Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 7-year-old boy, ichthyosis vulgaris was treated with a 10% ointment for application over a large area of the body surface. In this way, the child received 400 g salicylic acid (0.6 g/kg body weight per day) percutaneously over a period of 4 weeks. The patient was referred to hospital by the family doctor: he was in a deep somnolent state, apparently caused by hyperventilation following wheezing, vomiting, tinnitus and vertigo. Salicylate intoxication was suspected because of metabolic acidosis, an anion gap and respiratory overcompensation. The diagnosis was confirmed by a serum salicylate level of 985 micrograms/ml (therapeutic level 150-300 micrograms/ml). Following forced diuresis and alkalization with sodium bicarbonate, haemodialysis was unnecessary. As the salicylate level declined to values within the therapeutic range, the patient started to recover consciousness, waking on the 4th day. By day 6 there were still obvious neurological deficiencies. Fecal incontinence, bilateral ptosis and intermittent diverging strabismus on the right persisted for some weeks. It was 6 months before complete neurological resolution was achieved. The pathogenesis of salicylate toxicity and the need for safer therapies for ichthyosis vulgaris are discussed.
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PMID:[Life threatening salicylate poisoning caused by percutaneous absorption in severe ichthyosis vulgaris]. 896 5

From 1974 to 1995, 19 children with achalasia of the esophagus have been treated at our institution. Presenting symptoms included vomiting (n = 14), dysphagia (n = 13), failure to thrive (n = 6), and odynophagia (n = 1). Diagnosis was established by a barium swallow in 19, with eight also undergoing esophageal manometry. Six boys and 13 girls with an average age of 10 years (range, 1.3 to 17.6) underwent a transthoracic, modified anterior Heller esophagomyotomy (HM). Five underwent a concomitant, modified, Belsey fundoplication (BF). Follow-up ranging from 6 months to 21 years (mean, 9 years) was accomplished in all 19 patients by both office visits and telephone interviews. Early postoperative follow-up showed initial swallowing difficulty in two (14%) patients with a HM alone and in four out of five (80%) patients treated with a HM and BF. All patients (n = 5) with a HM and BF and one with a HM alone required one esophageal dilation during the first postoperative year. These initial swallowing difficulties resolved in all six patients during this first postoperative year. Late postoperative follow-up, however, indicates occasional, mild dysphagia in two out of five with an HM and BF resulting in complete relief of presenting symptoms in 17 of the 19 patients (90%). All patients rated their overall result as either excellent (68%) or good (32%) with none rating it as fair or poor. None of the 19 patients had clinical evidence of gastroesophageal reflux, although five patients had evidence of nonpathologic reflux noted during upper gastrointestinal x-ray. Recurrent vomiting, asthma, wheezing, or esophagitis symptoms have not been reported by any patients. No patients required reoperation, and there were no deaths or postoperative complications. Modified Heller esophagomyotomy is safe (0% mortality) and effective (90% relief of symptoms) in children with achalasia. A concurrent modified Belsey fundoplication results in early and late mild postoperative dysphagia that was responsive to esophageal dilation. The transthoracic, modified Heller esophagomyotomy without a fundoplication is currently our treatment of choice for achalasia in children.
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PMID:Efficacy of the transthoracic modified Heller myotomy in children with achalasia--a 21-year experience. 904 49

