Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously, we reported the effectiveness of treatment with oxatomide (O), an antihistamine, plus dextromethorphan (D), and that of Bakumondo-to (B), an herbal drug that inhibits the activation of C-fibers, in patients with persistent coughing after upper-airway infection. In this study, we evaluated the efficacy and side effects of combination therapy (O + D + B) in patients with postinfectious persistent cough. Patients who had been coughing for more than three weeks and had a history of upper-airway infection took part in the study. None had any history of nasal disease, gastroesophageal reflux, bronchial asthma, or other chronic pulmonary disease. All patients were non-smokers, and none used angiotensin converting enzyme (ACE) inhibitors. All had normal chest roentgenograms and normal pulmonary function. The following hematological data were obtained before treatment: peripheral eosinophil counts. CRP levels, serum IgE concentrations, and titers of cold agglutinins and antibodies to Mycoplasma pneumoniae. The effects of one week of treatment with O + D + B on the severity of coughing, as estimated with a cough diary, were examined. Thirty-six patients entered the study, but only 18 with normal hematological findings who satisfied the study criteria were eligible for efficacy and side-effect analyses. Cough scores decreased significantly from 5.1 +/- 2.4 (range, 2-9) to 1.2 +/- 1.9 (range, 0-6), and the rate of cough disappearance was 50%. Two patients reported slight drowsiness. Therapy with O + D + B reduced perception of coughing as estimated with a cough diary. These results suggest that this therapy (O + D + B) may be useful in patients with postinfectious persistent cough.
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PMID:[A pilot phase II study of combination therapy with oxatomide, an antihistamine, plus dextromethoraphan and bakumondo-to, an herbal drug, in patients with postinfectious persistent cough]. 969 46

The prevalence of cow's milk allergy is stable, between 2% and 5%. Clinical symptoms are numerous. Gastroesophageal reflux and persistent constipation have been recently described. The main point is the increasing prevalence of multiple food allergens. Double blind placebo controlled milk challenges are mandatory for the diagnosis, sometimes eight days long. The proof of the IgE-dependent sensitization, or of lymphocyte activation is not always brought. ECP, methylhistamine and tryptase dosages coupled to challenges are not clearly informative tests. The eviction of dairy products is completed by substitution by casein hydrolysates or pork collagen or soy hydrolysates, or by formula made from amino acids. Tolerance protocols are not standardized, however valuable. Review documented by 98 references.
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PMID:Cow's milk allergy. 1044 1

Cow's milk allergy affects approximately 2% of infants under 2 years of age. This review summarizes the recent advances in understanding its pathophysiology and immunological mechanisms. Apart from IgE-mediated atopic manifestations, T cell-mediated reactions have been demonstrated in infants with cow's milk allergy. The clinical spectrum ranges from immediate-type reactions, presenting with urticaria and angioedema to intermediate and late-onset reactions, including atopic dermatitis, infantile colic, gastro-oesophageal reflux, oesophagitis, infantile proctocolitis, food-associated enterocolitis and constipation. The exact mechanisms of these disorders are still poorly understood. Double-blind, placebo controlled food challenge, the definitive diagnostic test for cow's milk allergy, is increasingly being replaced by the measurement of food-specific antibodies, in combination with skin-prick or atopy patch testing. The treatment of cow's milk allergy relies on allergen avoidance and hypoallergenic formulae, or maternal elimination diets in breast-fed infants.
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PMID:Cow's milk allergy in infancy. 1204 18

