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Query: UMLS:C0242429 (sore throat)
 2,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A few minutes after sucking a lozenge for a sore throat a 68-year-old man developed an anaphylactic shock. At a heart rate of 110/min there was no palpable blood pressure. A red confluent exanthem, predominantly of the trunk, was noted. After brief intensive-care treatment the patient was completely well again and diagnostic tests for allergy were performed. The prick test for the 14 individual ingredients of the throat lozenge produced massive reddening and urticaria on the test arm with carbowax, a polyethylene glycol which serves as a vehicle in the remedy and does not have to be listed. Later there were an urge to cough and urticaria all over the trunk. There was no systemic reaction. Neither specific IgE antibodies nor any complement-consuming reaction could be demonstrated. Thus the precipitating mechanism remains unexplained.
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PMID:[Anaphylactic shock after sucking on a throat lozenge]. 169 39

Ingestion of commercially processed honeybee-collected pollen produced potentially fatal consequences in a 19 year old asthmatic male. Symptoms of sore throat, facial itch and swelling, difficulty in breathing and stridor lasted for approximately two hours and was followed by clinical respiratory distress with widespread wheeze on auscultation of his chest. RAST and skin test data suggest that these complications appear to be mediated by IgE antibodies directed against the processed pollen, but not bee venom. Consumption of processed pollen by atopic individuals is, therefore, a potentially hazardous procedure with little therapeutic benefit.
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PMID:Acute hypersensitivity to ingested processed pollen. 386 27

Acid anhydrides are low-molecular-weight chemicals known to cause respiratory irritancy and allergy. Skin allergy has on rare occasions been reported. 2 workers contracted hives and itching on uncovered skin after 2 months exposure to methyltetrahydrophthalic anhydride (MTHPA) and methylhexahydrophthalic anhydride (MHHPA), to which they had airborne exposure. Later, the patients also developed conjunctivitis, rhinitis, sore throat, cough or asthma. In addition to MTHPA, 1 worker was also exposed to unsaturated polyester resin (UP). Both patients' immediate allergy to MTHPA and MHHPA was verified by positive prick tests to MTHPA and MHHPA, conjugated with human serum albumin (HSA), and positive radioallergosorbent tests (RASTs) to these anhydrides. On prick testing, both patients also reacted to a phthalic anhydride (PA)-HSA-conjugate and 1 of the patients to UP-HSA-conjugate. Specific immediate allergy to UP was shown by RAST. RAST inhibition with MTHPA, MHHPA and UP-resin conjugates confirmed IgE-mediated allergy and cross-reactivity between anhydrides. Our patients had developed airborne contact urticaria caused by phthalic anhydrides, in addition to respiratory allergy. Phthalic anhydride contained in the UP resin was possibly responsible for the immediate reaction of the skin.
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PMID:Immunologic contact urticaria due to airborne methylhexahydrophthalic and methyltetrahydrophthalic anhydrides. 760 Jul 75

The purpose of this study was to determine the value of conventional and newer serological tests (toxoplasmic serological profile) in the diagnosis of toxoplasmic lymphadenitis (TL). We studied 40 consecutive patients with biopsy-proven TL. Cervical, axillary, or occipital adenopathy was present in 72.5%, 20%, and 7.5% of the patients, respectively. Low-grade fever, fatigue, general malaise, or sore throat were present in only 6 (15%) of the 40 patients. A positive result for all serological tests was time dependent from the clinical onset of lymphadenopathy. The initial serum samples were positive for antibody for each patient, as shown by a Sabin-Feldman dye test. Between 3 and 6 months after clinical onset of TL, all of the patients had antibody titers of > or = 1:1,024. The ELISA was positive for IgM antibodies in all of the patients in the first 3 months. Detection of IgA or IgE antibodies or an acute pattern in the differential agglutination test was helpful in diagnosing TL in those patients who had negative, low-positive, or equivocal titers of IgM antibodies (as measured by ELISA) after 3 months. A toxoplasmic serological profile on the first serum specimen drawn after clinical onset of TL had a sensitivity of 100%. It is advisable to obtain such a serological profile in cases of asymptomatic lymphadenopathy before biopsy is carried out, especially for those individuals who have negative or equivocal IgM antibody titers.
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PMID:Studies on the serodiagnosis of toxoplasmic lymphadenitis. 779 74

