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Macrophage colony-stimulating factor (M-CSF) is a cytokine involved in the development and proliferation of the monocyte/macrophage lineage cells. M-CSF has also been reported to participate in the induction of osteoclasts, and may be important in the destruction of bone and cartilage and the periarticular osteoporotic changes seen in patients with rheumatoid arthritis (RA). We developed a new ELISA technique to measure M-CSF levels in synovial fluid with high sensitivity and reproducibility. The mean M-CSF level in the synovial fluid of patients with RA was 1.38 +/- 0.56 ng/ml, and that of patients with osteoarthritis (OA) was 0.67 +/- 0.13 ng/ml. In contrast, serum levels of M-CSF in patients with RA and in normal controls were 1.32 +/- 0.50 ng/ml and 0.90 +/- 0.09 ng/ml, respectively. These differences were both statistically significant. Since serum M-CSF levels correlate with inflammatory signs obtained from examination of blood, they indicate the general condition of patients with RA. Synovial fluid M-CSF levels increase even in the early phase of RA and remain high despite drug therapy, which suggests that they reflect the condition of affected joints including joint spaces and inflamed synovia more directly than do the levels of serum M-CSF. Measurement of the M-CSF level in the synovial fluid may be useful in the diagnosis, clinical evaluation, and assessment of the effects of treatment in patients with RA.

A 64-year-old male patient with postinfarction complete anterior papillary muscle rupture and massive mitral regurgitation is presented. The diagnosis was suspected clinically and confirmed by transesophageal echocardiography. One week after the episode of acute myocardial infarction (AMI) the patient had a sudden onset of severe congestive heart failure with pulmonary edema and was transferred to our hospital. The patient underwent an emergency mitral valve replacement with a SJM29M prosthetic valve. Histological examination revealed an acute coagulation necrosis of the anterior papillary muscle without specific inflammatory change. To our knowledge this is the second case with successful surgery for a complete rupture of the anterior papillary muscle following AMI in Japan.

A 23-year-old female in the 28th week of pregnancy was admitted with an acute abdominal distension. The plain X-ray films showed a marked gaseous dilatation of the colon from the cecum to the splenic flexure. A tube colostomy was performed. Her postoperative course was uneventful and she improved progressively. Her pregnancy and delivery elapsed uneventfully there after. After the delivery she again complained of marked abdominal distension. The colonoscopic decompression in combination with the administration of Cisapride was successfully accomplished. Ogilvie's syndrome is characterized by an unobstructed colon which progresses to marked dilatation. When the colonic diameter becomes 12cm or more, surgical decompression should be recommended to avoid the hazard of spontaneous rupture. This is the first reported case of Ogilvie's syndrome in pregnancy in Japan.

Patients having previously not received cefotiam (CTM), a recently introduced cephem antibiotic, were subjected to skin tests with a 300 micrograms/ml solution of CTM in physiological saline before and after CTM therapy to detect sensitization with the drug. Anti-CTM antibody titration was carried out on sera from patients who showed a positive skin test and those who developed signs of hypersensitivity during CTM therapy. The results were as follows: Of 1,927 patients examined by skin test with CTM prior to initiation of CTM therapy, 31 patients (1.61%) showed positive reactions with formation of a wheal and erythema. There were 7 patients (0.36%) who proved negative in the skin test but developed mild symptoms of hypersensitivity in association with the skin test. The 847 patients negative on the CTM skin test were retested after a completion of CTM therapy, of whom 6 (0.71%) were found to have become positive showing formation of a wheal and erythema and 3 others (0.35%) showing a negative skin test developed mild adverse reactions associated with the skin test. Sixty-eight serum samples collected from the patients positive on the CTM skin test and those who developed manifestations of hypersensitivity following CTM therapy were examined for anti-CTM antibody by the Prausnitz-K ustner reaction, passive cutaneous anaphylaxis test and hemagglutination test. All proved negative in these tests. Of various background factors assessed, none was found to have causal relation to the skin reaction in any of the patients showing positive skin reactions to CTM.