PubMed Health⌕ Search

Biomedical subjects

O Sodeinde

Publications and source records attributed to O Sodeinde.

At least 19 recordsLinked to original sources

Variation in the relationship between anti-MSP-1(19) antibody response and age in children infected with Plasmodium falciparum during the dry and rainy seasons.

Malaria remains a major parasitic disease in Africa, with 300-500 million new infections each year. There is therefore an urgent need for the development of new effective measures, including vaccines. Plasmodium falciparum merozoite surface protein-1(19) (MSP-1(19)) is a prime candidate for a blood-stage malaria vaccine. Blood samples were collected from children aged 10 days to 15 years in the months of January-March (N = 351) and October-November (N = 369) corresponding to the dry and rainy seasons, respectively. P. falciparum infection was determined by microscopy and enzyme linked immunosorbent assay (ELISA) was used to determine the total IgG and IgG subclasses. There was a significant increase in the mean anti-MSP-1(19) antibody titre in the dry season (p < 0.05), compared to the rainy season. A significantly positive correlation between the anti-MSP-1(19) antibody titre and parasite density (p < 0.01, r = 0.138) was observed. In the rainy season, unlike in the dry season, P. falciparum positive children had higher anti-MSP-1(19) antibody titres than P. falciparum negative children and this difference was significant (p < 0.05). When all individuals were grouped together, the anti-MSP-1(19) antibody titre increased with age in both seasons (r = 0.186 and 0.002), this increase was more apparent in the dry season. However, when the study population was divided into P. falciparum positive and negative groups, it was observed that in the rainy season, there was a negative correlation between anti-MSP-1(19) titre and age in P. falciparum positive individuals, while those who were P. falciparum negative had a positive correlation between anti-MSP-1(19) titre and age. Analysis of anti-MSP-1(19) IgG subclass showed that IgG1 and IgG3 mean titres were highest in both the dry and rainy seasons with an increase in the mean antibody titres for IgG1, IgG2 and IgG3 in the rainy season. In the dry season there was a positive correlation between IgG1, IgG2, and IgG3 titres with age, while IgG4 was negative, whereas in the rainy season there was a positive correlation between IgG2 and IgG4 (non-cytophilic antibodies) with age and a negative correlation for IgG1 and IgG3 (cytophilic antibodies) with age. Seasonal differences in the level of MSP-1(19) IgG subclass titres were observed for P. falciparum negative and positive individuals. Only samples, which were positive for IgG2 and IgG4, showed positive correlation between parasitemia and total IgG. The incidence of P. falciparum infection, which increases during the rainy season, might be an important determinant of anti-MSP-1(19) antibody levels in children living in Igbo-Ora and the results point to the fact that non-cytophilic antibodies to MSP-1(19) in children might be associated with an increase in total IgG and parasitemia.

Adolescent↗

Stroke in Nigerian children with sickle cell disease.

We reviewed our records over a 15-year period to determine whether or not the impression that stroke complicating sickle cell disease was less common than reported in North America. Records of children aged 16 years and below with a diagnosis of stroke seen at the University College Hospital, Ibadan, Nigeria between 1988 and 2002 were examined. Thirty-nine such patients were identified but only 31 had detailed records available for study. Twenty-seven of these had sickle cell disease, 26 with haemoglobin genotype SS and 1 with Hb S+C. Sickle cell disease was therefore responsible for 87% of stroke seen in children at our centre. With an average clinic population of about 500 patients with sickle cell disease, the hospital frequency of stroke among these patients is estimated at 5.4%. The mean age of occurrence of the first stroke was 6.8 years ranging from 17 months to 11 years. Of the 7 patients who had CT scans of the brain done, 5 had evidence of cerebral infarction while 2 had intracerebral haemorrhage. While only 2 deaths occurred among the cases reviewed, morbidity was significant with only 6 patients achieving complete recovery. Recurrent stroke occurred after an average of 25.6 months in 8 of 13 patients who were followed up (61.5%). The incidence of stroke among African children with sickle cell disease appears to be not as high as reported in patients from North America.

Adolescent↗

Certain red cell genetic factors and prevalence of chloroquine-induced pruritus.

