Current management of the gastrointestinal complications of systemic sclerosis.

Systemic sclerosis is a multisystem autoimmune disorder that involves the gastrointestinal tract in more than 90% of patients. This involvement can extend from the mouth to the anus, with the oesophagus and anorectum most frequently affected. Gut complications result in a plethora of presentations that impair oral intake and faecal continence and, consequently, have an adverse effect on patient quality of life, resulting in referral to gastroenterologists. The cornerstones of gastrointestinal symptom management are to optimize symptom relief and monitor for complications, in particular anaemia and malabsorption. Early intervention in patients who develop these complications is critical to minimize disease progression and improve prognosis. In the future, enhanced therapeutic strategies should be developed, based on an ever-improving understanding of the intestinal pathophysiology of systemic sclerosis. This Review describes the most commonly occurring clinical scenarios of gastrointestinal involvement in patients with systemic sclerosis as they present to the gastroenterologist, with recommendations for the suggested assessment protocol and therapy in each situation

Autoimmune disease after neonatal injection of semi-allogeneic spleen cells in mice: involvement of donor B and T cells and characterization of glomerular deposits.

Balb/c neonates injected with semi-allogeneic (A/J x Balb/c) F1 hybrid spleen cells develop an autoimmune disease associated with an immune-complex glomerulonephritis. The successful induction and maintenance of B cell chimerism is required for the occurrence of autoimmunity. The percentage of chimeric mice displaying autoimmune features increases in parallel with the number of cells injected at birth. T cell depleted inocula although readily inducing B cell chimerism were found unable to induce hypergammaglobulinaemia, circulating immune complexes and glomerulonephritis. IgG1 is the most and IgG3 the least represented IgG isotype among the immunoglobulins deposited in the glomeruli. Immunoglobulins bearing donor (A/J) allotype are detected in the glomeruli of six out of 11 chimeric mice. Rheumatoid factor activity is significantly concentrated within the immunoglobulins eluted from the kidneys, whereas anti-DNA activity is not

Early renal graft failure due to recurrence of Wegener's granulomatosis under cyclosporine therapy

Recurrence of Wegener's granulomatosis led to loss of the graft within 34 days in a patient receiving cyclosporine. Review of the literature confirmed the rarity of recurrence of this disease after transplantation in azathioprine-treated recipients, but this complication was recently described in 3 patients (including our case) who were on cyclosporine immunosuppression. Further experience will be needed to establish the optimal regimen for renal transplantation in patients with Wegener's granulomatosis.SCOPUS: NotDefined.jFLWNOinfo:eu-repo/semantics/publishe

The effect of exogenous interferon: acceleration of autoimmune and renal diseases in (NZB/W) F1 mice.

To determine the effect of prolonged administration of exogenous interferon on the autoimmune disease of NZB/W female mice, forty-four NZB/W mice received three injections per week of 6.4 x 10(4) interferon units from birth to 33 weeks, forty mice were injected with mock interferon and forty-eight mice were left untreated. In mice injected with interferon growth was delayed, survival was decreased, and the severity of the glomerulonephritis was enhanced. Interferon increased the titre of serum anti-ssDNA and anti-soluble nucleoprotein antibodies, but had no effect on the circulating immune complex load. These results suggest that interferon in some way affects local deposition of immune complexes within the glomerulus