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Biomedical subjects

P Fondu

Publications and source records attributed to P Fondu.

At least 109 records · Page 6Linked to original sources
PubMed1980

The erythrocyte membrane disturbances in protein-energy malnutrition: nature and mechanisms.

In protein-energy malnutrition (PEM), as observed in Kivu, the RBC have an increased ratio of surface area to volume which is demonstrated by the presence of target cells on light microscopy and cup cells with scanning electron microscopy. The osmotic fragility is decreased. These abnormalities can be attributed to the accumulation of cholesterol and phosphatidylcholine (PC) in the RBC membrane. The molar ratio of cholesterol to phospholipids is moderately increased. Several findings suggest that the cholesterol and PC build-up results from disturbed exchanges in these lipids between the RBC and the plasma lipoproteins. Firstly, the osmotic fragility of a patient's RBC gradually becomes normal when the cells are transfused into a healthy recipient. Secondly, the cholesterol flux between the RBC and the plasma LDL seems to be low. Thirdly, the increase in RBC PC cannot be explained by a diminished fatty acids transport between the deep RBC PC pool and the RBC phosphatidylethanolamine (PE) pool. Finally complex disturbances of the plasma lipoproteins are obvious. It is improbable that the cholesterol and PC build-up accounts for the premature RBC destruction which has been described in Kivu PEM. However, the observation of an increased fatty acid turnover in RBC PC and PE, as well as other data previously obtained in Kivu PEM, lead to the conclusion that membrane peroxidation may be a major cause of the shortened erythrocyte life-span in this syndrome.

Child↗
PubMed1978

Protein-energy malnutrition and anemia in Kivu.

Protein-energy malnutrition in Kivu is associated with a discrete normocytic, normochromic anemia. An attempt to define the physiopathology of this anemia disclosed the following results. As compared with local controls, both iron and total iron binding capacity were low, but with siderophilin saturation and sideroblast counts either normal or elevated; serum and erythrocyte folate was normal, plasma vitamin B12 was normal or elevated, and serum ascorbic acid was normal or elevated. The riboflavin nutritional status was normal. During refeeding, iron and riboflavin deficiencies became apparent. Characteristic findings on admission were the presence of giant erythroblasts and a diminished erythrocyte survival time implicated to an intracorpuscular hemolysis. Two results from the present study could contribute to explanation for the aforementioned abnormalities: low plasma vitamin E levels and, perhaps more importantly, low plasma selenium levels. In conclusion, the anemia of protein-energy malnutrition, as observed in Kivu, is a classifiable nonadaptive anemia that cannot be explained by isolated iron or vitamin deficiencies and whose physiopathology is distinct from that of the anemia of chronic disorders. It is suggested that a selenium deficiency may play an important role in the pathogenesis of this anemia.

Anemia↗
PubMed1978

The regulation of erythropoiesis in protein-energy-malnutrition.

The erythropoietin (ESF) content of plasma and urine has been studied in children with protein-energy-malnutrition (PEM) living in the Kivu province at an altitude of 1467--2000 m. On admission, packed cell volume (PCV) was moderately reduced; after 2 months of refeeding PCV had increased but was still lower than in the controls. Plasma ESF was increased on admission and in patients refed for 2 months. The expected positive correlation between serum and urine ESF levels was found after refeeding but not on admission; the last finding could not be explained by the presence of erythropoiesis inhibiting factor(s) in the urine. In spite of the normal 2,3-DPG and P50 previously described in PEM in Kivu, the anaemia associated with this disease is not merely an adaptation to lowered oxygen consumption and there must be some disturbances in the responsiveness of bone marrow to ESF. The high ESF values observed after 2 months of refeeding confirm that the restoration of the red cell volume proceeds slowly.

Adolescent↗
PubMed1977

A reassessment of intravascular volume measurements in protein--calorie malnutrition.

Accurate determination of plasma volume is difficult in oedematous protein--calorie malnutrition, but present studies on the equilibrium of labelled red cells have shown that red cell volume measurements are valid in this syndrome. The red cell volumes have been measured in afflicted Bantu children during a refeeding programme. Expression of the results in ml/kg, ml/m2 or ml/cm is misleading and has been replaced by expressing the results as a percentage of the means of the normal values for the height. The results show that the red cell volume increase that ought to occur at the end of refeeding programme (and hence the iron requirement) is far higher than suggested by the packed cell volume. With treatment the red cell volume increases slowly. The red cell volume and plasma volume changes that occur during treatment do not take place at the same rate.

