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Löfdahl CG, Sölvell L, Laurell AB, et al. Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome. Acta Med Scand. 1979;206(5):405-12doi: 10.1111/j.0954-6820.1979.tb13536.x.
Löfdahl, C. G., Sölvell, L., Laurell, A. B., & Johansson, B. R. (1979). Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome. Acta medica Scandinavica, 206(5), 405-12. https://doi.org/10.1111/j.0954-6820.1979.tb13536.x
Löfdahl, C G, et al. "Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome." Acta medica Scandinavica vol. 206,5 (1979): 405-12. doi: https://doi.org/10.1111/j.0954-6820.1979.tb13536.x
Löfdahl CG, Sölvell L, Laurell AB, Johansson BR. Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome. Acta Med Scand. 1979;206(5):405-12. doi: 10.1111/j.0954-6820.1979.tb13536.x. PMID: 525442.
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Acta Med Scand. 1979;206(5):405-12. doi: 10.1111/j.0954-6820.1979.tb13536.x.

Systemic capillary leak syndrome with monoclonal IgG and complement alterations. A case report on an episodic syndrome.

Acta medica Scandinavica

C G Löfdahl, L Sölvell, A B Laurell, B R Johansson

PMID: 525442 DOI: 10.1111/j.0954-6820.1979.tb13536.x

Abstract

A case of the rare systemic capillary leak syndrome (SCLS) is described. The patient suffered 9 attacks with muscle pain, weakness and profuse sweating. He showed increased Hct values up to 79 percent and a decreasing plasma volume to about 50 percent of normal. During the attacks the patient was in a state of shock and BP was unmeasurable. Studies with 131I-labelled albumin during attack showed an increased transcapillary escape rate to about 20 percent/hour, compared to 6 percent when he was without symptoms. A monoclonal IgG with a constant concentration of about 5g/l was found. Studies of the complement system during attack showed low C4 values, disproportions among the C1 subcomponents and C1r-C1s-C1IA complexes, suggesting a complement activation via the classic pathway. Hereditary angio-edema was excluded by normal C1IA values. The complement activation might be part of the pathogenesis of the increased macromolecular permeability in this syndrome. A short review of cases described earlier is given.

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