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A father and daughter both had multiple pathological fractures and nodal osteoarthropathy. The father, aged 50 years, had at least 20 healed fractures of the axial and appendicular skeleton, sustained by minor trauma over his 50-year lifespan, many of which had been surgically fixed prior to his first presentation to us. Fractures of the clavicles, thoracic cage and long bones of the arms and legs, had healed with malalignment and deformity. Healed fractures were complicated by ankylosis of the cervical vertebrae and both elbows. He also had osteoarthritis of the hands, with exuberant osteophytosis, and profound perceptive deafness. His general health was good, his intellect and facies were normal, and his sclerae were white. The daughter, aged 27 years, had sustained at least seven fractures of the axial and appendicular skeleton following trivial injuries, in distribution similar to those of the father.She had also experienced painful swelling of the fingers,which preceded progressive development of nodal osteoarthropathy.Her hearing was normal. In both individuals,biochemical and immunological investigations yielded normal results. It was not possible for molecular studies to be undertaken. Pedigree data were consistent with autosomal dominant transmission, and this disorder appeared to be a previously undocumented heritable skeletal dysplasia. [ABSTRACT FROM AUTHOR]

Anticholinergics are the mainstay of the pharmacological management of organophosphate poisoning (OPP). Atropine has the potential to cause central toxicity which may complicate the management of this lifethreatening condition. A combination of atropine and glycopyrrolate in equivalent dosages titrated to the peripheral muscarinic signs, theoretically reduces the central effect of the anticholinergics by 50% and thereby the risk of central toxicity, while it provides effective control of the peripheral manifestations of OPP. This study reports the clinical morbidity and mortality associated with the management of OP with this anticholinergic combination over a 4-year period, 2003 to 2006, at Tygerberg Academic Hospital (TAH). Two of the 53 patients treated for OPP died, with this mortality lower than that previously reported at TAH. Atropine toxicity was evident in 12 (22.5%) patients and responded to a temporary cessation of the combination infusion. The demographic profile, presenting symptoms, duration of stay and complications encountered were similar to previous reports from TAH. Patients treated with the infusion of a combination of atropine and glycopyrrolate had a lower mortality rate compared with earlier reports from the same unit, but the occurrence of atropine toxicity was unchanged despite the hypothesized theoretical advantage. [ABSTRACT FROM AUTHOR]

The article presents a study which determines whether the radiographic features of joint destruction in tophaceous gout (TG) imply a different pathophysiology to rheumatoid arthritis (RA) and psoriatic arthritis (PA). It carries a radiographic comparison of the articular damage in persons with RA, PA, and TG. It suggests that the pathophysiology of joint destruction in TG is different to that in RA and PA.

We report on a patient with seropositive polyarthritis retrospectively diagnosed as Poncet’s disease in the preclinical phase of seropositive rheumatoid arthritis. Our patient developed rheumatoid arthritis more than 2 years after being successfully treated for pulmonary tuberculosis and an initial inflammatory polyarthritis consistent with the diagnosis of Poncet’s disease. This case illustrates the importance of recognizing Poncet’s disease in a patient presenting with polyarthritis in order to avoid inappropriate long-term disease modifying antirheumatic treatment. It also illustrates the need for adequate follow-up of patients with Poncet’s disease after treatment with antituberculosis treatment so that progression to a primary inflammatory arthritis such as rheumatoid arthritis may be identified timeously. Although seropositivity for rheumatoid arthritis has been reported in Poncet’s disease as well as in tuberculosis, it is rather uncommon, and long-term follow-up of patients with Poncet’s disease is essential particularly if they have positive serological tests for rheumatoid arthritis. In this case report, we describe the first reported case of Poncet’s disease in the preclinical phase of rheumatoid arthritis and review the literature related to this rare disease presentation. [ABSTRACT FROM AUTHOR]