Profle and Characterized of Feses in Cow Milk Allergy
Widodo Judarwanto. Children Allergy Online Clinic, Jakarta Indonesia
Childhood cow’s milk allergy is a diagnosis encompassing various syndromes. Antigen-immunoglobulin E (IgE) antibody interaction is classically involved in mast cell degranulation in IgE-mediated food allergy, while non-IgE mediated cow’s milk allergy is mostly mediated by cellular mechanisms. TheA diagnosis of cow’s milk allergy largely relies on a good knowledge of the clinical expression of the disease. Growing evidence exists that exposure to cow’s milk elicits inflammation in the gut of infants with cow’s milk allergy, irrespective of symptoms.
Inflammation and increased protein leakage from the gut during a cow’s milk elimination-challenge test in fecal samples of infants presenting with different symptoms suggestive of cow’s milk allergy
Markers of inflammation in the feces
The concentrations of alpha1-antitrypsin (AT), eosinophil cationic protein (ECP), immunoglobulin (Ig) A, and cow’s milk-specific IgA antibodies, in fecal samples of 208 infants with a mean age of 7 months. Prechallenge samples were collected after a mean 3-week elimination period, and post-challenge samples were obtained 4 days after starting the challenge. Fecal levels of prechallenge total IgA and post-challenge AT were higher in infants with a positive challenge. Of these infants, pre- and post-challenge levels of ECP were higher in those reacting after 24 h than in those reacting within 1 h. Prechallenge levels of ECP were higher in those showing intestinal symptoms , and both pre- and post-challenge levels of total IgA were higher in those with an IgE-mediated reaction to cow’s milk. Regardless of the challenge result, total IgA increased during the challenge and was higher in those breast-fed until the challenge than in those fed formula only. Hence, in infants reacting to the cow’s milk challenge, higher prechallenge levels of fecal IgA indicate increased antigenic stimuli in the gut, and higher post-challenge levels of AT reflect increased protein loss as a result of intestinal inflammation. In infants with slowly evolving gastrointestinal symptoms, increased fecal ECP may help in distinguishing patients from those who tolerate cow’s milk. Individual serial follow-up of fecal IgA and ECP can be used to estimate the degree of inflammation in the gut and an appropriate time for a challenge test, but are not diagnostic tools for cow’s milk allergy
Fecal tumor necrosis factor alpha, eosinophil cationic protein
Infants with atopic eczema exhibit a specific fecal protein pattern after oral challenge with cow’s milk, characterized by an increase in both eosinophil cationic protein (ECP) and tumor necrosis factor (TNF)alpha. These study was to determine the pattern of these proteins in allergic infants with intestinal manifestations. TNFalpha, ECP and immunoglobulin E (IgE) were measured in stools from 13 infants with intestinal symptoms and 10 healthy infants. The allergic infants underwent two stool collections, one before a cow’s milk challenge and the other after the challenge, either at the onset of clinical manifestations or 15 days after the challenge if no clinical manifestations occurred. Baseline TNFalpha, ECP and IgE levels were low in all infants. The concentration of TNFalpha increased after the challenge in infants positive to challenge ( but not in those negative to challenge. ECP and IgE levels remained low after the challenge in all the allergic infants. These data confirm that fecal TNFalpha and ECP levels indicate various reaction types of food allergy and that different immunologic disturbances lead to atopic eczema or intestinal symptoms during food allergy. Fecal protein pattern can thus be a useful tool in diagnosing food allergy in infants with intestinal manifestations.
The use of fecal alpha1-antitrypsin in the monitoring of intestinal inflammation in infants with atopic eczema and food allergy was evaluated. The study material comprised 26 atopic infants with confirmed food allergy. Fecal samples were collected before an elimination diet and 3 months later for the determination of alpha1-antitrypsin.
Nine (35%) of the 26 patients demonstrated an increased fecal concentration of alpha1-antitrypsin (median 3 mg/g; range 2.8-6.4 mg/g). In all nine patients (100%) the oral cow’s milk challenge was positive as opposed to only six (35%) in those with normal alpha1-antitrypsin concentration. No further connections between alpha1-antitrypsin and other food allergies were detected. As a result of an adequate elimination diet, the fecal concentration of alpha1-antitrypsin was normalized in seven patients, with a favourable clinical response in atopic eczema in six and no improvement in one patient. These study indicate that serial determinations of fecal alpha1-antitrypsin provide a useful non-invasive tool for the detection and follow-up of intestinal inflammation in a certain group of atopic infants with cow’s milk allergy and severe inflammation of the gut.
Faecal eosinophil cationic protein and tumour necrosis factor-alpha
The concentrations of tumour necrosis factor-alpha, eosinophil cationic protein and alpha-1 antitrypsin in faeces as indicators of intestinal inflammation induced by double-blind placebo-controlled oral cow’s milk challenge in infants and young children with atopic eczema.
An increased alpha-1 antitrypsin concentration (> 2 mg/g) after cow’s milk challenge was detected in 43% of the infants positive as compared with 11% of the infants negative to challenge. The concentration of eosinophil cationic protein in faeces increased after cow’s milk challenge in patients positive to challenge but not in those negative to challenge. The concentration of eosinophil cationic protein was enhanced particularly in patients manifesting immediate-type reactions to the cow’s milk challenge. The concentration of tumour necrosis factor-alpha increased after cow’s milk challenge in patients positive to challenge but not in those negative to challenge. The concentration of tumour necrosis factor-alpha in faeces was enhanced particularly in patients manifesting delayed-type reactions to the cow’s milk challenge.
Children with atopic eczema food allergy is associated with intestinal inflammation indicating that more general immunologic disturbances than previously thought take place in these patients. Faecal eosinophil cationic protein, tumour necrosis factor-alpha and alpha-1 antitrypsin distinctly indicate various reaction types of food allergy. Parallel testing with eosinophil cationic protein and tumour necrosis factor-alpha may significantly enhance the accuracy in diagnosis of food allergy in patients with atopic eczema.
Probiotic effects on faecal inflammatory markers and on faecal IgA in food allergic atopic dermatitis syndrome infants.
Probiotic bacteria are proposed to alleviate intestinal inflammation in infants with atopic eczema/dermatitis syndrome (AEDS) and food allergy. In such infants we investigated effects of probiotic bacteria on faecal IgA, and on the intestinal inflammation markers tumour necrosis factor-alpha (TNF-alpha), alpha1-antitrypsin (AT), and eosinophil cationic protein (ECP). Infants with AEDS and suspected cow’s milk allergy (CMA) received in a randomized double-blinded manner, concomitant with elimination diet, Lactobacillus GG (LGG), a mixture of four probiotic strains (MIX), or placebo for 4 wk. Four weeks after treatment, CMA was diagnosed with a double-blind placebo-controlled milk challenge. Faecal samples of 102 infants, randomly chosen for analysis, were collected before treatment, after 4-wk treatment, and on the first day of milk challenge. After treatment, IgA levels tended to be higher in probiotic groups than in the placebo group, and AT decreased in the LGG group, but not in other treatment groups. After challenge in IgE-associated CMA infants, faecal IgA was higher for LGG than for placebo, and TNF-alpha was lower for LGG than for placebo, but non-significantly. In conclusion, 4-wk treatment with LGG may alleviate intestinal inflammation in infants with AEDS and CMA.
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