Seven repair technicians (RT, site A) repeatedly exposed to facsimile machine fume developed recurring sore throat, fever, lymphadenopathy, chest tightness, dry cough, and dyspnea. The fume concentration was low (0.6 mg/m3 of breathing-zone air) but it contained butyl methacrylate (BMA), a known skin sensitizer. Although chest radiographs were normal, three of the seven RT-A had lung crackles and spirometric abnormalities, and increased serum levels of immunoglobulins IgE or IgM. Symptoms and most other abnormalities improved when exposure to BMA was stopped. We later evaluated workers in two other sites (B and C). Six RT-B had daily contact with BMA fume (0.14 to 0.40 mg/m3 of air) at a field repair depot. Six administrative and six sales staff members (AS-B, SS-B) without regular fume exposure served as controls. All RT-B had elevated serum IgE levels (202+/-69 U/mL [SEM]; normal <41 U/mL). IgE and fume levels were positively correlated (r=0.83). four RT-B had lung crackles, but few symptoms and normal results of spirometry. The crackles cleared 8 weeks after substitution of a BMA-free paper, but IgE levels remained high (201+/-69). The nonexposed AS-B and SS-B had no crackles. Their IgE levels were normal (19+/-4 U/mL [SEM]; p<0.01). The crackles suggest BMA fume might have caused inflammation in terminal airways units. The significance of the IgE elevations is also uncertain since this class of antibodies is usually associated with asthma, not pneumonitis. In view of these uncertainties, BMA was eliminated from the facsimile transceiver process. Follow-up of group C workers (n=32) found no symptoms, lung crackles, or abnormal results of spirometry. However, IgE concentrations were elevated in 15 and remained so for 21 months, perhaps because of continuing exposure to residual low levels of BMA. These findings suggest that BMA-bearing facsimile fume caused increased IgE levels in RT at sites A, B, and C, and might have resulted in permanent lung injury if such exposure had continued.
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PMID:Pulmonary abnormalities and serum immunoglobulins in facsimile machine repair technicians exposed to butyl methacrylate fume. 863 24

Airborne fungi have been postulated as a cause of symptoms among office workers. Using the MAST chemiluminescent system, this study evaluated 36 IgG and 36 IgE antibody levels in 47 office workers from an area with elevated airborne fungal concentrations and 44 office workers from an otherwise similar area with lower airborne fungal exposure. No difference was found in IgG antibody to fungi between the lower and higher exposure areas, but high IgG antibody to one or more of the fungi studied was detected in 67% of all the workers tested. IgE antibody to one or more antigens was detected in 40% of the participants. Workers who reported atopic symptoms (sneezing, runny nose, and itchy eyes) or "sick building" symptoms (any three of the following temporally related to work: headache, fatigue, stuffy nose, irritated eyes, or sore throat) were more likely to have one positive IgE antibody test. Type I hypersensitivity to aeroallergens besides fungi may play a role in some symptoms reported by some participants in this office building.
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PMID:The relationship between symptoms and IgG and IgE antibodies in an office environment. 951 63

Formaldehyde (FA) is an occupational and general indoor hazard often affecting the respiratory airways. One of the main causes of multiple chemical sensitivity is gaseous FA, and it has become an important social problem in developed countries. FA concentrations in anatomy dissection classrooms are thought to be higher than under usual circumstances. The number of students developing physical symptoms during the anatomy dissection course in our university has been increasing over recent years. We planned to clarify the causes of such symptoms. Ninety-five medical students were interviewed using a questionnaire about allergic histories, physical symptoms developed during the anatomy dissection course, and symptoms related to chemical sensitivity up to three months after the course had finished. We measured total IgE, specific IgE to FA and specific IgE to house dust mites. Eighty-three percent of students had experienced symptoms, such as burning eyes, nasal discharge, sore throat, general fatigue or skin irritation during the course. Fifty percent of students had a past history of atopic disease. Fifty-eight percent of students tested positive to specific IgE to house dust mites; however, only one student, who did not complain of any symptoms during the course, tested positive to FA-IgE. Students with atopic factors (present histories of atopic diseases and higher total IgE) and/or chemical sensitivity demonstrated worse physical symptoms during the anatomy dissection course than students without such histories. In conclusion, it is suggested that gaseous FA exposure may exacerbate basic allergic symptoms, and moreover that people with chemical sensitivity demonstrated worse symptoms following gaseous FA exposure. Nevertheless, in our study we find no relationship between FA-IgE and the physical symptoms of gaseous FA exposure during or following an anatomy dissection course.
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PMID:[Relationship between atopic factors and physical symptoms induced by gaseous formaldehyde exposure during an anatomy dissection course]. 1124 81

An increasing number of human cases of gnathostomiasis have been reported in Sinaloa, Mexico, most of whom have a custom of eating of raw fish dishes such as 'cebiche'. Here we report five adult patients, three women and two men, having an acute episode of vomiting and abdominal pain a few minutes after eating a dish of cebiche prepared from a spotted sleeper perch (Eleotris picta) fished from a nearby lake in southern Sinaloa. All five patients experienced acute throat pain, chest and joint pains, headache and fever. One patient, a 55-year-old male, was hospitalized with suspected pancreatitis and pneumonia. By 8-9 days later, all five patients developed between three and 12 edematous, migrating skin lesions on the back, abdomen, upper and lower extremities, face, eye and scalp. By ELISA, all of them were sero-positive to Gnathostoma doloresi antigen and had elevated IgE levels. Eosinophilia was found in two patients. These patients lived in an agricultural and fishing community. In this community we carried out a sero-epidemiological survey and study of living conditions in a random sample of 309 individuals distributed in 74 households. Frequent consumption of raw fish was reported in 36% of households, and 12 individuals had a clinical history of migrating skin lesions. The sero-prevalence to Gnathostoma antigens was 34.95%. Five fish species and four species of ichthyophagous birds collected from three lakes in the village and a nearby estuary were infected with the advanced third-stage larvae of G. binucleatum, a species found in Ecuador and Mexico. The results describe the first known outbreak of acute gnathostomiasis on the American continent.
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PMID:Acute outbreak of gnathostomiasis in a fishing community in Sinaloa, Mexico. 1279 24

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