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Secondary hypolactasia is a type of acquired hypolactasia caused by a diffuse lesion of the intestinal mucosa.
It occurs in persons with considerable enzymatic activity who suffer a diffuse lesion of the intestinal mucosa develops
due to different causes. When the microvellosities are damaged, this leads to a reduction in the activity of all the
disaccharides, but lactase is the enzyme most affected (1). In fact, intolerance to milk may be the only clinical
symptom of this generalised disaccharide deficit (1).
• The evolution of this secondary intolerance depends on the seriousness and progression of the damage caused to the mucosa.
• Of all the disaccharides studied, lactase is the one that is reduced the most in pathologies affecting the brush border membrane and in some cases it is the only disaccharide affected (2). As the cause leading to the damage to the mucosa starts to diminish, as occurs in celiac disease with a gluten-free diet, the enzymatic activity increases. The activity of saccharase and maltase quickly returns to normal but on the contrary, the lactase activity takes longer to recover. For this reason it can be considered that the activity of lactase is the one that is most sensitive to damage in the mucosa(1).
The causes of secondary hypolactasia include: diseases of the small intestine, multi-systemic diseases and
iatrogenic causes that refer to a state, disease or disorder caused by physicians, medical treatments or drugs (3,4).
The key causes of secondary hypolactasia are shown in the following table.
Causes of secondary hypolactasia include reference (4) • In AIDS, the prevalence of microsporidiosis associated with hypolactasia may reach 50%. 70% of patients
infected by HIV suffer from lactose malabsorption, unlike 34% of control patients. In addition, the severity
of the lactose malabsorption increases in more advanced stages of the disease. In general secondary
hypolactasia is reversible once the underlying cause has been treated, but recovery may require 6 months or
more of dietetic therapy (5).
• The intestinal inflammation is often associated with an alteration in absorbing fluids, electrolytes and
nutrients, both in inflamed areas and in non-inflamed parts of the intestine. Patients with Crohn’s disease show
a significant reduction in the enzymes of the brush border membrane (disaccharidases) but not in cytoplasmatic
enzyme activity (dipeptidases). In such patients, there are changes in jejunal disaccharide activity, shown in
abnormal lactose tolerance tests; this suggests a deficit in lactase activity (6).
• In Celiac disease, there is a moderate to severe atrophy of the intestinal microvilli, a reduction in the
epithelial surface and an alteration of the cell architecture which provokes a reduction in the disaccharide
activity. In these patients, enzymatic activity is improved with the recovery of the histological alterations in
patients with this disease in remission, after following a gluten-free diet. The detection of a deficit in lactase
activity is important, since eliminating the intake of dairy products in this type of patient leads to a great
improvement in their symptoms; so much so that patients with adult-type Celiac disease will not improve any
further after restricting gluten until milk has been removed from their diet (2).
• Diseases caused by parasites, such as giardiasis, cryptosporidiosis and others that affect the proximal
small intestine may lead to lactose malabsorption due to a direct effect on the intestinal epithelial cells (7).
• In Whipple’s disease, a chronic systemic bacterial infection which mostly affects middle-aged men, the
agent causing this disease has been identified as Tropheryma Whippelii. This condition is cured by anti-microbial
treatment. Weight loss and diarrhoea are the most common symptoms. The jejunal microvilli are distended
and infiltrated with macrophages, with variable atrophy. The area most affected is the intestine, with weight
loss, diarrhoea and malabsorption (the most frequent symptom) and to a lesser extent, abdominal pain (8). In
this disease the duodenum usually presents abnormalities and the clinical symptoms of intestinal bleeding and
anaemia suggest epithelial damage. Changes have been shown in the intestinal mucosa, indicating functional
deficits. The lactase activity is reduced or even absent (9).
• In children with gastroenteritis that is severe enough to warrant their being admitted to hospital, one
common complication is sugar intolerance. Of all the predisposing factors, the most important one is viral
infection, particularly due to rotavirus (10). The infection causes damage to the small intestine and a loss of
epithelial cells in the intestinal vellosities. The immature epithelial cells that replace the lost ones are often
lactase-deficient, which leads to a secondary lactase deficit and lactose intolerance (7). It is important to
recognise the presence of lactose malabsorption which may complicate acute gastroenteritis as a differentiating
condition from post-enteritis syndrome, which may cause diarrhoea and difficulties in recovery (9).
1. Bayless TM, Christopher NL. Disaccharidase deficiency. Am J Clin Nutr. 1969 Feb;22(2):181-90.
2. Plotkin GR, Isselbacher KJ. Secondary disaccharidase deficiency in adult celiac disease (nontropical sprue) and other malabsorption states. N Engl J Med. 1964 Nov
12;271:1033-7.
3. Alliende FG. Intolerancia a la lactosa y otros disacáridos. Gastr Latinoam 2007; 18(2):152-6
4. Swagerty DL, Walling, AD Klein RM. Lactose Intolerance. American Family Physician 2002; 65(9):1845-50.
5. Book Review: Coulston AM, Boushey CJ (editors). Nutrition in the Prevention and Treatment of Disease. 2nd ed. Elsevier Academic Press; 2008. 912 pp. ISBN 13:978-012-
374118-9.
6. Dunne WT, Cooke WT, Allan RN. Enzymatic and morphometric evidence for Crohn’s disease as a diffuse lesion of the gastrointestinal tract. Gut. 1977 Apr;18(4):290-4.
7. Luna Gil NCI, Pereira Scromeda MC, Elena TorresE, Rott CM. Intolerancia a la lactosa en pediatría. Revista de Posgrado de la VIa Cátedra de Medicina Febrero 2010; 198:16-20.
8. Ratnaike RN. Whipple’s disease. Postgrad Med J. 2000 Dec;76(902):760-6.
9. Ectors NL, Geboes KJ, De Vos RM, Heidbuchel HP, Rutgeerts PJ, Desmet VJ, Vantrappen GR. Whipple’s disease: a histological, immunocytochemical, and electron microscopic
study of the small intestinal epithelium. J Pathol. 1994 Jan;172(1):73-9.
10. Trounce JQ, Walker-Smith JA. Sugar intolerance complicating acute gastroenteritis. Arch Dis Child. 1985 Oct;60(10):986-90.

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