The hypothesis that chloroquine-induced pruritus (CIP) may be determined by certain genetic factors was tested by investigating the epidemiology of CIP with respect to certain genetic red cell markers namely, haemoglobin genotype, glucose-6-phosphate dehydrogenase (G6PD) deficiency and the ABO blood groups. Three hundred consecutive patients treated for malaria with chloroquine at the University College Hospital, Ibadan, Nigeria were recruited into the study. They were observed over 3 days for presence of CIP. ABO blood groups, G6PD and Hb genotypes were determined appropriately for each patient. One hundred and twenty four (41.3%) of the patients responded positively to CIP. There was a reduced frequency of the sickle cell trait (HbAS) among itchers relative to non-itchers. This suggests that the trait may be protective against CIP. G6PD deficiency was also found to be relatively more common among itchers than non-itchers. This indicates that G6PD deficiency may increase susceptibility to CIP. There was however no difference in the distribution of itchers among the different ABO blood groups. It was concluded that CIP may be associated with certain genetic red cell markers particularly Hb and G6PD types which are known malaria markers but not ABO blood groups.

Adolescent↗

Glucose-6-phosphate dehydrogenase-6-phosphogluconolactonase. A novel bifunctional enzyme in malaria parasites.

Plasmodium falciparum glucose 6-phosphate dehydrogenase (Pf Glc6PD), compared to other Glc6PDs has an additional 300 amino acids at the N-terminus. They are not related to Glc6PD but are similar to a family of proteins (devb) of unknown function, some of which are encoded next to Glc6PD in certain bacteria. The human devb homologue has recently been shown to have 6-phosphogluconolactonase (6PGL) activity. This suggests Pf Glc6PD may be a bifunctional enzyme, the evolution of which has involved the fusion of adjacent genes. Further functional analysis of Pf Glc6PD has been hampered because parts of the gene could not be cloned. We have isolated and sequenced the corresponding Plasmodium berghei gene and shown it encodes an enzyme (Pb Glc6PD) with the same structure as the P. falciparum enzyme. Pb Glc6PD is 950 amino acids long with significant sequence similarity in both the devb and Glc6PD domains with the P. falciparum enzyme. The P. berghei enzyme does not have an asparagine-rich segment between the N and C halves and it contains an insertion at the same point in the Glc6PD region as the P. falciparum enzyme but the insertion in the P. berghei is longer (110 versus 62 amino acids) and unrelated in sequence to the P. falciparum insertion. Though expression of this enzyme in bacteria produced largely insoluble protein, conditions were found where the full-length enzyme was produced in a soluble form which was purified via a histidine tag. We show that this enzyme has both Glc6PD and 6PGL activities. Thus the first two steps of the pentose phosphate pathway are catalysed by a single novel bifunctional enzyme in these parasites.

Amino Acid Sequence↗

The disposition of chloroquine and its main metabolite desethylchloroquine in volunteers with and without chloroquine-induced pruritus: evidence for decreased chloroquine metabolism in volunteers with pruritus.

The pharmacokinetics of chloroquine and its main metabolite desethylchloroquine have been carried out in volunteers with and without chloroquine-induced pruritus. It was shown that the volunteers with pruritus tended to metabolize chloroquine slower than the volunteers without pruritus because the metabolic ratio was lower in the volunteers with pruritus than that in the volunteers without pruritus. However, the overall pharmacokinetic patterns were comparable between the two groups and agreed with published data. The 24-hour urinary collections in the two groups of volunteers indicated that the volunteers with pruritus excreted more chloroquine (although not statistically significant) than the volunteers without pruritus. This also indicates that they metabolized less chloroquine. There were no side effects of note in any of the volunteers. The volunteers who gave positive histories of chloroquine-induced pruritus had mild episodes of itching after intake of the drug; the pruritus subsided within 48 hours in all instances.

Adult↗

Identification of a subpopulation of immune Nigerian adult volunteers by antibodies to the circumsporozoite protein of Plasmodium falciparum.

