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.