Hepatic Injury in Chronic Hypervitaminosis A

Abstract

A 6-year-old girl who suffered from chronic hypervitaminosis A developed hepato\x=req-\ splenomegaly, hepatic dysfunction, and hypersplenism. A liver biopsy specimen displayed large lipid laden Kupffer's cells which were shown to contain vitamin A by fluorescence microscopy. Electron microscopically hepatic injury was indicated by increased lysosomes, focal cytoplasmic degradation, and numerous "light" and "dark" cells. These nonspecific indications of liver cell damage may reflect intracellular release of the biologically active alcohol of vitamin A.The association of hepatosplenomegaly and chronic hypervitaminosis A has been recognized since the description of Josephs ] in 1944. However, few clinicopathological correlations have been reported. In this communication we describe the hepatic changes observed by light, fluorescence, and electron micros¬ copy in a 6-year-old girl with he¬ patic dysfunction and hepatosplenomegaly resulting from chronic excess ingestion of vitamin A.

Accumulation of Vitamin A in the Hepatic Stellate Cell of Arctic Top Predators

“…As we demonstrated in this study, the localization of stored vitamin A in the arctic animals was essentially the same as that published previously in normal rat and human liver, namely HSCs (Wake, 1971; Wake, 1988; Blomhoff and Wake, 1991; Senoo et al, 2010, 2011). In hypervitaminosis A in human and rat (Stimson, 1961; DiBenedetto, 1967; Rubin et al, 1970; Muenter et al, 1971; Hruban et al, 1974; Russell et al, 1974; Jacques et al, 1979), vitamin A spills out from HSCs into the portal area (Glisson's sheath) (Wake, 1971; Wake, 1988; Blomhoff and Wake, 1991, plasma, and other organs (Rodahl and Davies, 1943; Rodahl and Moore, 1943; Rodahl, 1949, 1950; Biesalski, 1989). In polar bear, arctic fox, glaucous gull, and bearded seal, the liver has vitamin A levels that are comparable to hypervitaminosis A in human and rat, the portal area did not show vitamin A autofluorescence or positive gold chloride staining (Fig.…”

Hepatic Hypervitaminosis A

“…Chronic hypervitaminosis A, frequently responsible for bone, cutaneous, or neurologic manifestations, also causes hepatic injury. Although the liver involvement was recognized very early (I), clinicopathological correlations have been reported only in seven pediatric patients (2)(3)(4)(5)(6)(7). We report four new cases of the same sibship, and the evolution of two of them after vitamin A withdrawal.…”

Vitamin A abuse: development of cirrhosis despite cessation of vitamin A. A six‐year clinical and histopathologic follow‐up

“…Chronic liver hypervitaminosis A may remain unrecognized for many years, but eventually results in severe liver disease. Histological changes include hypertrophy and an increased number of perisinusoidal lipocytes (Ito cells), damage to the sinusoidal barrier and fibrosis (2)(3)(4)(5)(6). The Ito cells contain an enhanced amount of lipid vacuoles.…”

“…Their hyperplasia can also be observed in the absence of concomitant hepatic fibrosis (7). Examination of fresh material under UV light demonstrates fading vitamin A fluorescence in these perisinusoidal storage cells (2)(3)(4)(5)(6)(7).…”