PubMed Health⌕ Search

Biomedical subjects

C L Sezi

Publications and source records attributed to C L Sezi.

8 recordsLinked to original sources
PubMed1996

Effect of protein deficient cassava diet on Cercopithecus aethiops hearts and its possible role in the aetiology and pathogenesis of endomyocardial fibrosis in man.

Despite the current hypotheses for its causation, the exact cause of endmyocardial fibrosis is unknown. However, endomyocardial fibrosis being a disease of the low socio-economic groups who feed on low protein high carbohydrate diets consisting exclusively of cassava in Uganda and the demonstration by the author of a bimodal age distribution among the female patients and monomodal pattern in the male patients, led the author to suspect protein deficiency and cassava as aetiological factors thereby attributing the first mode to the increased but unmet protein needs for childhood growth and the second mode to the increased but unmet protein needs for pregnancies and lactation in the 20-40 year age groups. Consequently a new hypothesis that "prolonged ingestion of tuber (cassava/tapioca) crops associated with extreme deprivation of protein causes EMF" was formulated. In order to verify this hypothesis, three Cercopithecus aethiops were fed on uncooked banana diet while another three were fed on uncooked cassava and hearts harvested for histology whenever the animal health deteriorated. Changes in the endomyocardium included cell vacuolation, interstitial fibrosis and endocardial thickening by the 130th day in the animals on cassava but the animals on bananas were free from such changes. By the 160th day, the former exhibited marked thickening of the endocardium, interstitial fibrosis, fibrous septa formation, pappillary muscle fibrosis as well as apical fibrosis of the left ventricle, which findings occur in the human disease. Calcification and inflammatory cells were absent. A repeat of the experimental feeding with cassava using a batch of five animals, one of which survived up to seven months revealed cardiac findings similar to those seen at 160 days. Thus, the pathogenetic process, hitherto obscure, begins with cardiac cell necrosis followed by fibrosis consequent upon the failure of cardiac cell repair due to protein deficiency caused by the protein free cassava diets since the animals on bananas, which also lacked protein did not develop similar changes. The low plasma amino acid profiles in EMF prone subjects, the poor blood supply and the great apical mechanical stress are incriminated for the severe apical lesions. This study shows that the disease can be experimentally induced in the monkey thereby validating the postulated hypothesis.

Adolescent↗
PubMed1996

Effects of cassava diet on Cercopithecus aethiops livers: a case for cassava as the cause of both tropical splenomegaly syndrome (TSS) and endomyocardial fibrosis (EMF).

The aetiology of endomyocardial fibrosis (EMF) and tropical splenomegaly syndrome (TSS) though speculative, was considered by the author to be the same or related since the two diseases may occur in the same individual and locality. Accordingly, when attempting to prove a hypothesis for the causation of EMF that prolonged ingestion of tuber (cassava/tapioca) associated with extreme deprivation of protein causes EMF; one group of three Cercopithecus aethiops was fed on uncooked cassava while a second group was fed with uncooked bananas and in addition to harvesting the hearts whenever the animal health deteriorated, livers were also harvested for histological changes. While hearts from the animals on cassava revealed changes seen in human EMF the livers from the same animals exhibited Kupffer cell hyperplasia and hypertrophy as well as sinusoidal lymphocytosis, features seen in human TSS thereby confirming that the aetiology of these two diseases is the same. However, the banana diet did not produce such changes.

Age Distribution↗
PubMed1995

Response of Plasmodium falciparum to chloroquine and Fansidar in vivo and chloroquine and amodiaquine in vitro in Uganda.

The response of P. falciparum to chloroquine and pyrimethamine-sulfadoxine in vivo and chloroquine and amodiaquine in vitro was investigated in parasitaemic school children from six locations. Mean parasite sensitivity to chloroquine at day 7 was 74% (range 61-97) with parasite clearance rates between 2-3 days and complete defervescence in 85% of febrile children. Sensitivity declined in the four sites followed up to day 14 to 45% (range 37-53). Parasites were significantly more sensitive to pyrimethamine/sulfadoxine at 5/6 sites (100% day 7) but 5% of subjects became parasitaemic by day 14. In vitro isolates were significantly less sensitive to chloroquine than to amodiaquine with a mean 99% effective concentration of 348 mumol/L compared to 6.44 mumol/L. Clearly the role of chloroquine as the primary therapy for uncomplicated P. falciparum malaria should be reconsidered especially in the light of increasing disease severity and resurgence. Amodiaquine may be suitable alternative with pyrimethamine/sulfadoxine as second line and for more severe malaria prior to referral. The cost of alternative antimalarials and the dynamic and deteriorating pattern of resistance are powerful arguments for more objective slide diagnosis to minimise drug pressure and a regular drug sensitivity surveillance system. We believe that the latter should concentrate on measuring clinical drug efficacy in symptomatic outpatients rather than in asymptomatic children while the former needs more pragmatic and economical strategies possibly centred on seasonality and risk.

Amodiaquine↗