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Biomedical subjects

A F Fleming

Publications and source records attributed to A F Fleming.

At least 91 records · Page 5Linked to original sources
PubMed1979

Treatment of iron deficiency in Nigerians with daily intramuscular Ferastral.

Treatment of severe iron deficiency with iron-poly(sorbitol-gluconic acid) complex (Ferastral) intramuscular 10 ml (iron 500 mg) on alternate days has been shown highly effective and well tolerated. In order to see whether the time of treatment could be shortened, 20 Nigerians with severe iron deficiency (mostly from hookworm infection) were treated with daily intramuscular Ferastral 10 ml until their calculated total requirement of iron was met. The total iron deficit was 877-2763 mg (mean 1875 mg). Supportive treatment included antimalarials, folic acid and anthelmintics. No patient complained of undue pain at injection sites or of any other undesirable side-effects. There was no evidence of hepatic or renal toxicity in any patient, including eight who were followed at intervals up to eight weeks from the start of treatment. The initial haemoglobin (Hb) level was 2.2-7.8 g/dl (mean 4.6 g/dl). Daily regeneration of Hb in the first 14 days was 0.12-0.49 g/dl (mean 0.30 g/dl), and haematological indices were generally normal by eight weeks. Recovery was slow or incomplete in six patients, all of whom had complications other than iron deficiency. Serum iron was measured in five patients, rose to around 8000 micrograms/dl on about day 4, and fell to physiological levels by day 14. The serum unsaturated iron binding capacity fell to nil in five out of six patients on around day 3, and reappeared between days 7 and 10. Five patients who had persistent blood loss from continued hookworm infestation received a further single dose of Ferastral (iron 1000 mg) 10 ml into each buttock after four weeks, and one patient after two weeks. This large dose was also acceptable to patients if given slowly; it was followed by an accelerated Hb regeneration, but no toxicity. Daily intramuscular Ferastral 10 ml until the calculated iron requirements are met (usually in less than five days) is recommended for the treatment of severe iron deficiency. Patients with continued blood loss or Hb less than 10 g/dl after four weeks without other cause of anaemia, may receive a boost of one intramuscular injection of Ferastral 20 ml (10 ml into each buttock).

Adolescent↗
PubMed1979

Abnormal haemoglobins in the Sudan savanna of Nigeria. I. Prevalence of haemoglobins and relationships between sickle cell trait, malaria and survival.

The prevalence of different haemoglobins and their interaction with malaria have been studied in Garki, Kano State, Nigeria. Sickle cell trait was present in 24% of newborn and 29% of those aged over five years. Hb.AC was present in 0.7%. Frequency of both haemoglobin variants was greater in Hausa than Fulani. Sickle cell anaemia was almost invariably fatal in early childhood. The distribution curve of percentage of Hb.S in sickle cell trait subjects was normal, and did not demonstrate any high frequency of a gene for alpha-thalassaemia. The presence of beta-thalassaemia minor could not be tested, but Hb.S/beta-thalassaemia was not detected. Hb.S gene frequency appears to have been maintained by a fitness in heterozygotes of 21% over normal homozygotes; increased fertility and high mutation rate did not make any apparent contribution. Hb.AS subjects had on average lower frequency and considerably lower densities of Plasmodium falciparum trophozoites than Hb.AA from the age of 30 to 59 weeks; density was less in sickle cell trait up to age three years in the dry season only. It is suggested that the survival advantage and hence the prevalence of sickle cell trait may be greatest in some hyperendemic areas and less where malaria transmission is extremely high or when it is high and unvaried.

Adolescent↗
PubMed1979

Abnormal haemoglobins in the Sudan savanna of Nigeria. II. Immunological response to malaria in normals and subjects with sickle cell trait.

