3例とも入院中に末梢血中の芽球の消失を認めたため化学療法を行わなかったが，2例は肝線維症が進行悪化し死亡した。肝病理検査では全例で芽球は検出されなかったが，さまざまな程度に線維化を認めた。さらに，中等度以上に進行した肝線維化の所見を認めた症例の生命予後は不良であった。日齢34に肝生検，ならびに日齢90に剖検を行った児では，生検施行前に芽球が消失していたにも関わらず，小葉構造の乱れを伴う肝線維症が進行していた。
肝線維化マーカーについては，ヒアルロン酸は胆汁鬱滞型肝障害の臨床経過と類似の傾向を示したが，その他のマーカーは臨床経過との明らかな相関を示さなかった。
今回の検討から，小葉構造の乱れを伴うほど線維化が進行した場合には，予後が悪い可能性が示唆された。また，肝線維化マーカーが肝線維化の有効な指標になりうるとはいえなかった。今後生検よりも非侵襲的でかつ的確に肝線維症の予後を予測しうる指標，ならびに，芽球消失後も進行し続ける肝線維化の病態の解明および治療法の確立が望まれる。
Chemotherapy was not selected as a clinical intervention because blast cells disappeared from peripheral blood in all three patients during hospitalization. In all patients, no blast cells were found in pathological examination of the liver specimens, although various levels of hepatic fibrosis were observed. Two infants with a histologically proven moderate to severe degree of hepatic fibrosis died of progressive hepatic fibrosis. We observed the progression of fibrosis in one patient after the disappearance of blast cells, at biopsy at 34 days and autopsy at 90 days of age.
Among the serum markers for hepatic fibrosis, the level of hyaluronic acid varied with the degree of hepatic fibrosis during the development of liver damage with cholestasis； however, the other markers showed no clear correlation with the clinical course. In summary, prognosis is poor for infants with TAM, in whom hepatic fibrosis progresses to destroy the hepatic lobular architecture. However, we cannot be certain that the serum markers for hepatic fibrosis can predict hepatic fibrosis to the same degree as does pathological examination of liver specimens. A less invasive method than liver biopsy should be investigated. Finally, the need exists for an appropriate medical intervention protocol in the management of TAM.
