Flåøyen A, Borrebaek B, Nordstoga K
Department of Large Animal Clinical Sciences, Norwegian College of Veterinary Medicine, Oslo.
Vet Res Commun. 1991;15(6):443-53. doi: 10.1007/BF00346541.
Alveld is a hepatogenous photosensitization disease seen in lambs grazing Narthecium ossifragum pastures in Norway. Mycotoxins, possibly sporidesmin, have been suspected to cause the liver damage in alvled as in facial eczema. The histological changes in the liver of alveld cases and in lambs photosensitized after experimental sporidesmin intoxication were compared. The liver damage, characterized by necrosis in single centrilobular hepatocytes, was of the same type in both conditions. Minor to moderate portal fibroplasia and bile duct proliferation were almost always present. Accumulated glycogen was seen in hepatocytes in the centrilobular areas. This was significantly correlated to the enzymatically measured glycogen content and there was good correlation between parenchymal damage and glycogen accumulation. The glucose-6-phosphatase and glycogen phosphorylase activities were normal. These findings indicate that parenchymal damage, rather than obstruction of the bile ducts, caused the retention of phylloerythrin both in alveld cases and in experimentally sporidesmin-intoxicated lambs. The accumulation of glycogen could not be explained.
阿尔维尔德病是一种发生在挪威食用碎米荠属牧草的羔羊身上的肝源性光敏性疾病。人们怀疑霉菌毒素，可能是孢子菌素，与面部湿疹一样，会导致阿尔维尔德病中的肝脏损伤。对阿尔维尔德病病例的肝脏组织学变化与实验性孢子菌素中毒后光敏化羔羊的肝脏组织学变化进行了比较。两种情况下的肝脏损伤均以单个小叶中央肝细胞坏死为特征，属于同一类型。几乎总是存在轻度至中度的门静脉纤维增生和胆管增生。在小叶中央区域的肝细胞中可见糖原积累。这与酶法测定的糖原含量显著相关，实质损伤与糖原积累之间也有良好的相关性。葡萄糖-6-磷酸酶和糖原磷酸化酶活性正常。这些发现表明，在阿尔维尔德病病例和实验性孢子菌素中毒的羔羊中，实质损伤而非胆管阻塞导致了叶红素的潴留。糖原的积累无法解释。
