We thank our correspondents for the interesting contributions in response to our article on carbohydrate malabsorption (1).
In actual fact, in routine clinical practice? the terms of hereditary fructose intolerance (metabolic defect) are often confused with fructose malabsorption. For this reason we separated these terms in our article, and gastrointestinal carbohydrate intolerance relates only to resorption disorders of the bowel.
The main focus of our article in particular was on carbohydrate mediated intolerance mechanisms. For this reason, hereditary causes need to be included in the differential diagnostic evaluation, especially as these disorders often manifest after ingestion of foodstuffs containing fructose or galactose and are then misinterpreted as allergies to milk/fruit or lactose maldigestion. We thank Professor Mönch for mentioning galactose 1 phosphate uridyltransferase and the neonatal screening program introduced in 2002. Owing to space restrictions we listed in Table 1 only one of the possible enzyme defects in galactosemia, as an example: the reaction catalyzed by galactokinase.
As Riechmann et al. say in their letter to the editor, standardized provocation tests for the normal population to confirm the diagnosis of carbohydrate intolerance and for reporting real prevalence rates are lacking. For this reason we included under “Definition of carbohydrate intolerance” the estimated data for the population of Europe (lactose 7–20%, fructose 15–25%, sorbite 8–20%); the variations show that substantial differences exist within Europe and that people of southern or Asian origins are far more likely to suffer from lactose maldigestion.
The “prevalence of 30–40%” cited by Riechmann and colleagues relates to all non-immunological food intolerances (carbohydrate intolerance, alcohol intolerance, fat intolerance syndrome, biogenic amines, salicylates, sulfites, etc), which cumulatively can account for 30–40% (1–3).
The gold standard for the diagnostic evaluation of carbohydrate intolerance is the oral provocation test in patients, which is best combined with an H2 breath test. As we underlined, the mere rise in the hydrogen gas curve in asymptomatic patients is a mere sign of asymptomatic malabsorption, which by itself does not require any dietary restrictions. Overestimating the meaningfulness of the H2 breath test alone would certainly incur a risk of panic (1, 2, 4).
We mentioned that patients with carbohydrate intolerance confirmed in such a way can tolerate a certain amount of carbohydrate up to the individual threshold level, so that individual dose adjustment is required. It is therefore an essential therapeutic task to restore a dose reduction in carbohydrates into limited range by means of professional diet advice and training for patients.
Compared with the estimated prevalence rates of gastrointestinal malabsorption that we reported, the prevalence rates of carbohydrate intolerance are much higher in patients with functional symptoms, such as irritable bowel syndrome, and allergies (1, 4).
In this setting, the differential diagnostic evaluation should actively search for such intolerances (see also Table 2 in ), because certain patient cohorts can receive crucial help thanks to this knowledge (1, 2, 4).
On behalf of the authors
Prof. Dr. med. Peter Christopher Konturek
Klinik für Innere Medizin II, Thüringen Klinik Saalfeld
Rainweg 68, 07318 Saalfeld
Conflict of interest statement
The author declares that no conflict of interest exists.
|1.||Raithel M, Weidenhiller M, Hagel AFK, Hetterich U, Neurath MFK, Konturek PC: The malabsorption of commonly occurring mono- and disaccharides—levels of investigation and differential diagnosis. Dtsch Aerztebl Int 2013; 110(46): 775–82 VOLLTEXT|
|2.||Stein J, Kist M, Raithel M: Erkrankungen durch Nahrungsmittel (Food-borne diseases) 1st edition. Stuttgart: Wissenschaftlich Verlagsgesellschaft 2011; 1–472.|
|3.||Skypala I: Adverse food reactions – an emerging issue for adults. J Am Diet Assoc 2011; 111: 1877–91 CrossRef MEDLINE|
|4.||Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG: A diet low in FODMAPs reduces symptoms of Irritable Bowel Syndrome. Gastroenterology 2014; 146: 67–75 CrossRef MEDLINE|