ABSTRACT
The therapeutic benefits of camel milk consumption are a supplement to routine sickle cell disease management. In maintaining hemolytic crises in sickle cell anaemia, patients were assessed during a six weeks study. Throughout the study, 20 patients were recruited for the study and divided into 4 groups, 5 patients per group. Group 2, 3 and 4 were treated with daily consumption of raw camel milk (100 ml, 50 ml + Folic acid + Paludrin and 100 ml + Folic acid + Paludrin respectively). In all groups, the foetal haemoglobin (Hb F), packed cell volume (PCV), platelet, red blood cell (RBC) and white blood cell (WBC) count were measured before initiation of the study and monitored at 2 weeks intervals for 6 weeks. In the group that took camel milk (50 ml in addition to Folic acid and Paludrin), there was a significant increase in WBC (8.16 ± 4.12 to 16.68 ± 3.53), a significant increase in PCV (21.28 ± 1.23 to 25.24 ± 1.11) with decrease in platelet (311.80 ± 61.93 to 260.40 ± 29.22) and significant increase in Hb F (7.06 ± 2.42 to 10.02 ± 2.41) compared to group 1 (control). However, there was no significant difference in the haematological parameters of group 2 and 4. The results implied that the consumption of camel milk in sickle cell patients resulted in an increase in foetal hemoglobin concentration which prevented crises in almost all the patients. Increase in foetal haemoglobin has been postulated to reduce hemolytic crises in sickle cell anaemia patients. Based on these findings, camel milk consumption may, therefore, be considered useful in the management of sickle cell diseases.
ABSTRACT
The aqueous root extract of Cochlospermum tinctorium (CTR) was investigated for its phytochemical composition; acute oral toxicity and hepatoprotective effect on carbon tetrachloride (CCl4) induced liver damage in rats. Phytochemical screening indicates the presence of alkaloids; tannins; cardiac glycosides; saponins; flavonoids; triterpenes; cyanogenic glycosides and volatile oils while steroids and anthraquinones were absent. Administration of 5000 mg/kg (body weight) of the extract orally did not produce any death in the rats within the observable period. The extract at 100 - 300 mg/kg (body weight) significantly and dose dependently reduced the levels of Alanine aminotransferase (ALT); Aspartate aminotransferase (AST) and Alkaline phosphatase (ALP) enzymes levels in the CCl4 -treated rats. The values of serum albumin; serum total protein and reduced glutathione in the extract treated groups of rats remained comparatively higher than its values in the CCl4 - treated group. The pretreatment of the rats with the extract produced a significant (P 0.05) reduction in blood clotting time. The histopathological findings were in support of the biochemical changes recorded during the study. These results suggest that aqueous root extract of CTR possess hepatoprotective effect against CCl4- induced liver damage in rats and the extract at 5000 mg/kg body weight appeared to be safe when administered orally