We investigated symptoms suggestive of swallowing problems in patients with primary biliary cirrhosis, some of whom displayed features of sicca complex. A prospective study of 95 consecutive patients with primary biliary cirrhosis was conducted at a single teaching hospital using a questionnaire administered over the telephone. Some symptoms of sicca complex (dry mouth and/or dry eyes) were found in 65 patients (68.4%). Subjective xerostomia alone was present in 45 patients (47.4%). The questionnaire revealed an increase in incidence of dysphagia in xerostomia subjects, affecting 21 of 45 patients, compared with 6 of 50 non-xerostomia patients. Multivariate logistic regression analysis showed that confounding factors such as age, obesity, cigarette smoking, and medications associated with a dry mouth could not explain these findings. Twenty-eight patients complained of hoarseness, 23 of coughing, and 14 of wheezing, all of which were significantly more frequent than in the 50 patients without xerostomia. Heartburn affected 17 xerostomia patients and 15 non-xerostomia patients, indicating no difference in frequency between these two groups, even after age, obesity, cigarette smoking, and medications associated with heartburn were considered in the multivariate analysis. Acid regurgitation, nausea, and vomiting were also similar in frequency between patients with and without xerostomia. Swallowing problems, manifested primarily as dysphagia, are common in primary biliary cirrhosis patients who have subjective xerostomia.
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PMID:Primary biliary cirrhosis, sicca complex, and dysphagia. 919 Jan 3

Recently, the efficacy of oral vitamin A supplementation for measles and respiratory syncytial (RSV) infection has been evaluated in developing countries. However, in developed countries where vitamin A deficiency is little worth consideration, few studies have been conducted on the effect of vitamin A supplementation. The effect of oral vitamin A (100,000 IU) supplementation was evaluated in 105 children with measles (age 5 months to 4 years) and in 96 children with RSV infection (ages a month to 2.5 years) in Fukushima, Japan. Comparisons were made of clinical signs, duration of hospitalization and complications between treated groups and non-treated groups. Treated group (measles n = 47, RSV n = 54) and non-treated groups (measles n = 58, RSV n = 42) had similar baseline characteristics. Patients with measles given a vitamin A supplementation had a shorter duration of cough (7.2 +/- 1.6 vs 9.2 +/- 1.8 days, p < 0.05) and patients with severe RSV infection given a vitamin A supplementation had a shorter duration of retraction (3.6 +/- 1.4 vs 5.3 +/- 0.8 days, p < 0.05) and wheezing (4.4 +/- 1.7 vs 6.3 +/- 1.5 days, p < 0.05). Toxicities, including excess vomiting and bulging fontanel were not observed. Our findings may suggest the efficacy of oral vitamin A supplementation for measles and severe RSV infection, in children who have no malnutrition.
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PMID:[The efficacy of oral vitamin A supplementation for measles and respiratory syncytial virus (RSV) infection]. 1021 86

Gastroesophageal reflux (GER) is implicated in the pathogenesis of respiratory symptoms in childhood. It should be taken into account especially in the differential diagnosis of children presenting with wheezing. Although, oesophageal pH monitorization has been reported to be the best technique in the evaluation of GER, radionuclide studies have also been shown to be very sensitive recently. In this study, 82 children presenting with recurrent wheezing (n = 74) and/or vomiting (n = 28) (mean age 17.4 months; range 3-48 months) were evaluated. GER scintigraphy was performed to determine the frequency of GER. GER was determined in 18 of the 82 cases (21.9%). The GER was found in 21.1% of children with recurrent wheezing and in 16.6% of children suffering from recurrent vomiting. GER scintigraphy should be kept in mind in the evaluation of children with the complaint of recurrent wheezing since it is a noninvasive and easily applicable method.
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PMID:Results of the gastroesophageal reflux assessment in wheezy children. 1079 82

