Details

Autor(en) / Beteiligte

• BEKAERT, E. D.
• DOLE, E.
• DUBOIS, D. Y.
• BOUMA, M.-E.
• LONTIE, J-F.
• KALLEL, R.
• MALMENDIER, C. L.
• AYRAULT-JARRIER, M.

Titel

Alterations in lipoprotein density classes in infantile visceral Leishmaniasis: presence of apolipoprotein SAA

Ist Teil von

• European journal of clinical investigation, 1992-03, Vol.22 (3), p.190-199

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

1992

Quelle

MEDLINE

Beschreibungen/Notizen

• . This study describes the alterations in the plasma lipoproteins from nine young Tunisian children with active visceral Leishmaniasis. The plasma lipid profile from affected patients was characterized by a marked hypertriglyceridaemia associated with reduced levels of total and high density lipoprotein (HDL)‐cholesterol and a significant increase in the plasma ratio of unesterified to total cholesterol. Quantitative determination of plasma apolipoproteins revealed significantly decreased levels of all measured apolipoproteins, especially of apolipoproteins A‐I and A‐II, with the exception of apolipoprotein E, the levels of which were markedly increased. Moreover, at least two isoforms of the apolipoprotein serum amyloid A (SAA), an acute phase protein, were detected in all patients' plasma using two‐dimensional electrophore‐sis. Immunochemical evidence was presented that apolipoproteins E and SAA, although both primarily associated with apolipoprotein A‐ (A‐I and A‐II) as well as with apolipoprotein B‐containing lipoproteins, could occur as LP‐E and LP‐SAA subspecies, devoid of apolipoproteins A and B. However, it should be pointed out that LP‐SAA particles were found in HDL2 from only two patients whereas the abnormal LP‐E particles were detected in LDL and HDL2 from all investigated patients. The polydispersity and heterogeneity of patients' HDL3 were assessed by electron microscopy. It was further suggested that the profound changes in the lipoprotein metabolism of these young patients may be due to the increased hepatic synthesis of apolipoprotein SAA and/or to their altered immune function during active visceral Leishmaniasis.