Body Constitution↗
PubMed1977

Intramural hematoma of the alimentary tract in two hemophilic children.

The occurrence of an intramural hematoma of the alimentary tract is reported in two hemophilic children. In both cases, the hematomas may be the result of a mild unrecognized trauma. The first patient presents large duodenal hematomas with secondary rupture into the retroperitoneal space. Death occurs despite medical and surgical treatment. The second patient presents an intramural hematoma of the colon, which is treated medically. In both cases factor VIII inhibitors developed during the course of therapy. Indications for medical or surgical treatment are discussed.

Barium Sulfate↗
PubMed1977

[Iron metabolism during proteoenergetic malnutrition in children].

The iron stores are normal in marasmic kwashiorkor in kivu, but they notably decrease on re-feeding. On admission, the total iron binding capacity depends not only on the severity of the protein depletion but also on the iron stores. There exists an abnormality of the iron release from the stores; this cannot be attributed to the hypotransferrinemia or to the hypoceruloplasminemia, which are too moderate, nor to an ascorbic acid deficiency, but possibly to the inflammatory state which is a feature of kwashiorkor. The iron deficiency which occurs on re-feeding is not explained by abnormalities of iron absorption or by increased iron loss, but by the raised requirement for iron. Parental iron treatment alone is required to normalise the packed cell volume and the red cell volume after re-feeding.

Child↗
PubMed1976

[Prognosis and treatment of idiopathic thrombocytopenic purpura in children].

The following conclusions can be drawn from the study of 55 cases of I.T.P. of childhood. 1. I.T.P. evolving more than 6 months must always be considered as chronic, the disease having in these cases few chances of recovery without splenectomy. After 6 months evolution, it is probably possible to establish a prognosis and a therapeutic approach with little risk of error. 2. Among the clinical and biological criteria noted at the onset of the disease, the intensity of thrombopenia alone is statistically different in acute and chronic I.T.P. Consequently, there are few criteria allowing the early recognition of evolution to chronic I.T.P. 3. The corticoids have no curative value in I.T.P. Prolonged corticotherapy is therefore useless in this disease. 4. As a palliative, the value of the corticoids can only be statisfactorily demonstrated in chronic I.T.P. Here it is certain in 6 cases on 16. 5. The value of corticoids for capillary resistance is evident, even in small doses. 6. Splenectomy must be considered in all cases of severe or corticodependant chronic I.T.P. Cure is obtained in most cases. 7. The contribution of immunosuppressive agents and in particular azathioprine, cannot be usefully assessed on the basis of the series studied. In the absence of decisive results, it would be worthwhile to evaluate this treatment by means of a greater number of clinical trials.

Acute Disease↗
PubMed1975

Serial measurements of vitamin B-12 and vitamin B-12-binding capacity in marasmic kwashiorkor.

Vitamin B-12 and total vitamin B-12-binding capacity (TBBC) have been determined by a radio-saturation assay in the blood of a large group of patients suffering from marasmic kwashiorkor on admission, and during their whole re-feeding. The results have been compared with values obtained in control children of the same ethnic group and with normal children living in Belgium. Vitamin B-12 levels are high on admission and only normalize during the second month of re-feeding. TBBC is normal on admission but significantly increases during re-feeding.

Black People↗
PubMed1975

Marasmic kwashiorkor anemia. III. Hemoglobin oxygen affinity.

Oxygen-hemoglobin dissociation curve, 2,3-diphosphoglycerate (2,3-DPG), and adenosine triphosphate (ATP) have been studied in marasmic kwashiorkor before re-feeding, after re-feeding, and in control children. P 50 and 2,3-DPG level are normal on admission, but high after re-feeding. Patients studied on admission were separated into 2 groups according to whether they presented active erythropoiesis (group I) or erythroblastopenia (group II). In group I, the sum 2,3-DPG + ATP correlates with the hemoglobin level. In group II, the sum 2,3-DPG + ATP correlates with the blood pH but not with the hemolobin level. It is suggested that marasmic kwashirokor anemia is an adaptation to a reduced metabolic activity. The hematological picture could proceed in 2 stages in this disease. In a first stage, the erythropoiesis is normal or increased because of the existence of a decreased red cell life span; a low hemoglobin level is observed, but there is no apparent hypoxia. At a more advanced stage of the disease, the tissue metabolism falls dramatically, the erythropoiesis is no loner stimulated, and the erythrocyte volume decreases notably.

Adenosine Triphosphate↗