Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major use of N-acetylcysteine in clinical toxicology is in the treatment of acetaminophen (paracetamol) overdosage. The hepatorenal toxicity of acetaminophen is mediated by a reactive metabolite normally detoxified by reduced glutathione. If glutathione is depleted, covalent binding to macromolecules and/or oxidation of thiol enzymes can lead to cell death. Oral or intravenous N-acetylcysteine or oral D,L-methionine mitigates acetaminophen-induced hepatorenal damage if given within 10 hours, but becomes less effective thereafter. In vivo, N-acetylcysteine forms L-cysteine, cystine, L-methionine, glutathione, and mixed disulfides; L-methionine also forms cysteine, thus giving rise to glutathione and other products. Oral therapy with N-acetylcysteine or methionine for acetaminophen poisoning is contraindicated in the presence of coma or vomiting, or if activated charcoal has been given by mouth. Nausea, vomiting, and diarrhea may also occur as a result of oral N-acetylcysteine administration. Anaphylactoid reactions including angioedema, bronchospasm, flushing, hypotension, nausea/vomiting, rash, tachycardia, and respiratory distress may occur 15-60 minutes into N-acetylcysteine infusion (20 hours intravenous regimen) in up to 10% of patients. Following accidental intravenous overdosage, the adverse reactions of N-acetylcysteine are similar but more severe; fatalities have occurred. A reduction in the loading dose of N-acetylcysteine may reduce the risk of adverse reactions while maintaining efficacy. Administration of N-acetylcysteine for a longer period might provide enhanced protection for patients in whom acetaminophen absorption or elimination is delayed. N-acetylcysteine may also have a role in the treatment of toxicity from carbon tetrachloride, chloroform, 1,2-dichloropropane, and other compounds. The possible use of N-acetylcysteine and other agents in the prevention of the neuropsychiatric sequelae of acute carbon monoxide poisoning is an important area for future research.
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PMID:Use of N-acetylcysteine in clinical toxicology. 192 4

During her 26th week of pregnancy a 20-year-old woman developed generalized pruritus, urticaria, flushing, tinnitus, and tachycardia during plasmapheresis with 5% human serum albumin (HSA) as adjunctive treatment for anti-Kell isoimmunization. The reaction was controlled with intravenous diphenhydramine. Despite pretreatment with diphenhydramine and betamethasone a subsequent attempt to perform plasmapheresis with infusion of 5% HSA resulted in a more severe reaction which progressed to respiratory distress. Intradermal skin testing with 5% HSA produced a 9 x 11-mm wheal and 17 x 21-mm erythema at 15 minutes. An enzyme-linked immunoassay was positive for IgE antibody to 5% HSA before and after dialysis for removal of Na caprylate. These results are consistent with an IgE-mediated basis for this patient's reaction to HSA.
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PMID:Anaphylaxis to human serum albumin. 230 85

Impotence, a common problem especially among older men, can now be treated with Viagra, This oral pill, unlike previous approved treatments mostly involving local injections, does not directly cause penile erection, but increases response to sexual stimulation. It acts by enhancing the relaxant effects of nitric acid on smooth muscle, and thus increases blood flow to certain areas of the penis, leading to erection. It has been evaluated in many randomized trials and in all was more successful in inducing erection than placebos. The most common side-effects include headache, flushing and indigestion, but there have also been reports of fatalities. We describe a 75-year-old man who had an acute myocardial infraction in the past and who had maturity-onset diabetes and hypertension. In the week prior to admission he had a cardiac scan following a few weeks of exacerbation of anginal pain for which he had been taking nitrites. He took a Viagra pill without prescription or medical advice and 2 hours later, during intercourse with his wife, developed audible respiratory distress and lost consciousness. His wife started cardiac massage but not mouth-to-mouth breathing. The emergency team found ventricular fibrillation and gave 5 electrical shocks and amines and atropine. He remained unconscious, but his pulse returned and he was hospitalized. He then had several generalized convulsions treated with i.v. valium. 20 minutes after admission there was asystole and all attempts at resuscitation failed. Cardiovascular status must be considered prior to prescribing Viagra, and the associated risk evaluated.
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PMID:[Viagra--the first oral treatment for impotence that is not lacking in fatal effects]. 1090 27

