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Recessively inherited ovalocytosis in coastal Melanesians is associated with widespread, but selective, depression of blood group antigens in homozygotes, who comprise about 15% of these populations. It is suggested that a membrane anomaly exists, and that the series of depressed determinants all depend, for their full expression, upon the same membrane component(s), the proper synthesis of which is being genetically affected. Affected antigens would thus be associated by position and/or structure. Antigens subject to depression include IT, IF, LW,D,C,e,S,s,U,Kpb,JKa,JKb,Xga,Wrb,Scl and Ena, which are simultaneously affected when present on oval cells. Reactivity of A1,ID,i,P1,M,N,Lub,k,Fya,Coa, Vel and Gea appears to be within the normal range on depressed cells, as does sialic acid content. Indirect evidence suggests that Z (associated with S and s) is among the depressed series, while NA and Leb are not. High H variants, common among Melanesians, seem absent among depressed bloods, and when such variants were excluded, H, A and B did not appear subject to depression. The distribution pattern of ovalocytosis suggests that it may confer some selective advantage in the tropical coastal environment. The findings also have implications concerning population genetic work in New Guinea.

All cases of leukaemia diagnosed between 1968 and 1976 in the Melanesian population of Papua New Guinea have been analysed, and comparisons made with an earlier series from this country and with findings reported from elsewhere. The major findings were: a low overall incidence (0.79/100,000), absence of a childhood or old age peak in incidence, a relatively lower proportion of acute lymphoblastic leukaemia in childhood, more than the expected proportion of cases of chronic granulocytic leukaemia under 20 years of age, and the rarity of chronic lymphocytic leukaemia.

A distinctive type of hereditary ovalocytosis has been found in Papua New Guinea and a few areas of Southeast Asia. Its main features include a high incidence among tropical lowland dwellers, autosomal recessive inheritance, specific depression of a number of red cell antigens, a characteristic morphology in blood films, and an effect on the erythrocyte sedimentation rate. Speculation has occurred as to whether the high incidence of ovalocytosis in malarious areas may be related to a selective advantage possessed by ovalocytics with regard to severe malaria. Preliminary data tend to support this hypothesis, but the evidence is not conclusive and much further work is needed.

An example of von Willebrand's disease in a Papua New Guinean female is described; this is believed to be the first time that this disorder has been documented in a Melanesian. Some salient features of the diagnosis and management of the disease are discussed. Bleeding disorders in Papua New Guinea have been found with increasing frequency in recent years, and it is not unreasonable to expect that their true incidence will be similar to those seen elsewhere.

Severe, acute and sometimes fatal intravascular haemolysis has occurred on several occasions in Papua New Guinea families after the ingestion of apparently 'stale' sago. Earlier cases had been recorded only from the Maprik area; however, we now report the occurrence of two similar outbreaks, involving a total of 14 persons, in the Western Province. Several bacteria and fungi were isolated and identified in a sample of suspect sago from one of the outbreaks. None of these, however, to our knowledge, has ever been incriminated as a cause of haemolysis, and the aetiological agent(s) and mechanism of haemolysis thus remain to be elucidated. No mycotoxins were detected in one sample available for analysis. It is suggested that the eating of sago stored for a long time be discouraged; and further that, if a meal of sago tastes abnormal, additional mouthfuls should not be eaten and the remaining portion should be sent for analysis or discarded.

A case of Glanzmann's thrombasthenia is documented in a Melanesian child, and the diagnosis and treatment of this disorder are discussed. This is the third inherited bleeding disorder to be reported in Papua New Guinea, haemophilia A (Factor VIII deficiency) and Factor XIII deficiency having been described previously.

Hereditary ovalocytosis in Papua New Guinea is restricted to areas of endemic malaria and may confer increased resistance to the disease. The incidence of malaria was investigated in 1616 Melanesiams of known red cell morphology and severity of infection determined in a smaller subsample. Ovalocytics tended to be more resistant to severe malarial infections than normocytics. The ratio of parasitaemia in 112 ovalocytics compared with 741 normocytic children was 1.05 for P. falciparum; 0.90 for P. vivax; 0.54 for P. malariae, and 0.91 for infection with any species. The difficulties in conclusively demonstrating any selective advantage of the condition are discussed.