Collections of human sera from malaria-endemic areas would be valuable for identifying and characterizing antigens as malaria vaccine candidates if the contributing serum donors' ability to resist infection were fully characterized. We prepared such a serum collection from 26 apparently immune Nigerian adults who failed to develop patent parasitemia for at least 20 weeks following a documented increase in antibodies to the circumsporozoite protein (CSP) from Plasmodium falciparum. Volunteers were evaluated five times per week for malaria symptoms and bimonthly for parasites by examining thick blood smears. The incidence rate over 13 months for the cohort was 42% (47 malaria-confirmed volunteers) and the risk of infection was 1.3 infections/year. Responses to CSP did not correlate with protection. Because antibody responses to antigens other than CSP may be associated with protection, the sera from these immune individuals may be useful for identifying and characterizing other potential malaria vaccine candidates.

Adult↗

Body temperature is a poor predictor of malaria parasitaemia in children with acute diarrhoea.

In order to ascertain the usefulness of a temperature > or = 38 degrees C or a history of fever in detecting malaria parasitaemia in children with diarrhoea as recommended by the World Health Organization (WHO), 522 children aged from 6 to 60 months presenting with acute diarrhoea were studied in Ibadan, Nigeria. The overall prevalence of malaria parasitaemia was 13%. There was no significant difference in the prevalence of parasitaemia between patients with a temperature > or = 38 degrees C and those < 38 degrees C. Neither was any difference found in the prevalence of parasitaemia between those with and those without a history of fever. Temperature > or = 38 degrees C had a low sensitivity (53%) and specificity (57%) and a low positive predictive value (16%) in detecting malaria parasitaemia. A history of fever had a higher sensitivity (79%) than temperature > or = 38 degrees C in detecting malaria parasitaemia but a low specificity (27%) and low positive predictive value (14%). Similar results were obtained in a simultaneously studied non-diarrhoea control group of 313 children. The implications of using the current WHO guidelines is that many diarrhoea patients with malaria would not be identified, while many patients without malaria would be treated unnecessarily. The latter situation may be associated with the development of drug-resistant malaria parasites while the children are unnecessarily exposed to the risk of drug-related complications. It is recommended that while the search for better guidelines continues children should be screened for malaria parasitaemia before treatment, where facilities are available.

Acute Disease↗

The clinical manifestations of cerebral malaria among Nigerian children with the sickle cell trait.

In order to describe the interaction between haemoglobin type and the clinical manifestations of cerebral malaria, we studied 60 children aged between 6 and 60 months at University College Hospital, Ibadan, Nigeria. Haemoglobin AS individuals with cerebral malaria did not exhibit major differences in clinical and laboratory characteristics when compared with their haemoglobin AA counterparts. There were no deaths among the Hb AS children compared with an 18% mortality in the Hb AA group. Blood transfusion rates were higher in the AS than in the AA children (86% vs 44%). The higher transfusion rates in the AS group is consistent with in-vitro observations of sickling of parasitized red cells containing Hb S which in vivo would be cleared by the reticuloendothelial system. It is concluded that the clinical manifestations of cerebral malaria are essentially similar in children with haemoglobins AS and AA but the former have higher transfusion needs and are less likely to die.

Blood Transfusion↗

Protein energy malnutrition and cerebral malaria in Nigerian children.

Eight (14 per cent) out of 57 consecutive cerebral malaria patients (all < 5 years old) were malnourished, including one with marasmus and another recovering from kwashiorkor. This was significantly lower than among other paediatric patients in the same children's emergency ward (112/319, i.e. 35 per cent, P < 0.01). Poor outcomes (death or recovery with neurological deficits) were commoner in the malnourished group (4/8) than the well nourished group (7/49) (P = 0.037, Fisher's exact test). Malnourished children should receive malaria chemoprophylaxis during nutritional rehabilitation.

Chi-Square Distribution↗

Lack of association between falciparum malaria parasitemia and acute diarrhea in Nigerian children.