Rotavirus and respiratory syncytial virus (RSV) infections represent up to 30% of the totality of nosocomial infections in paediatric wards. We studied the importance of these infections in the paediatric wards of the University Hospital Center of Poitiers, France, from October 1996 to September 1998. We defined as nosocomial an infection acquired after 3 days of hospitalization for rotavirus and after 7 days for RSV. The 274 cases of children presenting rotavirus gastroenteritis or RSV infection within this period were studied. Rotavirus was detected in stools by using an agglutination test and RSV was diagnosed in nasopharyngeal aspirations by direct examination with an immunofluorescence assay (IFA), cell culture and serotyping with IFA. We noted 50 rotavirus and 224 RSV infections, with a first epidemic of RSV subgroup B (49.5%) and a second epidemic of subgroup A (44.9%). 19 (38%) were rotavirus nosocomial infections and 5 (2.2%) were RSV nosocomial infections. The majority of the nosocomial infections occurred before the age of one year and particularly before the age of 6 months (42.2% for rotavirus, 60% for RSV). In comparison to community-acquired infections, children with rotavirus nosocomial infections were younger (9 months versus 12.5 months) which was the opposite for RSV nosocomial infections (10.8 months versus 6.5 months). The sex-ratio of children with community-acquired infections was 2.1 that was not reported in nosocomial infections. The length of stay in hospital was always longer in nosocomial infections (11.7 days versus 3.6 days for rotavirus; 38.8 days versus 4.8 days for RSV). Diarrhea (p = 0.007) and vomiting (p = 0.013) for enteric infections and wheezing (p = 0.02) for respiratory infections were more often observed in community-acquired infections. This study emphasizes the frequency and the consequences of rotavirus and RSV nosocomial infections in paediatric wards and the importance of the hygienic rules to prevent these infections.
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PMID:[Nosocomial infections due to rotavirus and respiratory syncytial virus in pediatric wards: a 2-year study]. 1102 3

We report a case of a patient who suffered generalized urticaria, chest tightness, wheezing, nausea, vomiting, hypotension, and loss of consciousness. Two hours earlier she had taken Eulitop Retard following lunch. She had tolerated all the implicated food after the reaction. Allergy evaluation revealed intense positive responses to intradermal tests with bezafibrate active component and Eulitop Retard (skin tests in control subjects were negative). Specific IgE tests (RAST) to Eulitop Retard were negative. An IgE mechanism is suggested to be responsible for this adverse reaction on the basis of the positive skin tets. The delayed onset (two hours) of this anaphylactic shock is unusual. Although infrequent, it may be caused by the specific pharmacokinetic characteristics of this drug, which is a slow releasing agent, mainly absorbed in the gut. The drug was taken just after lunch, and this concomitant food ingestion could also have produced a delay in gastric drainage and a retarded drug absorption. An IgE-mediated accelerated type reaction could also explain this delay. Apparently the patient reacted after the first contact to the drug, and the absence of a sensitization period is not usual in this type of immune reponse. Finally, we recommend the performance of prick and intradermal skin tests prior to any systemic challenge when allergic reactions to fibric acid derivatives are suspected.
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PMID:Bezafibrate-induced anaphylactic shock: unusual clinical presentation. 1143 73

In non-smokers the underlying causes for chronic persistent cough (CPC) e.g. chronic cough without diagnostic chest X-ray or pulmonary function test--are usually as follows: several common upper airways diseases, bronchial (cough type) asthma, gastrooesophageal reflux or treatment with an ACE (angiotensin converting enzyme)--inhibitor. In 10% of CPC however the cause remains uncertain. We report a 30 year old non-smoker with severe coughing and repeated vomiting for two months. No laboratory or technical data could be collected suggestive of a common cause of CPC: Upper airways disease, bronchial flow limitation or hyperresponsiveness, ACE inhibitor medication, B. pertussis infection, gastrooesophageal reflux disease (by 24 hours pH-probe) were ruled out. Fiberbronchoscopic findings remained unremarkable, except for the bronchial biopsy specimen, which showed moderate eosinophilic inflammation of the mucosa and marked thickening of the subepithelial layer. Since the cough was non-productive, sputum induction with 3 ml nebulised 3% NaCl solution was performed. 28% of the granulocytes were eosinophil stained. A low quality morning sputum (< 1 ml) showed 21% eosinophilia. Thus, the diagnosis of eosinophilic bronchitis was established. 400 micrograms budesonide dry powder inhalations b.i.d. for one week resolved the cough, treatment was stopped after three weeks. No recurrence was seen two months later. Both the cough type asthma and the eosinophilic bronchitis could represent a form fruste of classical bronchial asthma beyond wheezing or dyspnoea, but with the common main symptom: cough. Since hyperresponsiveness and cough are phenotypic hallmarks of cough variant asthma, in eosinophilic bronchitis--beside cough--another two features of asthma are present: eosinophilic inflammation of the mucosa along with sputum eosinophilia and subepithelial layer thickening. Not surprisingly, eosinophilic bronchial inflammation could be shown in patients with cough variant asthma as well, who--up to 56% during a four year-period--develop classic asthma. The long-term outcome of eosinophilic bronchitis is not known, however. Thus, asthma, cough variant asthma and cough due to eosinophilic bronchitis can mirror different phenotypes or phases of the same entity. CPC due to either the cough type asthma or the eosinophilic bronchitis is like asthma fast responding to inhalative steroids. (Induced) sputum staining should be added to the diagnostic armamentarium of CPC.
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PMID:[Eosinophilic bronchitis without asthma--an additional rare cause for chronic persistent cough (CPC)? A 30-year old patient with severe CPC due to eosinophilic bronchitis without asthma or hyperreactivity]. 1144 11