Children born in areas hyperendemic for Plasmodium falciparum are protected by maternal antibodies for up to about five months of life, after which they are subject to intense infection until they acquire sufficient immunity--by about five years of age. Children with sickle cell trait (Hb.AS) are at an advantage during these critical years, probably because of preferential phagocytosis of parasitized red cells. This could lead to either (i) early processing of antigen by macrophages and an accelerated immune response, or (ii) less antigenic stimulus and hence lower antibody production. Immunoglobulin (Ig)G and IgM determinations, agar gel diffusion (Ouchterlony) against soluble P. falciparum antigen, the indirect fluorescent antibody (IFA) test using P. falciparum and P. malariae antigens, and the indirect haemagglutination (IHA) test with P. falciparum antigen were performed on sera from a population with different Hb electrophoretic types in the hyperendemic malarial area of Garki, Kano State, Nigeria. Plasma immunoglobulins and antimalarial antibodies rose with age. After the first year of life, lower mean concentrations of immunoglobulins (especially IgM), and lower mean titres of antibodies specific against P. falciparum (Ouchterlony, IHA and less significantly IFA) were present in Hb.AS compared to Hb.AA; these differences increased with age. Antimalarial intervention was followed by a decline of all values and final levels showed little difference between haemoglobin types. It was unlikely that either a relative inability to produce antibody or a more rapid catabolism of immunoglobulins was responsible for the lower levels in sickle cell trait. The observations are more easily explained by the hypothesis that Hb.AS persons have less antigenic stimulus due to the early removal of parasitized sickled cells by macrophages, which then degrade the antigens. The antibody difference between Hb.AA and Hb.AS increased throughout life, suggesting that this process remained a feature of sickle cell trait even after parasite frequencies and densities were similar in the two Hb groups. These observations have implications in the aetiology of tropical splenomegaly syndrome, which is rarely seen in sickle cell trait subjects. Mean IgG and IgM were slightly higher in Hb.AS than Hb.AA infants, the difference for IgG achieving significance. This suggested that during infancy early phagocytosis of parasitized cells had led to enhanced processing of antigen and hence an earlier immune response in Hb.AS, but this was unlikely to be a major factor in survival. IFA titres against P. malariae were slightly but not significantly lower in Hb.AS, possibly as a result of cross-reaction with P. falciparum antibody or of a slight degree of protection against P. malariae.

Adolescent↗
PubMed1979

Abnormal haemoglobins in the Sudan savanna of Nigeria. III. Malaria, immunoglobulins and antimalarial antibodies in sickle cell disease.

Subjects with sickle cell disease were identified in (i) a whole population sample (2742) Garki District, Kano State, Nigeria, and in (ii) the 534 infants born into the population during five years. Eleven (2.1%) newborn had Hb.SS, as was expected from gene frequency (0.146). Prevalence was maintained in the first year of life, but fell to 0.4% at one to four years and to 0.05% (one person) over the age of nine years. Antimalarial intervention for two transmission seasons was followed by an apparent but not significant decrease in Hb.SS mortality. There was one male aged about 40 years who had Hb.SC (the expected number was three). Hb.SS children were compared to normal subjects at the same age, the same village and the same survey; they had significantly less than the expected Plasmodium malariae infection (P less than 0.01) and lower than median P. falciparum densities while below five years (P less than 0.05). Over one year of age, they tended to have below average indirect fluorescent antibody (IFA) (P less than 0.01), indirect haemagglutinating antibody (IHA) (P less than 0.01) titres and number of precipitin rings (not significant) against P. falciparum antigen, and IFA against P malariae (P less than 0.01). They had above average IgM (P less than 0.05), but their IgG concentrations did not differ from normal. We conclude that (i) sickling is sufficient to protect against P. malariae in Hb.SS but not Hb.AS; (ii) sickling prevents intense P. falciparum infection in Hb.SS, as in Hb.AS; (iii) in Hb.SS, there is less antigenic stimulus and hence less antibody against P. falciparum (like Hb.AS) and P. malariae (unlike Hb.AS); (iv) although less intense, malaria is frequently fatal in Hb.SS, especially in age-group one to four years (unlike Hb.AS); (v) IgM levels are high in Hb.SS in response to frequent infections other than malaria (unlike Hb.AS).

Adolescent↗
PubMed1979

Abnormal haemoglobins in the Sudan savanna of Nigeria. IV. Malaria, immunoglobulins and antimalarial antibodies in haemoglobin AC individuals.

