Imported cerebral malaria complicated with glucose 6 phosphate dehydrogenase deficiency

Two cases of cerebral malaria imported from Guyana and Ghana are reported. These are the first cases of cerebral malaria diagnosed and treated in Trinidad and Tobago since malaria was eradicated. The management of both these cases was complicated because the patients' erythrocytes were glucose-6-phosphate dehydrogenase-deficient, and by the occurrence of blackwater fever, cerebral manifestations, renal impairment, hyperglycaemia and thrombocytopenia. The symptoms of cerebral malaria resolved following treatment with quinidine and doxycycline and quinidine and clindamycin. (AU)

Imported cerebral malaria complicated with glucose-6-phosphate dehydrogenase deficiency

Two cases of cerebral malaria imported from Guyana and Ghana are reported. These are the first cases of cerebral malaria diagnosed and treated in Trinidad and Tobago since malaria was eradicated. The management of both these cases was complicated because the patients' erythrocytes were glucose-6-phosphate dehydrogenase-deficient, and by the occurrence of blackwater fever, cerebral manifestations, renal impairment, hyperglycaemia and thrombocytopenia. The symptoms of cerebral malaria resolved following treatment with quinidine and doxycycline and quinidine and clindamycin (AU)

Methylene blue reduction and disorders of the pentose phosphate pathway - abstract

When methylene blue (MeB) is incubated with normal blood it is reduced to leucomethylene blue. This has been utilized as the basis of a screening test for glucose-6-phosphate dehydrogenase (G6PD) deficiency by Sass and others +. The absorbance (As) at 615 nm of the supernatant abtained following centrifugation of blood samples of 72 normal males and 108 females incubated with MeB was less than 0.22. For 25 G6PD deficient males and 32 G6PD deficient females As > 0.28, but for two males and 26 females with apparently normal G6PD activity As > 0.23. Evidence is presented to support the view that such anomalous results may be due to 6-phosphogluconate dehydrogenase deficiency or to variable X-inactivation in G6PD deficient females (AU)

Observations on the origin of liver fat in infantile malnutrition

Liver samples were obtained by biopsy from malnourished children in Jamaica, and also from a group of children who had recovered from malnutrition. The activity of glucose-6-phosphatase was significantly reduced in the liver of the malnourished children. The ability of liver homogenates to synthesize fat from acetate was less in the malnourished children than in the recovered group, but the difference was not significant. In the malnourished children, the fasting levels of nonesterified fatty acids (NEFA) and glycerol in the plasma were increased. The origin of the excess liver fat in kwashiorkor is discussed, and it is concluded that it is derived directly from dietary carbohydrate (Summary)

Glucose 6 phosphate dehydrogenase deficiency in Curacao

This report dealt with cases of blood transfusion reactions, hematesis and hemolytic jaundice of the newborn due to the defect. The inheritance was discussed: it was found to be incomplete, sex-linked, dominant with a variable expression in the female and intermediate in the male (AU)

Some aspects of erythrocyte Glucose-6-Phosphate dehydrogenose deficiency in Trinidad

The glucose-6-phoshate dehydrogenose (G6PD) activity of erythrocyte samples in Trinidad was investigated, using the Motulsky cresyl blue decolourization test. Of 91 specimens taken from normal negroes, 12.1 percent showed absent enzyme activity and of 71 specimens from East Indians, 7 percent showed the same deficiency. As was to be expected (G6PD) deficiency being inherited as a sex linked character) in both groups there was a preponderance of males having the enzyme defected. Three out of thirteen (23.1 percent) of children with severe cerebral palsy and five out of twenty-seven (18.5 percent) of mentally defective children were found to be G6PD deficient as compared with 12.1 percent of normal controls. The role of virus infection in precipitating hemolytic episodes in people with G6PD deficiency was investigated. G6PD deficient and normal erythrocytes were incubated for 60 minutes with a standard dose (approx. 3,000 PFU) of VEE virus and were then stained for Heinz bodies. Whereas Heinz body counts of 0.5 percent or less were found in samples of normal erythrocytes, levels of 1.5 percent or more were found in erythrocytes with G6PD deficiency. Erythrocyte G6PD deficiency is then shown to be present in Trinidad (more frequently in the negro population than in East Indian); the percentage of negroes with this enzyme deficiency is close to that reported from the U.S.A. It is suggested that this enzyme deficiency may play a part in the aetiology of cerebral palsy and that virus infections may be concerned in the precipitation of hemolytic episodes (AU)