging, Japanese senile independence score, history of vertebral compression fracture, and incidents of another vertebral compression fracture during the observation period were significantly different between those with and without edema. CONCLUSION: It has been suggested that hospitalized patients with subcutaneous edema on their back often have a history of vertebral compression fracture and experience another vertebral compression fracture during the observation period. Hospitalized patients with subcutaneous edema on their back should have their osteoporosis treated more carefully.

High diagnostic value of anticalpastatin autoantibodies in rheumatoid arthritis detected by ELISA using human erythrocyte calpastatin as antigen.

OBJECTIVE: To develop a quantitative method of measuring autoantibodies against human calpastatin in rheumatoid arthritis (RA) and to determine their diagnostic value compared with other autoimmune and articular diseases. METHODS: We performed a highly sensitive ELISA for IgG and IgM anticalpastatin autoantibodies in human sera using human erythrocyte calpastatin as an antigen. Samples were diluted 1:2000 for the measurement of IgG and 1:400 for IgM. RESULTS: IgG anticalpastatin antibodies were found in the sera of 48 of 58 patients (82.8%) with RA. In contrast, IgG anticalpastatin antibodies were found in the sera of only 2 of 11 (8.3%) patients with osteoarthritis (OA). Compared to sera from patients with other autoimmune diseases, anticalpastatin antibody sensitivity for RA was better than that of systemic lupus erythematosus (5.6%), systemic sclerosis (0%), mixed connective tissue disease (0%), and Sjögren's syndrome (20%). IgG anticalpastatin antibodies also showed high specificity (96.1%) for RA. Almost 90% of patients with RA were positive for IgG or IgM anticalpastatin antibodies. CONCLUSION: We have developed a simple, sensitive, specific, and quantitative ELISA for anticalpastatin antibodies that may have a high diagnostic value for RA.

A case of female premenopausal tophaceous gout requiring surgical management.

We report a case of tophaceous gout in a 32-year-old woman who had suffered from anorexia nervosa since the age of 15. She had been taking a diuretic, mainly furosemide, to lose weight since she was 18. She was referred for orthopedic surgery because of a tophus at her right metatarsophalangeal joint. Because of a discharging sinus associated with the tophaceous deposits, surgery was performed. Use of the diuretic was stopped after surgery and the serum uric acid concentration returned to normal. It was thought that long-term abuse of a diuretic induced the tophaceous gout in this premenopausal woman.

Relationship between histological findings and clinical findings in rheumatoid arthritis.

The aim of the present study was to compare histological findings and clinical symptoms of patients with advanced stages of rheumatoid arthritis (RA). Synovial tissue specimens were obtained during reconstructive knee surgery from 93 RA patients (18 men; 75 women). The histological assessments of specimens were evaluated using two histological scoring systems reported by Rooney and Koizumi. Clinical symptoms (duration of morning stiffness, joint score, grip strength), laboratory data (erythrocyte sedimentation ratio, C-reactive protein (CRP), rheumatoid factor), X-ray findings (Larsen score) and drug usage were assessed before surgery. Significant statistical correlations between both histological scoring systems were observed; however, there was no significant correlation between the clinical findings and the histological scoring systems. A statistically significant correlation was found between the levels of CRP and Koizumi's scoring system. In addition, Koizumi score correlated significantly to X-ray findings. Rooney's scoring system had an inverse correlation to methotrexate history. Histological findings do not correlate to simultaneous clinical symptoms in advanced RA patients. However, our data indicate that observed histological changes reflect X-ray damage.

Antirheumatic effects of humanized anti-Fas monoclonal antibody in human rheumatoid arthritis/SCID mouse chimera.

OBJECTIVE: Anti-Fas monoclonal antibodies (Mab) are considered to be a potential therapeutic agent for rheumatoid arthritis (RA). However, Fas mediated liver and chondrocyte damage is a serious problem in its clinical application. m-HFE7A, a novel anti-Fas Mab, selectively induces apoptosis in inflammatory cells. We succeeded in humanizing m-HFE7A to obtain h-HFE7A. We investigated the therapeutic effects of h-HFE7A Mab in RA. METHODS: We investigated the apoptosis-inducing activities of h-HFE7A on human Fas ligand transfected cells and cultured human activated lymphocytes (human peripheral blood mononuclear cells and isolated human RA synovial lymphocytes), synoviocytes, and chondrocytes. We then examined the effects of h-HFE7A Mab in vivo using SCID-HuRAg mice implanted with human RA tissue. RESULTS: Administration of h-HFE7A Mab alone did not induce apoptosis in cultured human Fas ligand transfected cells and activated lymphocytes. However, apoptosis-inducing activities were noted by this Mab crosslinking with a secondary antibody or Fcgamma receptor positive cells. In contrast, no apoptosis induction by h-HFE7A was observed on cultured synoviocytes and chondrocytes with or without crosslinking. Thus the crosslinking with Fcgamma receptor positive cells is essential for the efficacy of this Mab in vivo. In the implanted tissue of the SCID-HuRAg mice, the number of inflammatory cells was significantly decreased in the h-HFE7A Mab treated group compared to the IgG treated control group. Moreover, there were only negligible effects in synoviocytes and chondrocytes with the h-HFE7A Mab. CONCLUSION: Administration of this novel humanized anti-Fas Mab may provide a new treatment for RA by inducing Fas mediated apoptosis in inflammatory cells.

Treatment with the angiogenesis inhibitor endostatin: a novel therapy in rheumatoid arthritis.

OBJECTIVE: An endostatin that inhibits angiogenesis dependent tumor growth is being tested as an antitumor agent. The neoangiogenesis condition of cancer is essentially identical to that of rheumatoid arthritis (RA). Thus antiangiogenic treatment has potential for treatment of RA. We investigated the effects of human recombinant endostatin on human RA synovial tissue by use of a novel model of RA, in which human RA tissue is grafted into SCID mice (SCID-HuRAg). METHODS: Ten or 50 mg/kg of human recombinant endostatin was administered by percutaneous direct intrasynovial injection in each of 7 SCID-HuRAg mice. We examined the volume of the grafted tissue mass and the histological changes 7 days after endostatin administration. Six control mice received phosphate buffered saline in the same manner. RESULTS: The grafted synovial volume of SCID-HuRAg mice was significantly decreased by endostatin administration. The number of inflammatory cells (macrophages and lymphocytes) was also significantly reduced in a dose dependent manner. The number of vessels that were counted by von Willebrand factor VIII and type IV collagen positive cells was decreased, although apoptotic cells were increased in RA synovia. CONCLUSION: The results suggest that antiangiogenesis treatment using endostatin represents a potential new therapeutic strategy for RA.