Kubanek B, Heimpel H, Paar G, Schoengen A
Blut. 1977 Aug 29;35(2):115-24. doi: 10.1007/BF00996291.
Nine patients with anorexia nervosa were studied, who had varying degrees of bone marrow failure ranging from a slight neutropenia to severe pancytopenia. In addition to routine laboratory work bone marrow biopsies were performed at admission and during the course of disease. In four of those patients erythropoietin excretion per 24 hours was measured by the bioassay in the polycythemic mouse at least twice during the course of treatment. At admission most bone marrow showed a marked although varying hypocellularity with grossly apparant background gelatinous material, which appeared to consist of acid mucopolysaccharides. Leukopenia and the changes of the bone marrow morphology reversed to normal after refeeding. Erythropoietin excretion was only elevated in patients who were anemic and returned to normal when the haematocrit reached normal levels. It seems therefore unlikely that an impaired production of erythropoietin or other postulated humoral factors cause the haemopoietic changes in anorexia nervosa. A direct effect of fat or carbohydrate depletion and/or of the increased mucopolysaccharides upon the proliferation of the haemopoietic cells can be suggested, but is an entirely speculative preposition.
对9例神经性厌食症患者进行了研究,他们有不同程度的骨髓衰竭,从轻度中性粒细胞减少到严重全血细胞减少。除了常规实验室检查外,入院时和病程中均进行了骨髓活检。其中4例患者在治疗过程中至少两次通过对红细胞增多症小鼠的生物测定法测量24小时促红细胞生成素排泄量。入院时,大多数骨髓显示出明显但程度不同的细胞减少,伴有明显的背景胶状物质,其似乎由酸性粘多糖组成。再喂养后白细胞减少和骨髓形态改变恢复正常。促红细胞生成素排泄仅在贫血患者中升高,当血细胞比容达到正常水平时恢复正常。因此,促红细胞生成素或其他假定的体液因子产生受损似乎不太可能导致神经性厌食症中的造血变化。可以推测脂肪或碳水化合物消耗和/或增加的粘多糖对造血细胞增殖有直接影响,但这完全是一种推测性的假设。