Unfortunately, surfactant therapy is not routinely available to infants in some parts of the world because of its cost. It is the hypothesis of this article that in situations where surfactant is not available, there may be a role for antenatal thyrotropin-releasing hormone (TRH) plus glucocorticoid therapy. Data from randomized clinical trials, which compared therapy with antenatal glucocorticoid plus TRH to that with glucocorticoid alone were extracted and subjected to meta-analysis. The trials that incorporated surfactant therapy were analyzed separately from those in which surfactant was not used. In addition, because surfactant therapy was only available to some patients in the Australian ACTOBAT trial, each group analysis was performed with and without the ACTOBAT data. A characteristic of the earlier presurfactant trials is that few were designed for "intention to treat" analysis. In most of these studies, it was decided a priori to include babies who delivered within a specified time period after hormone therapy. The addition of TRH did not decrease respiratory distress syndrome in those trials in which surfactant therapy was used. In the presurfactant trials, respiratory distress syndrome was significantly decreased when "intention to treat" data were examined, as well as in those infants who delivered between 1 and 10 days after maternal therapy. There was also a significant decrease in oxygen dependency at 28 days after birth, and in oxygen dependency or death at this time, in those infants who delivered 1 to 10 days after treatment. Antenatal TRH had no significant effect of on neonatal complications such as air leak, intraventricular hemmorhage, patent ductus arteriosus, retinopathy of prematurity, or necrotizing enterocolitis. However, TRH did produce transient suppression of the pituitary thyroid axis. There were also a variety of transient complications in the mothers, including nausea, vomiting or flushing, light-headed feeling, and increased blood pressure. The authors conclude that the implementation of appropriate antenatal glucocorticoid treatment is the first priority. Once this has been established, the data presented here suggest that addition of antenatal TRH should be considered in those situations where surfactant is not available.
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PMID:Is there a role for antenatal TRH therapy for the prevention of neonatal lung disease? 1177 11

Paclitaxel (Taxol) a taxane antineoplastic agent causing irreversible microtubule aggregation with activity against breast, ovarian, lung, head and neck, bladder, testicular, esophageal, endometrial and other less common tumors was derived from the bark of the Pacific yew (Taxus brevifolia). Phase I trials conducted in the late 1980s were almost halted because of the high frequency of hypersensitivity-like reactions. Respiratory distress (dyspnea and/or bronchospasm), hypotension, and angioedema were the major manifestations, but flushing, urticaria, chest, abdomen, and extremity pains were described also. Reactions occurred on first exposure in the majority of cases raising etiologic questions. The vehicle for paclitaxel Cremophor EL (polyoxyethylated castor oil in 50% ethanol) was strongly suspect as a direct (non-immunoglobulin E dependent) histamine releaser. Premedication regimens and longer infusion times lowered the incidence of reactivity allowing phase II and III trials to progress through the early 1990s. The mechanism(s) underlying paclitaxel hypersensitivity-like reactions is still unknown, and clinical data on probable complement and mast cell activation are lacking. The original clinical trial protocols for paclitaxel required discontinuation of therapy for patients who experienced hypersensitivity-like reactions. Here, we review the current etiologic knowledge of these reactions and describe our clinical approach to allow completion of chemotherapy with this powerful plant-derived agent.
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PMID:Taxol reactions. 1212 9

Hypersensitivity reaction (HSR) is still a major concern during cancer chemotherapy with paclitaxel. In the present study, we investigated retrospectively the incidence of HSRs to paclitaxel and the risk factors in 105 patients (553 courses) who received adjuvant chemotherapy (paclitaxel and carboplatin) for ovarian cancer. Moderate to severe HSRs that led to cessation or discontinuation of the chemotherapy, including respiratory distress and hypotension, were observed in 14 patients (13.3%) and 16 courses (2.9%), regardless of the use of conventional premedication with glucocorticoid, and histamine H(1) and H(2) antagonists. The incidence of HSRs to paclitaxel in patients with ovarian cancer seemed to be considerably higher than those reported by other investigators in patients with other carcinomas such as non-small-cell lung cancer and breast cancer. Four risk factors were identified: (1) history of mild dermal reactions such as facial flushing and urticaria in previous courses, (2) presence of respiratory dysfunction, (3) obesity (body mass index >25), and (4) postmenopausal at the time of ovariectomy. The incidence of hypersensitivity increased linearly as the number of risk factors increased (r=0.992, P=0.008). It is likely that disappearance of the estrous cycle facilitates the occurrence of HSRs to paclitaxel.
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PMID:Incidence and risk factors for paclitaxel hypersensitivity during ovarian cancer chemotherapy. 1579 61

