Leukotrienes in the pathophysiology of kwashiorkor
1993; Elsevier BV; Volume: 342; Issue: 8877 Linguagem: Inglês
10.1016/0140-6736(93)92003-c
ISSN1474-547X
AutoresErtan Mayatepek, Katja Becker, Georg F. Hoffmann, Michael Leichsenring, L Gana,
Tópico(s)Obstructive Sleep Apnea Research
ResumoAbstract Summary The actions of cysteinyl leukotrienes include production of oedema. We investigated whether these mediators might be involved in the oedematous malnutrition syndrome kwashiorkor. The capacity of leukotriene (LT) synthesis by stimulated whole blood and urinary LTE 4 excretion was measured in 12 children with kwashiorkor, and compared with that in 24 marasmic and 12 control children. Urinary LTE 4 excretion was significantly higher in patients with kwashiorkor than in controls (118·8 [SD 28 5] vs 31 1 [19·3] nmol/mol creatinine; p<0 01). Whole blood LTE 4 synthesis was increased in kwashiorkor patients by a factor of 3·5 (p<0 01). In marasmic children, LTE 4 excretion and synthesis did not differ from those in controls. Although glutathione, known to participate in LTC 4 synthesis, was subnormal in erythrocytes of all malnourished patients, whole-blood LTC 4 synthesis was higher in kwashiorkor patients than in controls (28·1 [5·0] ng/mL; p<0·05), and close to control values (9 8 [1 5] ng/mL) in marasmic children. LTB 4 synthesis, however, was greatly reduced in kwashiorkor patients (11·5 [2·4] vs 46·5 [6 4] ng/mL; p<0 01). Inability to synthesise the immunoregulator LTB 4 may lead to inefficient chemoattraction of phagocytes and an inadequate inflammatory response in kwashiorkor. The increased endogenous cysteinyl LT generation in kwashiorkor suggests that these lipid mediators are involved in the pathophysiology of the syndrome, particulary in oedema formation. Lancet 1993; 342: 958–60
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