Okada S, Yutaka T, Kato T, Ikehara C, Yabuuchi H, Okawa M, Inui M, Chiyo H
Eur J Pediatr. 1979 Apr 3;130(4):239-49. doi: 10.1007/BF00441360.
Neuraminidase deficiency towards fetuin, 2 leads to 3 sialyllactose and 2 leads to 6 sialyllactose was found in cultured skin fibroblasts from a 10-year-old Japanese girl who exhibits craniofacial dysmorphism, a short neck, vertebral and pelvic deformities and macular cherry-red spots. Neuraminidase deficiency in this case seems the primary enzyme defect because the enzyme activity of her parents was intermediate. In addition, beta-galactosidase in leukocytes and cultured skin fibroblasts from the patient was found to be severely deficient, but could be detected in serum and urine. In the parents, beta-galactosidase activity was normal. There were moderately increased levels of urinary sialic acid-rich oligosaccharides and glycopeptides in the patient. The clinical and biochemical observations suggest that this case is very close to mucolipidosis I.
在一名10岁日本女孩的培养皮肤成纤维细胞中发现,其对胎球蛋白的神经氨酸酶缺乏导致产生3 -唾液酸乳糖和2 -唾液酸乳糖。该女孩表现出颅面畸形、短颈、脊柱和骨盆畸形以及黄斑樱桃红斑。在这种情况下,神经氨酸酶缺乏似乎是主要的酶缺陷,因为其父母的酶活性处于中间水平。此外,发现该患者白细胞和培养皮肤成纤维细胞中的β-半乳糖苷酶严重缺乏,但在血清和尿液中可检测到。其父母的β-半乳糖苷酶活性正常。该患者尿中富含唾液酸的寡糖和糖肽水平中度升高。临床和生化观察表明,该病例与黏脂贮积症I非常接近。