Eosinophilic esophagitis, long known to be a feature of acid reflux, has recently been described in patients with food allergies and macroscopically furrowed esophagus. The pathophysiology and optimal management of patients with eosinophilic esophagitis is unclear. We describe our clinical experience related to eosinophilic esophagitis and obstructive symptoms in children and propose etiopathogenesis and management guidelines. Twelve children with obstructive esophageal symptoms (11 male), median age 5 years, and identified to have eosinophilic esophagitis with > 5 eosinophils per high-power field (eos/hpf) are reported. Of these, four had strictures, six had impactions, and two had only dysphagia. A diagnostic evaluation included esophagogastroduodenoscopy with biopsies in all and upper gastrointestinal series, IgE, radioallergosorbent tests, and skin tests for food allergies in some cases. Esophageal histology specimens were independently analyzed for eosinophil density by two authors. Four of five children with > 20 eos/hpf responded to elimination diets/steroids. The fifth child responded to a fundoplication. Seven children had 5-20 eos/hpf and three of them with no known food allergies responded to antireflux therapy alone. Three others in this group with positive food allergies responded to treatment with elimination diets and/or steroids. The seventh patient in this group was lost to follow-up. In conclusion, on the basis of response to therapy, eosinophilic esophagitis can be subdivided into two groups: those with likely gastroesophageal reflux disease if < 20 eos/hpf and no food allergies, and others with allergic eosinophilic esophagitis associated with food allergies and often with > 20 eos/hpf.
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PMID:Eosinophilic esophagitis: strictures, impactions, dysphagia. 1264 86

Eosinophilic bronchitis is a recently described condition in patients with chronic cough, sputum eosinophilia, normal spirometry and no evidence of bronchial hyperreactivity. The aim of the study was to assess the causes of chronic cough and to identify the prevalence of eosinophilic bronchitis as a cause of chronic cough. Thirty-six patients [mean age 45.4 +/- 14.3 years (range 16-69 years), M/F: 4/32] with an isolated chronic cough lasting for more than 4 weeks were recruited from the outpatient clinic. In all patients, after a full history and physical examination, blood eosinophil count, eosinophilic cationic protein (ECP), serum total and specific IgE levels were measured. Spirometry, methacholine provocation test, skin prick tests, ear, nose and throat examination, induction of sputum and esophageal pH testing were performed. The mean duration of cough was 31.3 +/- 52.3 months. Sputum eosinophilia greater than 3% was present in 12 (33.3%) patients and they were diagnosed as eosinophilic bronchitis. Their induced sputum had a mean eosinophil count of 8.3% and a mean ECP level of 98.5 mg x l(-1), which were higher than the others (P=0.003, both). The diagnosis of the remaining patients were postnasal drip syndrome in eight, gastroesophageal reflux disease in eight, post-infectious cough in two and cough-variant asthma in one patient. In conclusion, eosinophilic bronchitis is an important cause of chronic cough and should be considered in the assessment of patients before regarding them as having idiopathic chronic cough.
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PMID:Eosinophilic bronchitis as a cause of chronic cough. 1281 57

Twenty-two children (13 boys and 9 girls) with chronic cough were treated with the leukotriene receptor antagonist montelukast (Singulair tbl. 5 mg) administered once daily for four weeks. In 14 children (68%), the cough ceased during the third week of treatment. Children responding to montelukast were found to have higher blood levels of eosinophil cationic protein (S-ECP) in the pretreatment blood sample than children with no response (responders 14.88+/-2.651 microg/l versus nonresponders 6.62+/-0.948 microg/l; p<0.01). Blood S-ECP levels remained higher also in the post-treatment blood sample in responders (10.55+/-1.631 microg/l) compared to nonresponders (6.13+/-0.937 microg/l; p<0.05). The difference is statistically significant. There were also differences in absolute eosinophil blood count and IgE blood levels between the two groups in the pretreatment blood sample. Using 24-hour pH-metry, two children not responding to therapy were subsequently diagnosed to have gastroesophageal reflux. Judging from the results, one might deduct that patients with chronic cough who have increased levels of serum ECP and absolute eosinophil blood counts are likely to benefit from treatment with montelukast.
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PMID:Treatment of chronic cough in children with montelukast,a leukotriene receptor antagonist. 1558 30

