JOURNAL REPORT Lactose intolerance and Galactosemia Lactose intolerance: Common Misunderstanding Founded on the article's background, the lactose intolerance refers to the syndrome that condemned to the inadequate enzyme called lactase found in the brush border of the small bowel mucosa. This enzyme lactase is essential to convert lactose from galactose to glucose. If this lactose is not digested, it will threaten the fermentation of the gut microbiota which has led to the symptoms of lactose intolerance. It is also pointed out that the lactose intolerance and the cow's milk allergy present similarity based on the clinical manifestation of gastrointestinal disorder that could be misconception on their part. Based on the finding of this article, the difference between the lactose intolerance and cow's milk allergy is the adverse food reaction whereas the immune-mediated reactions in cow milk's allergy such as food allergy and celiac disease that are explicit by the proteins while the non-immune mediated in lactose intolerance comply to the food intolerances such as enzymatic defects, transport defects, pharmacological, and other unknown triggers. To extract this information let's talk about the lactose intolerance syndrome. It is stated that there are three types of lactose intolerance, and these various factors are intermitted to the lactase deficiency. First, the congenital lactase deficiency (CLD), this factor submerged to the low average of lactase activity from a mutation in lactase phlorizin hydrolase gene (LPH). Since it is adverse to the mutation in genes, it must be already distinguished from the third trimester of pregnant women that there is a lack of production in lactase. Second, factor of primary lactose intolerance or adult-type. This implies the intestinal lactase expressions which result to the difficulty of digesting dairy product in childhood or adolescence. This is the most common type of lactose intolerance that greatly affected 70% of the adult in global population. The main aspect of this factor is that those people who acquire primary lactose intolerance they produce a plenty of lactase in their starting life. As time passed by, as there are changes of food intake such as milk into other formulas, there will be decreasing production of lactase. Lastly, the secondary lactase deficiency which is derived from the intestinal damage that leads to pathologic condition. This means that any interruption occurs from small intestine will affect the production of lactase. In the management of lactose intolerance and CMA on nutritional issues, it is essentially to avoid causative food of the diet. Therefore, for lactose intolerance, it is better to avoid the food contain dairy products, all kinds of milk, butter, cottage cheese, ice cream and etc. On the other hand, cow's milk allergy (CMA), it is rather to avoid such small protein doses in the diet. In addition, clinical trials also play an important role to accumulate the safe and proper lactose dietary levels for moderately and severely undernourished children as stated in the article. The aspect of this article is help to conceptualize the major differences of lactose intolerance and cow's milk allergy that are often labeled as symptoms of "milk allergy". Both of these syndromes may have similar symptom, but they have different mechanisms. Therefore, it is very important to understand and identify these differences in order to avoid such an indication of food restriction or management. Thus, this article contributes to the patient and parents who are mistaken with the similarity of lactose intolerance from cow's milk allergy. Galactosemia Based on the exploratory article of galactosemia, it is initially described in the early 1900s by von Reuss. Galactosemia is defined as the autosomal recessive inborn error of carbohydrate metabolism that characterized by the inability to convert galactose to glucose. In this articulation, galactosemia exhibits pathway that was defined by Louis Leloir who won the Nobel Prize in Chemistry in year 1970. This pathway includes the three enzymes which is the active form in Leloir pathway namely; galactokinase (GALK), galactose-I-phosphate uridyltransferase (GALT), and uridine diphosphate (UDP)-galactose 4-epimerase (GALE). This enzyme is chained to one another, if there is a deficiency, it will results to form galactosemia. This deficiency will lead to causations over than 250 mutations in the GALT gene that mainly affect the newborn which will deteriorate the well-being of the patient. Furthermore, the galactose is the main unit of this topic; galactose is very essential carbohydrates to the supplementation for the infants that serve as a source of energy. This is evident in milk products which are present in both human and bovine milk. In typical galactosemia, it is found out that the main toxic metabolite present is the Gal-I-P and it acts as both the primary marker to identify affected patients and then as therapeutic in their management. Nevertheless, there are three categories of GALT deficiency includes the most severe is classic galactosemia, clinical variant galactosemia and Duarte galactosemia. These various categories differ in the residual enzyme activity. In this article, the different recommended formulas for infants with Galactosemia has presented such as the soy-based formulas including ProSobee, Similac Isomil, and the elemental formulas contain PurAmino, Nutramign, Pregestimil, Elecare, Alimentum and Neocate. This is very important information for those infants with Galactosemia that serves as alternation of milk products. In the early prognosis of galactosemia, it is strictly advised to place the newborn on newborn screening programs to alleviate and treat the possible concern on galactosemia. This definitive diagnosis is done by measuring galactose-I-phosphate levels and GALT enzyme activity and with molecular genetic testing. For the early detection of galactosemia on newborn, a galactose regimen should be prohibited. In conclusion, galactosemia is a genetic disorder that results in clinical manifestation such as feeding intolerance, jaundice lethargy, hypotonia, vomiting, and poor weight gain. If left untreated, it may lead to death or serious condition. Thus, an early prognosis may sustain the capability of the newborn to improve and may have early treatment for eradicating this condition. Therefore, this article contributes to the sense of parents, patients and public health to demand for the goodness of newborn screening program.
