Streptococcal toxic shock syndrome (STSS) is caused by infection with a toxicogenic strain of Streptococcus pyogenes. Clinical manifestations may be those of a mild illness, characterized by malaise, fever, and muscle pain, to severe sepsis and multisystem organ failure. The syndrome may be associated with several invasive infections including necrotizing fasciitis. Treatment is primarily surgical debridement of infected tissue with supportive care, antibiotics, and hemodynamic monitoring. Intravenous immunoglobulin (IVIG) is reported to have beneficial effects in the management of STSS associated with necrotizing fasciitis. The agent was successful in conjunction with surgical excision and antibiotics in a patient with necrotizing fasciitis, toxic shock, and multisystem organ failure. On the basis of this experience and a thorough literature review, we concur that IVIG may be a useful adjunct in the treatment of STSS associated with necrotizing fasciitis.

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One in five patients presenting with HNMSCC were deemed appropriate for palliative care at initial presentation and survived less than six months after diagnosis. More than one-third required surgical intervention, and 29 per cent never returned home.

Colonic infusion of short chain fatty acids (SCFAs) is trophic to rat jejunum and is associated with raised jejunal gastrin concentration. This study examined the hypothesis that the jejunal trophic effects of colonic SCFAs are mediated in part by gastrin. Forty six adult rats underwent caecectomy to reduce endogenous production of SCFA, ileocolonic anastomosis, and placement of a colonic infusion catheter. SCFA (70 mM acetate, 35 mM propionate, 20 mM butyrate) or saline were continuously infused into the colon for seven days. Rats received either a gastrin receptor blocker (L-365,260) or a control solution and animals were killed on day 8. SCFA infused into the colon acted systemically to significantly improve jejunal structure and increase jejunal gastrin concentrations. Gastrin receptor blockade abolished effects of SCFA on jejunal DNA, protein, crypt cell proliferation, and gastrin. Gastrin blockade did not reduce SCFA induced augmentation of villous height or crypt depth. It is concluded that the jejunal trophic effects of colonically infused SCFA are mediated in part by gastrin. (Gut1995;37:81-86)