Liver of cerebral malaria patient was void of retinol store: a first observation on vitamin a-storing cells from autopsy specimen

Abstract

Vitamin A supplement at high doses reportedly can help growth in children with malaria (Shankar, 2000; Serghides and Kain, 2002; Villamor et al, 2002). Whether the results are due to nutritional or therapeutic effect, or both, remains unclear. Literature about pathobiology of malarial liver is extremely sparse. Of rare occasion, we examined the liver of a man aged 22 years, body weight 52 kg, with Plasmodium falciparum infection who was referred to our hospital for severe cerebral malaria. The patient died at day 12 after admission, and autopsy conducted under informed consent of relatives. The removed dark brown liver, weighing 1,410 g, was investigated by fluorescence microscopy for vitamin A autofluorescence (Wake et al, 1987) and Golgi-Kopsch chromic silver technique (Wake et al, 1987) and Golgi-Kopsch chromic silver technique (Wake et al, 1988) plus opticoconfocal depth reconstruction imaging (Ekataksin et al, 2003) for visualization of hepatic stellate cells or retinol-storing arachnocytes (Ekataksin and Kaneda, 1999). Control liver was obtained from a forensic autopsy of a 45-year-old male with acute heart failure. Under wide ultraviolet, 330-385 nm excitation, the 50~100-mm-thick frozen sections of normal liver appeared with myriads of brightly glaring fluorescent spots distributed homogeneously in liver lobules, representing the lipid droplets containing vitamin A. The fluorescence faded in 20- 200 seconds. Higher magnifications revealed that each spot, located 30-50 mm apart along the sinusoids, was composed of globules of various sizes. Fluorescence was present within the lobules only, not found of the stroma. In malarial liver, the lobules were totally nonfluorescent. Hepatocytes were yellowish brown with distinct accentuation of light blue periportally. Dark pigments were discernible in the sinusoids. Under Golgi method, human arachnocytes exhibited a striking irregular shape, measuring 40-60 mm with several elongate slender processes characterized by knobs, segmental isthmi, and flexes, reminiscent of a rhizome studded with thread-like roots. Cell body was recognized with multiple lipid droplets. In malaria, the arachnocytes were visualized with more abundant cytoplasmic processes; lipid droplets were null or almost absent. The cells were not demonstrable in hematoxylin-eosin preparation, where bile plugs, intrahepatocellular biliary lysosomes, and phagosome-laden kupffer cells were prevailing. Findings are clear that in the malarial patient, liverstore of vitamin A is apparently diminished or depleted. Whether-How retinal metabolism is involved in the pathogenesis can not be determined with ceretainty in this single case observation. The present study is the first of its kind in demonstrating the retinal autofluorescence and in visualizing the arachnocyte reconstrction of human liver