Jubb T F, Jerrett I V, Browning J W, Thomas K W
University of Melbourne, Rural Veterinary Unit, Maffra, Victoria.
Aust Vet J. 1990 Mar;67(3):86-9. doi: 10.1111/j.1751-0813.1990.tb07710.x.
Postparturient haemoglobinuria occurred in 11 Holstein-Friesian cows in 8 dairy herds in East Gippsland, Victoria. The affected cows had a wide range of ages, body condition and production level. Seven of 9 cows sampled were hypophosphataemic, 4 of 8 cows examined had Heinz bodies present in erythrocytes and strong ketonuria was present in 6 of 10 urine samples tested. Herdmates having similar calving dates had mostly normal serum phosphorus levels and none had Heinz bodies. There was no evidence for dietary phosphorus (P) deficiency, hypocuprosis or excessive P drain from high production being predisposing factors. There were no cruciferous plants in the diet. Haemolysis persisted in 4 cows despite treatment to raise serum P levels. An hyposthesis is proposed for the sporadic nature and clinical manifestations of the disease. This is based on mechanisms of hypophosphataemia occurring in man and mechanisms of Heinz body formation and haemolysis in other circumstances. We suggest that hypophosphataemia occurs following recovery from preparturient keto-acidosis caused by undernutrition in late pregnancy and then becoming nutritionally replete in the early postparturient period. Circulating oxidants may cause erythrocyte damage which may be predisposed to by hypophosphataemia.
产后血红蛋白尿发生在维多利亚州东吉普斯兰地区8个奶牛场的11头荷斯坦 - 弗里生奶牛身上。患病奶牛年龄、体况和生产水平差异很大。9头采样奶牛中有7头低磷血症,8头检查奶牛中有4头红细胞内有海因茨小体,10份检测尿样中有6份强酮尿症。产犊日期相近的同群奶牛血清磷水平大多正常,且均无海因茨小体。没有证据表明日粮磷(P)缺乏、低铜血症或高产导致的磷过度流失是诱发因素。日粮中没有十字花科植物。尽管采取了提高血清磷水平的治疗措施,但仍有4头奶牛持续溶血。本文基于人类低磷血症的机制以及其他情况下海因茨小体形成和溶血的机制,对该病的散发性和临床表现提出了一种假说。我们认为,低磷血症发生在妊娠后期营养不良导致的产前酮酸中毒恢复后,然后在产后早期营养充足时出现。循环氧化剂可能导致红细胞损伤,而低磷血症可能易化这种损伤。