Cochet B, Griessen M, Balant L, Infante F, Vallotton M C, Bergoz R
Schweiz Med Wochenschr. 1981 Feb 7;111(6):192-3.
To determine the sensitivity and specificity of breath hydrogen (H2) in detecting lactase deficiency, breath H2 collected by end-expiratory sampling and capillary blood glucose were measured after ingestion of 50 g of lactose in 36 patients with biopsy-proved isolated lactase deficiency, 42 with normal lactase activity and 6 with lactase deficiency secondary to mucosal lesions. All patients had digestive symptoms clinically compatible with lactose malabsorption. The maximum increase in breath H2 concentration was more than 1.1 mumol/l (25 ppm) in all patients with isolated lactase deficiency, and less than 0.88 mumol/l (20 ppm) in 88% of patients with normal lactase activity; there were 5 false-positive results, attributed in one case to small bowel colonization and in another case to rapid transit after gastric surgery. Secondary lactase deficiency was accurately detected by neither breath H2 nor blood glucose.
为确定呼气氢(H₂)检测乳糖酶缺乏症的敏感性和特异性,对36例经活检证实为单纯乳糖酶缺乏症、42例乳糖酶活性正常以及6例继发于黏膜病变的乳糖酶缺乏症患者,在摄入50克乳糖后,通过呼气末采样测定呼气H₂,并检测毛细血管血糖。所有患者临床上均有与乳糖吸收不良相符的消化症状。所有单纯乳糖酶缺乏症患者呼气H₂浓度的最大增幅均超过1.1微摩尔/升(25 ppm),而88%乳糖酶活性正常的患者增幅小于0.88微摩尔/升(20 ppm);有5例假阳性结果,1例归因于小肠细菌定植,另1例归因于胃手术后肠道蠕动加快。呼气H₂和血糖均不能准确检测出继发性乳糖酶缺乏症。