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Flush resuscitation for group A streptococcus toxic shock: a possible role for continuous renal replacement therapy and plasmapheresis.

Group A streptococcus has emerged as a major cause of aggressive life-threatening deep-seated infections. In addition, toxic shock syndrome caused by Group A streptococcus was recognized in 1983. Group A streptococcus produces several potent exotoxins which explain the pathophysiology of these invasive infections. Other virulence factors such as M protein, which can impede phagocytosis, are associated with some Group A streptococcus. M protein and streptococcal pyrogenic exotoxins may act as super antigens. Host factors may influence the severity of infection. Blood purification techniques such as continuous renal replacement therapy and plasmapheresis can remove streptococcal exotoxins as well as inflammatory mediators. Replacement with fresh-frozen plasma corrects coagulopathy and may provide some antibody protection. Four patients with Group A streptococcus-toxic shock syndrome treated with continuous renal replacement therapy, plasmapheresis, or both showed dramatic, rapid improvement in cardiovascular dynamics and respiratory parameters. Two patients died. The mainstay of treatment for Group A streptococcus-toxic shock syndrome remains early diagnosis, aggressive surgical control of the infection, and appropriate antibiotics (i.e., penicillin and clindamycin). Flush resuscitation may rescue some patients from profound toxic shock. The mechanisms of action need to be delineated.

Anti-Bacterial Agents↗

Niacin skin-flush response and electrodermal activity in patients with schizophrenia and healthy controls.

Patients with schizophrenia have in different studies shown reduced niacin sensitivity and lower electrodermal activity (EDA) after auditory stimulation. Peripheral mediation of prostaglandins may have a physiological role in both responses. This motivates study of both niacin response and electrodermal responding in the same patients with schizophrenia. Thirty patients with schizophrenia and 17 controls were investigated with EDA and thereafter given 200mg niacin orally with continuous assessment of skin temperature. The patients showed a delayed temperature increase after niacin ingestion (P=0.002) and a higher frequency of electrodermal non-responding (P<0.05). Response/non-response for niacin correlated with EDA response/non-response in the patient group (P=0.009). The niacin test revealed a slower vasodilation reaction in the patients. The association between response patterns for the niacin test and EDA suggests that a common aberration in skin physiology may be of importance for both reactions in schizophrenia.

Administration, Oral↗