Mononeuritis multiplex and acute demyelinating polyneuropathy (Guillain-Barré syndrome) are well known in systemic lupus erythematosus (SLE). Chronic acquired demyelinating polyneuropathy has been reported rarely in SLE. Two young women had monophasic progressive weakness, areflexia, elevated CSF protein, and slow nerve conduction velocities as the first manifestation of SLE. Sural nerve biopsy in one patient revealed mild loss of myelinated fibers and an increased number of thinly myelinated fibers. Steroid therapy led to improvement in both patients. These patients demonstrate that chronic demyelinating polyneuropathy can be an unusual presentation of SLE, even preceding characteristic systemic disease by months.

Lyme disease is a recently described disease of unknown cause that may involve the skin, joints, heart, or nervous system with characteristic symptoms. The disease follows a bite from an Ixodes tick. Symptoms are generally self-limited and despite the varied and sometimes protracted manifestations, the outcome of the disease is favorable. The epidemiologic, clinical, and laboratory features and treatment of Lyme disease are reviewed.

Platelet serotonin levels were measured in 41 patients with systemic lupus erythematosus (SLE) and 36 normal controls. SLE patients had significantly lower mean serotonin levels (243 +/- 131 versus 414 +/- 175 ng/10(9) platelets, P less than 0.001); the lowest levels occurred in those patients with active disease. No differences in mean platelet serotonin levels were found when we compared patients with or without a history of renal disease, thrombocytopenia, or neuropsychiatric involvement. Decreased release of platelet granule constituents, as measured by plasma levels of the alpha-granule protein, beta-thromboglobulin.

Platelet aggregation was measured in 14 patients with systemic lupus erythematosus (SLE) and 13 normal controls. Ten SLE patients (group I) showed decreased responsiveness to collagen, while aggregation was normal in 4 (group 11). Group I patients also responded poorly to epinephrine. Platelets from SLE patients did not differ from controls in the production of malondialdehyde in response to N-ethylmaleimide, suggesting intact prostaglandin synthetic pathways. However, a significant decrease (P < 0.005) in platelet levels of the dense granule constituent, serotonin, was noted in group I SLE patients. Treatment of SLE platelet-rich plasma with deoxyribonuclease (DNase) resulted in enhancement of collagen-induced aggregation in 4 group I SLE patients, but not in 1 group I1 or 8 normal individuals. These results suggest that defective aggregation in SLE platelets may be partially related to a storage pool deficiency state. However, the ability to restore aggregation to collagen by digestion of platelet-rich plasma with DNase indicates that the defect is reversible and that it is perhaps mediated by plasma or platelet-associated DNA.In 1974, Regan et a1 (1) described abnormalities in the aggregation of platelets obtained from 12 of 21