Atopic dermatitis is a typical chronic inflammatory skin disease that usually occurs in individuals with a personal or family history of atopy. Children with atopic dermatitis frequently present IgE-mediated food sensitization, the most commonly involved foods being egg and cow's milk. However, controversy currently surrounds whether food allergy is an etiological factor in atopic dermatitis or whether it is simply an associated factor, accompanying this disease as one more expression of the patient's atopic predisposition. Approximately 40 % of neonates and small children with moderate-to-severe atopic dermatitis present food allergy confirmed by double-blind provocation tests but this allergy does not seem to be the cause of dermatitis since in many cases onset occurs before the food responsible for allergic sensitization is introduced into the newborn's diet.Studies of double-blind provocation tests with food in patients with atopic dermatitis demonstrate mainly immediate reactions compatible with an IgE-mediated allergy. These reactions occur between 5 minutes and 2 hours and present mainly cutaneous symptoms (pruritus, erythema, morbilliform exanthema, wheals) and to a lesser extent, digestive manifestations (nausea, vomiting, abdominal pain, diarrhea), as well as respiratory symptoms (wheezing, nasal congestion, sneezing, coughing). However, these reactions do not indicate the development of dermatitis.Some authors believe that responses to the food in provocation tests may also be delayed, appearing mainly in the following 48 hours, and clinically manifested as exacerbation of dermatitis. However, delayed symptoms are difficult to diagnose and attributing these symptoms to a particular foodstuff may not be possible.Delayed reactions have been attributed to a non-IgE-mediated immunological mechanism and patch tests with food have been proposed for their diagnosis. In our experience and in that of other authors, the results of patch tests with cow's milk do not seem very specific and could be due, at least in part, to the irritant effect of these patches on the reactive skin of children with atopic dermatitis.The involvement of foods in atopic dermatitis will always be difficult to demonstrate given that an exclusion diet is not usually required for its resolution. Food is just one among several possible exacerbating factors and consequently identification of its precise role in the course of the disease is difficult. Further double-blind prospective studies are required to demonstrate the effectiveness of exclusion diets in the treatment of atopic dermatitis.Apart from the controversy surrounding the etiological role of foods, the most important point in atopic dermatitis is to understand that the child is atopic, that is, predisposed to developing sensitivity to environmental allergens; in the first few years of life to foods and subsequently to aeroallergens. Consequently, possible allergic sensitization to foods should be evaluated in children with atopic dermatitis to avoid allergic reactions and to prevent the possible development of allergic respiratory disease later in life.
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PMID:[Etiologic implication of foods in atopic dermatitis: evidence against]. 1198 42

This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. Anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (Immunoglobulin E). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. Epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.
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PMID:Bugged. 1277 12


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