Vinceneux P, Pouchot J, Gaudin H
Service de médecine V, hôpital Louis Mounier, Colombes.
Presse Med. 1990 Jun 16;19(24):1147-9.
Increases in body temperature may be due to hyperthermia, i.e. imbalance between production and elimination of heat, or to fever, i.e. disregulation of the central thermostat by a humoral mediator now identified as interleukin I. The same mediator is involved in the production by the liver of inflammation proteins which, besides other actions, encourage the formation of rouleaux and produce an increase in erythrocyte sedimentation rate. However, it is not exceptional to find a rise in temperature associated with a normal erythrocyte sedimentation rate. When this situation does not reflect a technical error, it may guide the diagnostic approach of a febrile state and may suggest the existence of a non-inflammatory hyperthermia or of a fever associated with "paradoxical" normalisation of the erythrocyte sedimentation rate. The 1st hypothesis raises the possibility of a series of diagnoses ranging from fever of central origin to hyperthyroidism and drug-induced fever. The 2nd hypothesis leads to a search for plasma factors (low plasma fibrinogen level, hyperviscosity, cryoglobulin) or erythrocytic factors (polycythaemia, haemoglobinopathy) which inhibits the joining of red cells and artificially lower the erythrocyte sedimentation rate.
体温升高可能是由于热调节异常,即产热与散热失衡,也可能是由于发热,即由目前已确定为白细胞介素I的体液介质引起的中枢体温调节紊乱。同一种介质参与肝脏产生炎症蛋白的过程,这些炎症蛋白除其他作用外,还促进红细胞缗钱状形成并使红细胞沉降率升高。然而,体温升高而红细胞沉降率正常的情况并不罕见。当这种情况并非技术误差时,它可能指导发热状态的诊断方法,并可能提示存在非炎性热调节异常或与红细胞沉降率“反常”正常化相关的发热。第一种假设增加了一系列诊断的可能性,范围从中枢性发热到甲状腺功能亢进和药物性发热。第二种假设导致寻找抑制红细胞聚集并人为降低红细胞沉降率的血浆因素(低血浆纤维蛋白原水平、高粘滞度、冷球蛋白)或红细胞因素(红细胞增多症、血红蛋白病)。