Ann. Pak. Inst. Med. Sci. 2010; 6(2): 80-84

Objective: To compare the hepatic biochemical derangements induced by falciparum and vivax malaria
Study Design: A descriptive study
Place and duration of study: Department of Biochemistry, Basic Medical Sciences Institute, JPMC, Karachi from August 2005 to July 2006.
Materials and Methods: Total eighty-one patients of different ages and both sexes suffering from acute malaria, confirmed by peripheral blood smear were selected by convenient sampling. Nine out of eighty-one patients were infected by Hepatitis B and C infections and were excluded from the study. Out of seventy-two patients 48(70%) were suffering from malaria by Plasmodium falciparum and 24(30%) from Plasmodium vivax infection. The falciparum infected patients were divided into two groups on the basis of duration of illness. Group 1 comprised of 24 patients complaining of fever with or without rigors ranging from 1 – 7 days. Group 2 also consisted of 24 patients with duration of illness lasting from 8-20 days. Group 3 comprised of 24 Plasmodium vivax infected patients having illness of 1 – 20 days. Samples were analyzed in the Biochemistry Department at Basic Medical Sciences Institute, JPMC, Karachi.
Results: Liver was enlarged in 26 (54%) patients suffering from falciparum and
2 (8.3%) from vivax malaria. Spleen was also palpable in 23 (47.9%) patients from falciparum group and 4 (16.7%) from vivax group. This difference was statistically highly significant (P<0.001). Mean value of blood hemoglobin in Plasmodium falciparum group was 9.3±0.27, while in Plasmodium vivax group was 10.6±0.04 and the difference in haematocrit percentage was statistically highly significant (P<0.001). Hyperbilirubinemia was present in 52.7% of patients. The mean value of indirect Bilirubin in case of Plasmodium falciparum group is 2.4±0.32 comparatively higher than plasmodium vivax group showing a statistically significant P value (<0.01). Difference in the mean value of SGPT and SGOT are statistically highly significant (P<0.001) when results were compared with group I. The results of difference in mean value of alkaline phosphatase was statistically highly significant when group I and group II of Plasmodium falciparum infected were compared, which confirms that, as the duration of illness of Plasmodium falciparum progresses the level of alkaline phosphatase rises.
Conclusion: Although significant biochemical derangements were observed in both falciparum and vivax malaria, they were significantly more pronounced in Plasmodium falciparum infection, particularly in the later phase of illness. Therefore, liver function tests should be performed early in the course of Plasmodium falciparum malarial infections in order to prevent complications and to reduce mortality.
Key words: Plasmodium falciparum, Plasmodium vivax, Hyperbilirubinemia, hepatic biochemical derangements

Introducation

Malaria is responsible for 1-3 million deaths annually and 300-500 million infections world wide.¹ Most of deaths are due to severe malaria, with one or more complications in a patient showing asexual parasitaemia of falciparum malaria.² Malarial transmission occur through sporozoites injected in blood by female Anopheles mosquito, which attach to hepatocytes through receptor for thrombospondin and properdin.³ Tissue schizonts then produces large number of merozoites. Each merozoite is capable of invading red blood cells and establishing the asexual cycle of replication with the release of 24 to 32 merozoites.⁴ The clinical manifestations are consequent upon the release of cellular products and debris from ruptured erythrocytes and their phagocytosis by reticuloendothelial cells.⁵ Hyperplasia of the these cells in the liver occur as part of the response to malaria and is responsible for its enlargement.⁶ Plasmodium falciparum differs from other species in that its merozoites are capable of invading both older and younger red cells⁷ and is responsible for multiorgan dysfunctions.⁸ Liver involvement is common.⁵ Unconjugated hyperbilirubinaemia is attributed to hemolysis of both parasitized and non-parasitized erythrocytes and partly due to liver damage.⁹ Hyperbilirubinemia is often seen with acute renal failure, cerebral malaria and death.¹⁰ The coagulation system is adversely affected during severe malaria and is proportional to the severity of the illness.⁸ The elevated alkaline phosphatase activity indicates hepatic stage of parasites and significant perturbation in the hepatocytic membrane leading to its leakage.¹¹ Significantly decreased protein synthesis will not become apparent except in severe long standing hepatic diseases12 or might be due to increased capillary leakage.¹³ Hypoglycemia may have four reasons; (1) depletion of liver glycogen (2) glucose consumption by the parasites (3) hypoglycemic effects of elevated level of interleukin-1 and TNF-B and (4) release of insulin during treatment with quinine or quinidine.⁴
Present study was carried out to evaluate the acute hepatic damage induced by Plasmodium falciparum malaria, while Plasmodium vivax infected cases were included for comparative analysis.