Administration of a supramaximal dose of GRF 1-44 (200 micrograms, i.v.) to normal human volunteers increased GH levels while a further bolus of GRF (200 micrograms i.v.) given 2 hours later failed to increase plasma GH levels. In contrast, alpha-adrenergic receptor agonism with either propranolol-adrenaline infusion or clonidine increased plasma GH levels at a time when GH responses to this supramaximal dose of GRF were absent. This indicates that alpha-adrenergic pathways stimulate GH secretion through a non-GRF-dependent mechanism in normal human subjects.

Objective. To investigate the efficacy of high‐dose intravenous immunoglobulin (IVIg) in the treatment of refractory rheumatoid arthritis (RA). Methods. Ten patients with active, severe RA that was unresponsive to first‐ and second‐line agents were administered IVIg monthly, for 6 months. Results. Following IVIg treatment, there was significant improvement in both subjective and objective parameters of disease activity in all 9 patients who completed the protocol. This improvement was noted to occur as early as after the second infusion of IVIg. After discontinuation of the treatment, all patients had a relapse of the disease within a few weeks. Conclusion. Since the reduction in clinical activity paralleled a decrease in the CD4+CDw29+: CD4+CD45RA+ cell ratio, some of the therapeutic benefits associated with IVIg may be due to a direct influence on the CD4+CD45RA+ subset. Although the possibility of carrying out further controlled studies on a larger scale is limited by the high cost of the treatment, IVIg appears to be an effective therapy for refractory RA.

We describe a 68-year-old woman suffering from rheumatoid arthritis treated with low doses of prednisone who developed Kaposi's sarcoma (KS). This patient was not affected with AIDS, and two years previously, her sister had also complained of KS. In the literature only 8 rheumatoid arthritis patients who developed KS during steroid therapy have been reported. We present a review of the literature and question the responsibility of corticosteroids and autoimmune diseases as the cause of KS.

A 55-year-old woman with a six-year history of Sjögren's syndrome (SS) and the positivity of IgG and IgM antiphospholipid antibodies (aPL) developed a sudden onset of sensorineural hearing loss associated with vertigo. This suggested the presence of an atypical Cogan's syndrome (CS), which might be a focal, neurological complication of aPL.

The pharmacological treatment of systemic sclerosis (SSc) has been discouraging. In view of this, therapeutic trials with cyclosporine A (CyA) are outstanding particularly in patients with a rapid cutaneous involvement. We report the case of a patient whose SSc cutaneous manifestations dramatically improved with CyA therapy. Its subsequent withdrawal led to a quick onset of a fatal sclerodermal renal crisis. We believe that in our patient there could have been a cause and effect relationship between the suspension of CyA and kidney sclerodermal complication.