It is widely believed that malaria causes diarrhea. Yet, national and international diarrheal diseases control programs are silent about the overlap between these two major public health problems that coexist in most tropical countries. To test the hypothesis that malaria is associated with diarrhea and to define the role of malaria in morbidity due to diarrhea, 522 children 6-60 months of age presenting with acute diarrhea to the Children's Emergency Ward of the University College Hospital in Ibadan, Nigeria were routinely screened by means of thin and thick blood films for malaria parasitemia. Controls, without diarrhea, were studied in parallel. Detailed clinical features were recorded for every patient. Sixty-eight (13%) of the 522 diarrhea patients screened had malaria parasitemia. Among the controls (who had similar distributions of admission temperature, hemoglobin types, glucose-6-phosphate dehydrogenase deficiency, and prior treatment with antimalarial drugs), parasitemia was not significantly different, occurring in 56 (17.9%) of 313. In the dry season, however, a significantly higher prevalence of parasitemia was observed among the control group (15.5%) than in the diarrhea group (7.0%) (P = 0.004). Parasitemia was significantly more common in the dehydrated diarrhea patients than their well-hydrated counterparts (25% of 56 versus 11% of 466; P < 0.005). There were no significant differences in admission temperature, the presence of vomiting, or the home use of oral rehydration fluids between the dehydrated and the well-hydrated subsets of diarrhea patients. Consideration of parasite densities did not alter any of the foregoing relationships. These data contradict the widely held view that diarrhea is a symptom of malaria or that malaria causes diarrhea. They do, however, provide support for examining blood smears at least in dehydrated children with diarrhea in malaria-endemic areas and giving immediate antimalarial therapy to those who have malaria parasitemia.

Antimalarials↗

Persistent diarrhoea in Nigerian children aged less than five years: a hospital-based study.

To identify possible risk factors for persistent diarrhoea, 307 children with acute diarrhoea presenting at the University College Hospital, Ibadan, Nigeria over a 10-month period from July 1993 to April 1994 were followed up prospectively until the resolution of the illness. The children were aged 6-60 months. In 36 (11.7%) of them, diarrhoea became persistent (i.e. lasted more than 14 days). This hospital frequency of 11.7% of persistent diarrhoea is, as expected, higher than the figures from previous community-based studies of diarrhoea from Nigeria. The major factor associated with persistent diarrhoea was poor nutritional status. Mean z scores of weight-for-height and weight-for-age were significantly lower in the persistent diarrhoea group, while mean z scores of height-for-age were similar in the two groups. The frequencies of occurrence of undernutrition, marasmus and kwashiorkor were also higher in the persistent diarrhoea group. Therefore, in common with studies from other regions of the world, malnutrition is an important risk factor for persistent diarrhoea in this group of Nigerian children. The implication of these findings is that reduction in the prevalence of malnutrition may be associated with reduction in the proportion of acute diarrhoeal episodes that eventually progress to persistent diarrhoea.

Acute Disease↗

Interaction between acute diarrhoea and falciparum malaria in Nigerian children.

Although both malaria and diarrhoea are major public health problems in developing countries, and separately each has been the subject of intense research, few studies have investigated the interaction between these two conditions. The interaction between diarrhoea and malaria among children aged 4 months to 12 years in two tertiary health-care facilities, University College Hospital, Ibadan, and Lagos University Teaching Hospital, Lagos, Nigeria was studied. In Ibadan, the prevalence of diarrhoea among the cerebral malaria patients on admission as 11.7% (7/60) compared to 9.3% (215/2312) among other admissions in 1990 (chi square = 0.16; p = 0.6913). Similarly, no significant difference in the prevalence of diarrhoea was found between the cerebral malaria patients (14.3%) and other patients (16.1%) seen in Lagos in 1992 (chi square = 0.06, p = 0.81). Thus, cerebral malaria does not seem to be associated with an increased or decreased prevalence of diarrhoea when compared with other conditions. The prevalence of malarial parasitaemia among the 554 diarrhoea patients studied in Ibadan during 1993-1994 was 13.6% compared with 17.9% among the 347 controls (chi square = 3.75, p = 0.053). However, of the children with diarrhoea, malarial parasitaemia was more common among the dehydrated patients (25.4%) than among the well-hydrated patients (11.6%) (chi square = 8.11, p = 0.004). These data suggest that diarrhoea is merely coincidental in severe malaria and conversely, malarial parasitaemia is similarly coincidental in children with acute diarrhoea, although it may be more frequent among dehydrated diarrhoea patients than well-hydrated ones.

Acute Disease↗

Neonatal jaundice, aflatoxins and naphthols: report of a study in Ibadan, Nigeria.

