2005, Number 4
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Ann Hepatol 2005; 4 (4)
Liver dysfunction in steady state sickle cell disease
Kotila T, Adedapo K, Adedapo A, Oluwasola O, Fakunle E, Brown B
Language: English
References: 15
Page: 261-263
PDF size: 38.64 Kb.
Text Extraction
The Liver is one of the organs involved in the multiorgan failure that occurs in sickle cell disease, the pathophsiology of liver disease in this condition is complex because of the interrelated multifactorial causes. Liver dysfunction was assessed in both paediatric and adult sickle cell disease patients in the steady state. The transaminases and alkaline phosphatase were analysed by automation while coagulation studies were done manually. The mean (range) of Alanine transaminase (ALT), Aspartate transaminase (AST) and alkaline phosphatase (ALP) were 23.0 (2-77) IU, 48.5 (15-120) IU, 227.5 (37-1200) IU respectively. ALT and AST levels were less than 100 IU in over 95% of the patients. The gender or age of the patients did not significantly affect the level of these three enzymes. There was close association between the liver size and elevation of the liver enzymes except for alkaline phosphatase (ALT = .017, AST = .009, ALP = .056). Twenty-five percent of the patients had normal enzymes while 13% had derangement of the three enzymes, 19%, 50% and 74% had abnormal ALT, AST and ALP respectively. Only 22% and 5% had deranged PT and APTT respectively. In conclusion minimal elevation of the tramsaminases which is not gender or age dependent were observed in steady state sickle cell disease, higher levels of alkaline phosphatase may be due to associated vasoocclussive crises involving the bones rather than a pathology of the liver.
REFERENCES
Hassell KL, Eckman JR, Lane PA. Acute multiorgan failure syndrome: a potentially catastrophic complication of severe sickle cell pain episodes. Am J Med 1994; 96: 155-62.
Banerjee S, Owen C, Chopra S. Sickle cell Hepatopathy. Hepathology 2001; 33: 1021-28.
Ahn H, Li CS, Wang W. Sickle cell hepetopathy: clinical presentation, treatment, and outcome in paediatric and adult patients. Paediatr Blood Cancer 2005: 184-90
Schubert TT. Hepatobiliary system in sickle cell disease. Gastroenterology 1986; 90: 2013-21.
Brody JI, Ryan WN, Haidar MA. Serum alkaline phosphatase isoenzymes in sickle cell anaemia. JAMA 1975; 232: 738-41.
Aken’Ova YA, Olasode BJ, Ogunbiyi JO, Thomas JO. Hepatobiliary changes in Nigerians with sickle cell anaemia. Annals of Tropical Medicine and Parasitology 1993; 87: 603-606.
Bauer TW, Moore GW, Hutchins GM. The liver in sickle cell disease: a clinicopathologic study of 70 patients. Am J Med 1980; 69: 833-837.
Rosenblate HJ, Eisenstein R, Holmes AW. The liver in sickle cell anaemia. A clinical-pathologic study. Arch Pathol 1970; 90: 235-245.
Johnson CS, Omata M, Tong MJ, Simmons JF, Jr., Weiner J, Tatter D. Liver involvement in sickle cell disease. Medicine 1985; 69: 833-837.
Khurshid I, Anderson L, Downie GH, Pape GS. Sickle cell disease, extreme hyperbilirubinaemia, and pericardial tamponade: case report and review of the literature. Crit Care Med 2002; 30: 2363-2367.
Shao SH, Orringer EP. Sickle cell intrahepatic cholestasis: approach to a difficult problem. Am J Gastroenterol 1995; 90: 2048-2050.
Soliman AT, Bererhi H, Darwish A, Alzalabani MM, Wali Y, Ansari B. Decreased bone mineral density in prepubertal children with sickle cell disease: correlation with growth parameters, degree of siderosis and secretion of growth factors. J Trop Pediatr 1998; 4: 194-8.
Porter JB, Huchas ER. Transfusion and exchange transfusion in sickle cell anaemias, with particular reference to iron metabolism. Acta Haematol 1987; 78: 198-205.
Fasola FA, Odaibo GN, Aken’Ova YA, Olaleye OD. Hepatitis B and C viral markers in patients with sickle cell disease in Ibadan, Nigeria. Afr. J Med Med Sci 2003; 32: 293-295.
Allain JP, Daniel C, Soldan K, Sarkodie F, Phelps B, Giachetti C, Shyamala V, et al. The risk of hepatitis B virus infection by transfusion in Kumasi Ghana. Blood 2003; 101:2419-2425.