Sakurai I, Skinsnes O K
Int J Lepr Other Mycobact Dis. 1977 Oct-Dec;45(4):343-54.
Histochemical studies were made of pigmented cutaneous lesions from three cases of lepromatous leprosy treated with B663 to determine the nature and histogenesis of the brown pigmentation which develops as a side effect of the drug. One case of DDS-treated leprosy and four cases of untreated leprosy were also investigated histochemically as controls. The brown pigmentation of the skin is due to deposition of a ceroid-like substance in the macrophages, which is a yellowish-brown, acid-fast lipid pigment. It is insoluble in fat solvents and accepts lipid dyes even after lipid extraction by fat solvents. The macrophages in the B663-treated leprosy contain more neutral fat and less phospholipid than the untreated lepromatous leprosy tissues. Ceroid in the macrophages probably originated from unsaturated fatty acids of the leprosy bacilli through oxidation or their binding with the drug. Crystals of the drug were not found in the macrophages in this series, even on the tissues embedded in carbowax or frozen sections.
对3例用B663治疗的瘤型麻风患者的色素沉着性皮肤损害进行了组织化学研究，以确定作为药物副作用出现的褐色色素沉着的性质和组织发生。还对1例用氨苯砜治疗的麻风患者和4例未治疗的麻风患者进行了组织化学研究作为对照。皮肤的褐色色素沉着是由于类蜡样物质沉积于巨噬细胞内，这是一种黄棕色、抗酸的脂质色素。它不溶于脂肪溶剂，即使在用脂肪溶剂提取脂质后仍能接受脂质染料。与未治疗的瘤型麻风组织相比，用B663治疗的麻风患者的巨噬细胞含有更多的中性脂肪和更少的磷脂。巨噬细胞中的类蜡样物质可能源于麻风杆菌的不饱和脂肪酸通过氧化或与药物结合。在本系列中，即使在包埋于聚乙二醇或冰冻切片的组织中，也未在巨噬细胞中发现药物晶体。