This study set out to investigate the prevalence of naphthols and aflatoxins in the sera of babies with neonatal jaundice and their mothers in order to determine whether they contribute to the occurrence of unexplained neonatal jaundice in Ibadan. Blood was obtained from 327 jaundiced neonates and 80 of their mothers, and 60 non-jaundiced controls and seven of their mothers admitted to hospital between April 1989 and April 1991. Blood group, bilirubin concentration, erythrocyte G6PD status, aflatoxin and naphthol concentrations in blood were measured. Altogether, 30.9% of the jaundiced neonates were G6PD-deficient, compared with 13.3% of controls (chi 2 = 6.88; p = 0.009). Aflatoxins were detected in 27.4% of jaundiced neonates, 17% of their mothers, 16.6% of controls and 14.4% of control mothers. Naphthols were detected in 7.2% of jaundiced babies, 6.3% of their mothers, 6.25% of control babies and 14.4% of their mothers. Analysis of the data revealed that either G6PD deficiency or the presence of any serum aflatoxin is a risk factor for neonatal jaundice; odds ratio were 2.97 (95%) confidence intervals (CI): 1.31-6.74) and 2.68 (CI: 1.18-6.10), respectively. This study demonstrates that G6PD deficiency and/or the presence of serum aflatoxins are risk factors for neonatal jaundice in Nigeria. Aflatoxins are an additional risk factor not previously reported.

Aflatoxins↗

Hyponatraemia, birthweight and neonatal jaundice.

Cord serum sodium levels were estimated in 96 full term singletons delivered by spontaneous vertex delivery. Thirty-two of these infants had cord serum sodium of less than 130 mmol/L and 64 had cord serum sodium of > or = 130 mmol/L. Serum bilirubin estimated on day 4 of life of the babies demonstrated mean unconjugated bilirubin levels of 105.7 mmol/L (S.D.:87.04) and 89.4 mmol/L (S.D.:66.18) in the hyponatraemic and normonatraemic groups respectively (P < 0.05). The study also demonstrated a higher cord sodium and lower serum unconjugated bilirubin in those babies whose mothers did not receive parenteral fluids. It is suggested that hyponatraemia should be excluded in the aetiology of neonatal jaundice.

Adult↗

Detection of naphthols and aflatoxins in Nigerian cord blood.

Widespread use of napthol-containing compounds and frequent contamination of foods by aflatoxins occurs in Nigeria. Napthols cause haemolysis and aflatoxins are hepatotoxic. A study was carried out to determine the extent of fetal exposure to these compounds and their influence on birthweight. Cord blood samples were collected at delivery from 625 babies and their sera were analysed for aflatoxins and naphthols. Mothers' histories and babies' weights were recorded. Naphthols were detected in 6.9% and aflatoxins in 14.6% of serum samples. No correlation was found between the presence of either compound and birthweight. Reported exposure to naphthalene-containing compounds was not related to detection of serum naphthol. Results show considerable fetal exposure to these potentially toxic compounds in Ibadan, Nigeria.

Aflatoxins↗

Glucose-6-phosphate dehydrogenase deficiency.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy. Because its gene locus is on the X-chromosome it is more common in males than females in all populations. Prevalence rates vary from 62% among Kurdish Jews to the very low rates (0.1% or less in Japan, for example), which are compatible with sporadic cases arising from spontaneous mutations. However, there is at least one population in which G6PD deficiency has not been found, namely the indigenous (Amerindian) population of America. Approximately 400 variants have been described. Despite the clinical burden imposed by this enzymopathy, polymorphic frequencies have been reached in many populations. There is abundant epidemiological evidence that this has happened because of a biological advantage conferred on heterozygotes in falciparum malaria endemic areas. This advantage may apply to quartan malaria as well. Clinical severity varies, from the rare chronic nonspherocytic haemolytic anaemia to progressively milder forms like the Mediterranean and A- types. The other clinical syndromes, i.e. neonatal jaundice and haemolysis caused by infections, foods, drugs and chemicals, are not always predictable. This is because only a fraction of such enzymopathic persons develop these syndromes after exposure to the relevant stimulus. Modern techniques of molecular biology may elucidate why this is so. There is some emerging evidence that the genetic burden or survival value associated with G6PD deficiency may be relevant not only in tropical and infectious diseases, but also in their chemotherapy (e.g. malaria) as well as in the control of a long-recognized environmental pollutant such as lead.

Female↗