Cow milk protein intolerance (CMPI) affects 3% of infants under the age of 12 months and is often misdiagnosed as GERD or colic, risking dangerous exposure to antigens. Most infants out grow CMPI by 12 months; however, those with IgE-mediated reactions usually continue to be intolerant to cow's milk proteins and also develop other allergens including environmental allergens that cause asthmatic symptoms. Clinical manifestations of CMPI include diarrhea, bloody stools, vomiting, feeding refusal, eczema, atopic dermatitis, urticaria, angioedema, allergic rhinitis, coughing, wheezing, failure to thrive, and anaphylaxis. The research and literature showed that CMPI is easily missed in the primary care setting and needs to be considered as a cause of infant distress and clinical symptoms. This article focuses on correctly diagnosing CMPI and managing it in the primary care setting.
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PMID:The diagnosis and management of cow milk protein intolerance in the primary care setting. 1641 42

While most patients respond well to conventional antiasthmatic therapy as outlined in current guidelines, a small percentage, however, have severe disease which is relatively or completely unresponsive to inhaled as well as oral medications. These patients who often have a long-standing "career" in asthma are frequently labeled steroid-resistant or difficult-to-control but this group of patients is not well defined. It is likely that a number of mechanisms contribute to therapy-resistant asthma such as socioeconomic status, mental disturbances but also characteristics of the individual subgroups within the syndrome of asthma such as aspirin-exacerbated airway disease or intrinsic asthma. A thorough and systematic approach is required in the work-up of these patients which sometimes involves repeated evaluations to determine that asthma and not other diseases such as chronic obstructive pulmonary disease (COPD), emphysema, gastroesophageal reflux, congestive heart failure and many others which can mimic asthma are present. Issues relating to compliance with prior or future therapies are warranted and doctor-patient communication should be checked. A meticulous search for possible triggers such as cigarette smoking, occupational allergens and comorbid conditions should be included in the work-up. High-dose combination therapy including frequent bursts or maintenance therapy with systemic corticosteroids is often necessary. Alternative therapies such as methotrexate and other immunosuppressants should be avoided based on current data but recent evidence from controlled studies suggests that anti-IgE or anti-tumor necrosis factor-(TNF-)alpha strategies might be of benefit in these patients. There is data that different phenotypes of therapy-resistant asthma might exist but little if any evidence to suggest a single phenotype of therapy-resistant asthma.
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PMID:[Therapy-resistant asthma--a distinct phenotype?]. 1660 86

A 73-year-old woman without a history of allergic diseases visited our hospital complaining of sore throat and nocturnal cough. Blood tests showed marked eosinophilia (18000/mm(3);WBC 21900/mm(3), Eos 82.0%) with normal serum levels of C-reactive protein, non-specific and various allergen-specific IgE. Stool tests for protozoa or helminthic ova were negative. Chest X-ray films showed no pulmonary abnormalities. Endoscopic and histological examinations revealed reflux esophagitis (grade C according to the Los Angeles Classification System) with hiatal hernia with inflammatory infiltrates including eosinophils within the esophageal mucosa. A computed tomography showed the thickening of the esophageal wall. An administration of lansoprazole improved reflux esophagitis and also eosinophilia, and an alteration to famotidine caused heartburn with an increase in eosinophils. A re-alteration to omeprazole relieved the symptom and decreased eosinophils. It was shown that gastroesophageal reflux disease was one of the possible causes of eosinophilia.
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PMID:[A case of gastroesophageal reflux disease with marked eosinophilia]. 1740 63

The aim is to determine whether there is a pattern of allergic and immune abnormalities in children with complex medical problems. The authors retrospectively studied a convenience sample of 69 children in a case management program. Of 69 children, 42 underwent immunologic investigations during the selected time frame. Forty (95%) had 1 or more allergic disorder. Cow's milk sensitivity was present in 32 (76%). Abnormal immunoglobulin levels, IgG, IgA, and IgE were found at a greater frequency than in the general pediatric population (P <.005). Lymphocyte subset percentages were decreased for B cells (CD19) and natural killer cells (CD57, CD16/56; P <.05). Presence of a gastrostomy tube, gastroesophageal reflux disease, gastric acid suppression, and chronic constipation were common and failure to thrive, developmental delay, sleep disturbance, and recurrent otitis media were present in the majority. The authors report a higher than expected prevalence of allergic and immune abnormalities in children with complex medical problems.
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PMID:Prevalence of allergies in children with complex medical problems. 1851 21


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