8 male patients undergoing maintenance hemodialysis were studied to determine the effect of administering supplements of pyridoxine hydrochloride, 50 mg/day for 3–5 weeks, on tests of immune function. In the 3 patients who initially had abnormal nitroblue tetrazolium reduction tests, the values returned to normal with therapy (p < 0.05). The generation of chemotactic factors from plasma was defective in all evaluated patients and improved after pyridoxine therapy in 4 of 5 patients (p < 0.01). The lymphocyte subpopulations changed with a rise in the populations of null cells after supplementation with pyridoxine. In addition, lymphocyte transformation in response to mitogens improved in the 3 patients who initially showed low values in these assays. The improvements occurred with pyridoxine therapy even though some patients who responded had no evidence for vitamin B₆ deficiency before therapy, as indicated by a normal erythrocyte glumatic-pyruvic transaminase index. We conclude that several parameters of immune function are improved with pyridoxine supplementation. Studies are necessary to establish the minimum daily intake of pyridoxine which will maintain improved values of these tests of immune function in hemodialysis patients.

Twenty-three adults (11 males and 12 females) with well-defined relapsing polychondritis (RP) are studied in order to characterize the arthropathy of RP. Arthritis was found in 19 patients-as the presenting feature in 8 and as a significant symptom in 11 others. The usual pattern of involvement was migratory, asymmetric, nonnodular, nonerosive, and seronegative, and affected large and small joints as well as parasternal articulations. In addition RP was seen in 3 patients with preexisting chronic polyarthritis or associated rheumatic disease.Relapsing polychondritis (RP) is a rare rheumatic disorder consisting of an episodic, occasionally progressive, inflammation and degeneration of cartilaginous structures, and of inflammation of special sense organs including the eye and ear. A recent review by the authors documented 159 cases reported in the world From the

-353. Clinical and radiological survey of the incidence of osteoarthrosis among obese patients. Twenty-five grossly obese males were investigated for evidence of osteoarthrosis. A roentgenological survey of multiple joints obtained from 22 of these patients showed few significant degenerative changes. 6 patients (20 %) had previously incurred traumatic rents in their menisci necessitating meniscectomy. Our results refute previous claims that obesity is a factor in the genesis of osteoarthrosis but do indicate that obese individuals are more predisposed to traumatic injury of the knee.The role of obesity as an aetiological factor in osteoarthrosis (OA) remains controversial. It is thought that excessive weight is a factor in promoting joint degeneration, and invariably it is recommended to the obese patient with OA that he or she lose weight. The logic of this recommendation is irrefutable, but its basis in scientific fact is less clear.Large population studies of patients with OA have shown that a great number are obese (Kellgren and Lawrence, 1958;Kellgren, 1961;Lawrence, Bremmer, and Bier, 1966). A relationship has also been suggested between obesity and the development of OA in specific weight-bearing joints such as knees (Leach, Baumgard, and Broom, 1973) and hips (Law, 1964

A biopsy-proven case of scleromyxedema (papular mucinosis) with IgG lambda light chain paraproteinemia, eosinophilia and severe proximal myopathy is presented. Muscle biopsy revealed an atypical necrotizing vacuolar myopathy. Histochemical studies of cryostat sections revealed fiber necrosis, severe type II fiber atrophy, and fiber vacuolization with NADH tetrazolium reductase hyperactivity. Electron microscopy showed myocytolysis, reduplication of the basement membrane, and unit membrane-lined vacuoles negative for acid mucopolysaccharide.

A patient with biopsy-proven papular mucinosis, plus the characteristic IgG lambda light chain paraproteinemia, also developed a severe proximal myopathy, seronegative inflammatory polyarthritis, and marked eosinophilia. Muscle enzymes were elevated, EMG was compatible with polymyositis, and muscle biopsy revealed an atypical necrotizing vacuolar myopathy. Synovial biopsy revealed an inflammatory synovitis with Class I1 synovial fluid. No mucin deposition was detectable in muscle or synovium. During 7 years of observation, corticosteroids and various immunosuppressive agents were successively administered with little benefit. Recently, weekly intravenous methotrexate and low-dose oral corticosteroids have resulted in clinical and laboratory improvement. I t is suggested that the pathology in papular mucinosis may include serious rheumatic manifestations in addition to the cutaneous involvement.