Spontaneous tumor necrosis factor production in Kawasaki disease

Blanca A. Lang; Earl D. Silverman; Ronald M. Laxer; Allan S. Lau

doi:10.1016/S0022-3476(89)80746-2

Spontaneous tumor necrosis factor production in Kawasaki disease

Blanca A. Lang, Earl D. Silverman, Ronald M. Laxer, Allan S. Lau

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Resumen

Tumor necrosis factor production by peripheral blood mononuclear cells was measured in 18 patients with Kawasaki disease. In patients studied during the acute febrile phase of their disease, there was increased spontaneous TNF production (mean 26.9±40.3 U/ml) compared with that of control subjects (1.0±.86 U/ml) (p≤0.025). Spontaneous TNF production by patients tested in the subacute or convalescent phase of the illness was significantly lower than that in patients tested during the acute illness (p≤0.025). In all patients studied with serial acute and subacute-convalescent samples. TNF production was normal in the follow-up samples. Because TNF is a potent mediator of inflammation and causes damage to vascular endothelial cells, we suggest that TNF may be important in the pathogenesis of both the immune activation and endothelial cell damage characteristic of this illness.

Idioma original	English
Páginas (desde-hasta)	939-943
Número de páginas	5
Publicación	Journal of Pediatrics
Volumen	115
N.º	6
DOI	https://doi.org/10.1016/S0022-3476(89)80746-2
Estado	Published - dic. 1989
Publicado de forma externa	Sí

Nota bibliográfica

Funding Information:
Kawasaki disease is a systemic vasculitis primarily affecting infants and young children and characterized by a triphasic clinical course. The first, or acute, phase consists of prolonged fever, an erythematous rash, indurative edema and discoloration of the hands and feet, conjunctival injection, typical changes of the lips and oral mucosa, and cervical lymphadenopathy. 1 The subacute phase follows, usually within 10 days of disease onset, and is characterized by resolution of fever, desquamation of the skin of the fingertips and toes, thrombocytosis, and development of coronary artery abnormalities. The third, or convalescent, phase lasts from the period when all signs of the illness have disappeared until the sedimentation rate and platelet count have Supported by a grant from Hyland Division, Baxter HealthCare Corp., Glendale, Calif. Dr. Lang is a recipient of a fellowship from the Arthritis Society of Canada. Drs. Silverman and Laxer are recipients of associateships of the Arthritis Society of Canada. Dr. Lau is a recipient of a Young Investigator Award from the Canadian Infectious Disease Society. Submitted for publication March 29, 1989; accepted June 20, 1989. Reprint requests: E. Silverman, MD, Division of Immunology/ Rheumatology, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G IX8, Canada. 9/20/14728 returned to normal. 2 Up to 30% of untreated patients develop coronary artery abnormalities, 3 and in a small proportion of these, fatal complications develop as a result of coronary artery vasculitis and subsequen t thrombosis. 2 Multiple immunoregulatory abnormalities have been suggested to be involved in the pathogenesis of this illness. Studies have shown abnormal percentages of circulating T cell subsets, 4-7 increased numbers of activated CD4 + lymphocytes, 46 B cell hyperactivity, 5, 6 and increased endo-

ASJC Scopus Subject Areas

Pediatrics, Perinatology, and Child Health

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10.1016/S0022-3476(89)80746-2

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title = "Spontaneous tumor necrosis factor production in Kawasaki disease",

abstract = "Tumor necrosis factor production by peripheral blood mononuclear cells was measured in 18 patients with Kawasaki disease. In patients studied during the acute febrile phase of their disease, there was increased spontaneous TNF production (mean 26.9±40.3 U/ml) compared with that of control subjects (1.0±.86 U/ml) (p≤0.025). Spontaneous TNF production by patients tested in the subacute or convalescent phase of the illness was significantly lower than that in patients tested during the acute illness (p≤0.025). In all patients studied with serial acute and subacute-convalescent samples. TNF production was normal in the follow-up samples. Because TNF is a potent mediator of inflammation and causes damage to vascular endothelial cells, we suggest that TNF may be important in the pathogenesis of both the immune activation and endothelial cell damage characteristic of this illness.",

author = "Lang, {Blanca A.} and Silverman, {Earl D.} and Laxer, {Ronald M.} and Lau, {Allan S.}",

note = "Funding Information: Kawasaki disease is a systemic vasculitis primarily affecting infants and young children and characterized by a triphasic clinical course. The first, or acute, phase consists of prolonged fever, an erythematous rash, indurative edema and discoloration of the hands and feet, conjunctival injection, typical changes of the lips and oral mucosa, and cervical lymphadenopathy. 1 The subacute phase follows, usually within 10 days of disease onset, and is characterized by resolution of fever, desquamation of the skin of the fingertips and toes, thrombocytosis, and development of coronary artery abnormalities. The third, or convalescent, phase lasts from the period when all signs of the illness have disappeared until the sedimentation rate and platelet count have Supported by a grant from Hyland Division, Baxter HealthCare Corp., Glendale, Calif. Dr. Lang is a recipient of a fellowship from the Arthritis Society of Canada. Drs. Silverman and Laxer are recipients of associateships of the Arthritis Society of Canada. Dr. Lau is a recipient of a Young Investigator Award from the Canadian Infectious Disease Society. Submitted for publication March 29, 1989; accepted June 20, 1989. Reprint requests: E. Silverman, MD, Division of Immunology/ Rheumatology, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G IX8, Canada. 9/20/14728 returned to normal. 2 Up to 30% of untreated patients develop coronary artery abnormalities, 3 and in a small proportion of these, fatal complications develop as a result of coronary artery vasculitis and subsequen t thrombosis. 2 Multiple immunoregulatory abnormalities have been suggested to be involved in the pathogenesis of this illness. Studies have shown abnormal percentages of circulating T cell subsets, 4-7 increased numbers of activated CD4 + lymphocytes, 46 B cell hyperactivity, 5, 6 and increased endo-",

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N2 - Tumor necrosis factor production by peripheral blood mononuclear cells was measured in 18 patients with Kawasaki disease. In patients studied during the acute febrile phase of their disease, there was increased spontaneous TNF production (mean 26.9±40.3 U/ml) compared with that of control subjects (1.0±.86 U/ml) (p≤0.025). Spontaneous TNF production by patients tested in the subacute or convalescent phase of the illness was significantly lower than that in patients tested during the acute illness (p≤0.025). In all patients studied with serial acute and subacute-convalescent samples. TNF production was normal in the follow-up samples. Because TNF is a potent mediator of inflammation and causes damage to vascular endothelial cells, we suggest that TNF may be important in the pathogenesis of both the immune activation and endothelial cell damage characteristic of this illness.

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Spontaneous tumor necrosis factor production in Kawasaki disease

Resumen

Nota bibliográfica

ASJC Scopus Subject Areas

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