Haemoglobin (Hb) AC electrophoretic pattern was found in 0.7% of the population at Garki, Kano State, northern Nigeria, an area where malaria is hyperendemic. Twenty-one Hb.AC subjects at all ages did not differ from the rest of the population in their frequency or density of Plasmodium falciparum, P. malaria or P. ovale infections, nor in their IgM concentrations and titres of specific antimalarial antibodies. However, IgG levels in Hb.AC subjects were frequently above the average of the reference population (P less than 0.05), especially during a period of protection against malaria (P less than 0.01). These observations suggest that the Hb.C gene may be maintained in certain environments by an enhanced ability to produce IgG antibodies against an antigen or antigens other than malaria, and that its geographical relationship to malaria may be a coincidence. This hypothesis needs to be tested where Hb.C is seen at high frequency, in northern Ghana and Upper Volta or Gwoza (Nigeria).

Adolescent↗
PubMed1979

Tropical splenomegaly syndrome or chronic lymphatic leukaemia?

Four patients with the Tropical Splenomegaly Syndrome, showing marked lymphoid hyperplasia were studied, using immunological techniques. It has not been possible to decide on a definite diagnosis; chronic lymphatic leukaemia could not be excluded. Careful follow-up of similar patients may provide important clues to the pathogenesis of these diseases.

Adult↗
PubMed1978

Platelet function, factor VIII, fibrinogen, and fibrinolysis in Nigerians and Europeans in relation to atheroma and thrombosis.

Platelet function, factor VIII, fibrinogen levels, and fibrinolysis were studied in Europeans and in two groups of Nigerians living in Zaria, northern Nigeria, in order to see whether differences could help to explain the low incidence of atheroma and thrombosis in Nigerians. We confirmed the relative thrombocytopenia and observed a rapid disaggregation after ADP-induced platelet aggregation in Nigerians. The most striking difference was a reduced or absent ristocetin-induced platelet aggregation in Nigerian platelet-rich plasma, probably due to a plasma component interacting with the von Willebrand activity (VWF), since factor VIII coagulant activity, factor VIII related antigen, and isolated VWF were normal or high by European standards. Group II (rural population), but not group I (senior university staff in Zaria) of the Nigerians, tended to have high serum fibrinogen concentrations. Spontaneous fibrinolytic activity was enhanced in most Nigerians compared to the Europeans and was normally increased after venostasis in proportion to the initial activity. Fibrinolysis and ristocetin-induced platelet aggregation values for the Nigerians in group I were intermediate between European and Nigerian in the group II values, suggesting that differences were due more to environmental than to genetic factors.Relative thrombocytopenia, disaggregation after ADP-induced aggregation, inhibition of ristocetin-induced platelet aggregation, and active fibrinolysis help to explain the infrequency of thrombotic disease in Africans. Also the low incidence of atheroma may follow from less platelet adherence and less platelet release of mitogenic factors, which cause intimal hyperplasia.

Arteriosclerosis↗
PubMed1977

Iron-deficiency in the tropics.

Different populations in the tropics show wide variation in their iron status, even when living in the same area. These differences range from the most profound iron-deficiency anaemia to nutritional haemosiderosis. The extremes of dietary iron content so far reported are 5 mg per day in Mauritius to 180 mg per day in Ethiopia. Contamination with inorganic iron is an important source in some communities. Generally, the iron in food is in excess of requirement, but lumenal factors are all important in deciding how much is available for absorption. The iron of some diets is readily absorbed, but in other only a small percentage is utilizable. Hookworm infection is the commonest cause of severe iron-deficiency in many parts of the world. Its prevalence and its density depends on social habits, and may vary considerably even within tribes. The development of iron-deficiency anaemia depends on the hookworm load being sufficient to cause iron loss in excess of available intake. Anaemia impairs work capacity, reproductive ability of women and the development of children, and has wide social and economic repercussions. An intramuscular preparation by which 500 mg of iron may be administered in one injection has most useful application in areas where medical care is minimal.

Anemia, Hypochromic↗