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A knowledge of eosinophil granulocytes is indispensable for the study of hypereosinophilia. For this reason, the most recent findings relating to eosinophil morphology, production/regulation mechanism, and function are reported. Particular attention is given to enzyme populations, local control mechanisms and eosinophil cell surface receptors. Among the various enzymes present in the eosinophil, major basic protein (MBP), with its capacity to damage the cells of many organs, plays an important part; other enzymes include eosinophil peroxidase (EPO), arylsulphatase B, phospholipase D, histaminase and cationic proteins (ECP). Factors influencing eosinophil tissue concentrations and mode of action are considered. Recent findings agree on the role of eosinophils in immunological reactions and parasitic infestations: eosinophil plays a part in an immunological physiopathological sequence: it may, act as a killer cell with selective action against invading parasites, or it may be an immune modulator, anti-inflammatory cell able to surround inflammatory reactions and prevent them from spreading.

Following a previous note on the latest development in the study of eosinophilic granulocytes, a nosographic classification scheme is proposed for the problematic group of haematic eosinophilias. The scheme is based on the division of hypereosinophilias into three basic groups: benign idiopathic hypereosinophilias, hypereosinophiliasis caused by systemic eosinophilic blood diseases and symptomatic hypereosinophilias. Two rare events, hereditary familial eosinophilia and bening, non-familial idiopathic eosinophilia may be added to the benign idiopathic hypereosinophilias group. The group of hypereosinophilias caused by systemic eosinophilic blood diseases is still controversial and difficult to interpret. Particular attention is paid to the so-called "idiopathic hypereosinophilic syndrome" (HES), an umbrella term under which there is a current tendency to group a heterogeneous series of disorders characterised by long-lasting hypereosinophilia where there is no known reason for the increased eosinophilic granulocyte rate. Clinical and physiopathological features are then described to decide whether a given condition lies within the scope of this still little known syndrome.

Among the symptomatic hypereosinophilias and apart from pathologies covered in Note III, diseases of the connective tissue, neoplasias, blood diseases and other conditions are also examined. Two connective tissue diseases often accompanied by hypereosinophilias are Churg and Strauss angiitis and eosinophilic fascitis. Churg and Strauss angiitis (of which 2 personal cases are reported) is a systemic vasculitis usually seen in combination with bronchial asthma and haematic eosinophilia. Eosinophilic fascitis is quite rare and poorly understood. Its symptoms include hardening of the skin and eosinophilia and it is difficult to differentiate from progressive systemic sclerosis. The possible reasons why hypereosinophilia sometimes accompanies benign and more often malignant tumours are discussed. The pathogenesis of the hypereosinophilias encountered in diseases of the blood is still controversial. One hypothesis is that hypereosinophilia is an intrinsic symptom of the blood disease, others believe it to be an immunological response. In this context two personal cases are reported as examples: one of hypereosinophilia in a malignant non-Hodgkins lymphoma, the second in an IgG plasmacytoma. Particular attention was paid to the hypereosinophilia that accompanies the rare blood disease known as angioimmunoblastic lymphoadenopathy with dysproteinaemia (LAID) of which a personal case is reported.

The most frequently observed of the symptomatic hypereosinophilias are those caused by allergic, cutaneous, parasitic, infectious, pulmonary and gastroenteric conditions. Among the allergic conditions, particular attention is paid to the hypereosinophilias caused by allergic asthma, gastroenteritis and reactions to drugs. The most common skin conditions linked to hypereosinophilias such as bullous dermatites and angio-oedema are considered. Turning to the parasitic conditions, the various types of parasite that may produce hypereosinophilias by infesting the organs are examined. The aetiology of tropical eosinophilias and the pathogenetic mechanism that may trigger hypereosinophilias are discussed. It has been thought advisable to group the lung pathologies associated with hypereosinophilias under a separate heading, despite the indubitable importance of the allergic element in these events. Among gastroenteric conditions, the one considered is eosinophilic gastroenteritis whose clinical, anatomopathological and aetiopathogenic features are still not quite clear. Examples of certain forms of secondary hypereosinophilias are given in the form of four unusual personal cases of bronchial asthma, filariasis, an exceptional infestation by Hypoderma bovis and eosinophilic gastroenteritis.