Scombroid fish poisoning is an acute illness that occurs after eating fish containing high levels of histamine or other biogenic amines. Symptoms typically include facial flushing, sweating, rash, a burning or peppery taste in the mouth, diarrhea, and abdominal cramps and usually resolve within several hours without medical intervention. More severe symptoms (e.g., respiratory distress, swelling of the tongue and throat, and blurred vision) can occur and require medical treatment with antihistamines. In late 2006, two outbreaks of scombroid fish poisoning occurred, one in Louisiana and one in Tennessee. To determine the source of the outbreaks and to implement control measures, CDC and the state health departments in Louisiana and Tennessee conducted epidemiologic investigations, and the Food and Drug Administration (FDA) conducted traceback investigations of the product. This report describes the results of those investigations, which indicated that the outbreaks in Louisiana and Tennessee were associated with tuna steaks from Indonesia and Vietnam, respectively. The majority of seafood eaten in the United States is imported. FDA programs to identify and prevent seafood hazards such as scombroid fish poisoning have made substantial progress but are able to inspect only a small proportion of seafood entering the United States. The only effective method for prevention of scombroid fish poisoning is consistent temperature control of fish at </=40 degrees F (</=4.4 degrees C) at all times between catching and consumption.
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PMID:Scombroid fish poisoning associated with tuna steaks--Louisiana and Tennessee, 2006. 1770 71

Three mixed-bred raptors (Falco rusticolus x Falco cherrug) from a German falcon breeder were presented with a history of respiratory distress. In one bird a laryngeal stridor was noted, and oral examination revealed an epiglottal swelling. In the other two birds, nasal discharge and sneezing were the main clinical symptoms. Nasal flushing samples and biopsies were collected for pathologic, bacteriologic, and parasitologic examination. Results confirmed a cryptosporidial infection. Polymerase chain reaction (PCR) and DNA analysis identified the causative agent to be Cryptosporidium baileyi. No cryptosporidia were detected in fecal samples, indicating the infection was confined to the respiratory system. Analysis of prey animals (pigeons, quail) failed to identify the source of infection. Treatment was initiated with paromomycin in all three birds, whereas in two birds an additional therapy with azithromycin was given. However, no clinical improvement was seen after several weeks of treatment, and the birds either died or were euthanatized. To the authors' knowledge, these are the first confirmed cases of disease caused by cryptosporidia in the order of Falconiformes.
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PMID:Upper respiratory tract infection caused by Cryptosporidium baileyi in three mixed-bred falcons (Falco rusticolus x Falco cherrug). 1864 71

A healthy 1-year-old boy born at full term after an uncomplicated pregnancy presented to the dermatology clinic for a widespread eruption with gradual onset since 3 months of age. He was otherwise well, afebrile, feeding well, and gaining weight appropriately. The child was overall asymptomatic, though some of his lesions occasionally became red and pruritic. His mother noticed that after mild illnesses, he was more prone to these flares. She denied flushing, vomiting, diarrhea, respiratory distress, and irritability. He was meeting all developmental milestones and started walking at 11 months of age. The remainder of his review of systems was unremarkable, and family history was noncontributory. Physical exam revealed a well-appearing, well-nourished, playful, and interactive toddler. There were innumerable discrete and coalescing pink-brown macules and papules concentrated on the trunk and extending onto the proximal upper and lower extremities bilaterally, as well as the neck and lower face. Stroking the lesions quickly led to development of erythematous edematous wheals. There was no hepatosplenomegaly, and the lymph node exam was unremarkable.
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PMID:A 1-year-old boy with persistent, generalized eruption. Urticaria pigmentosa. 2454 82

A 74-year-old woman with known euthyroid multinodular retrosternal goiter necessitated an urgent intubation at home, due to acute respiratory distress evoked by tracheal compression. Extubation after a few days failed, and she underwent an urgent total thyroidectomy. During postoperative extubation the patient developed suddenly unilateral facial flushing and sweating at the left side, without ptosis of the left levator palpebrae superioris. These symptoms persisted during the next 24 hours. The skin at the right side of the face remained uninvolved. In the early postoperative period this appearance recurred at moments of emotions, exercise or heat. Beside this, the patient had a normal recovery. Six weeks later this reaction couldn't be provoked anymore. 'Harlequin' syndrome (unilateral facial flushing and sweating) is caused by a lesion of the controlateral sympathetic chain at the levels T2 and T3. It is unknown if the sweating and vasodilation at the "healthy" side is normal or if it is a reaction of hyperactivity.
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PMID:Harlequin syndrome after thyroidectomy for compressive retrosternal goiter. Case report and review of the literature. 2510 14


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