Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of the urine histamine metabolite, N-methylhistamine (N-MH), as a parameter of histamine release in immediate allergic reactions was investigated. Baseline levels were determined in 34 normal control subjects and 29 atopic patients. Increases of urine N-MH values were measured during histamine infusions and in venom-allergic patients receiving bee-sting challenges. N-MH was determined by a newly developed radioimmunoassay. Baseline levels in control subjects and atopic patients demonstrated no significant differences. With regard to challenge tests, fluctuation of N-MH levels during a 6-hour period was measured. Random 6-hour increases in healthy and atopic subjects ranged from 5% to 41%. Before infusion of histamine (0.25 micrograms/kg/min for 30 minutes), baseline values were 137 +/- 11.4 micrograms N-MH per gram of creatinine and 9 +/- 1.1 micrograms N-MH per hour (n = 9). Levels peaked 1 hour after infusion at 275 +/- 45 micrograms/gm of creatinine and 44 +/- 5.6 micrograms/hr and decreased to resting levels after 2 hours. Metabolization by N-MH accounted for 9.5% +/- 4.9% (range, 2.4% to 18.4%) of infused histamine in the urine of the nine subjects. Bee-sting challenges were performed in 12 patients and three control subjects. Only in three patients experiencing generalized urticaria, nausea, dyspnea, and hypotension were significant increases of urine N-MH levels (138%, 144%, and 238%) observed. All other patients and three normal control subjects demonstrated normal local reactions without increase of N-MH values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determination of N-methylhistamine in urine as an indicator of histamine release in immediate allergic reactions. 170 26

A phase I study of carboplatin (CBDCA) was performed in 40 children with advanced cancer. A single course of CBDCA consisted of 4 weekly 1-hour infusions followed by a 2-week rest. The starting dose of 100 mg/m2/week was 66% of the maximum tolerated dose in adults. Escalated dose levels given were: 125, 150, 175, and 210 mg/m2. Myelosuppression was dose limiting, with thrombocytopenia more pronounced than leukopenia. There was no evidence of cumulative toxicity. The maximum tolerated dose for children with solid tumors was 210 mg/m2/week X 4. Other side effects included transient nausea and vomiting at the higher dose levels and non-dose-related, reversible changes in creatinine clearance. One patient developed hives. No hepatic toxicity was seen. Among the 28 evaluable patients with solid tumors, one of ten with osteogenic sarcoma had complete disappearance of a lung nodule for 15+ months. Two of four patients with medulloblastoma had partial responses by clinical and computerized tomographic scan for 4 and 10 months. All three responders had received prior cisplatin therapy. CBDCA has major advantages over cisplatin in terms of reduced toxicity. Responses observed in patients previously treated with cisplatin are encouraging. The recommended phase II dose for children with solid tumors is 175 mg/m2/week X 4 with a 2-week rest.
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PMID:Phase I study of carboplatin (CBDCA) in children with cancer. 352 46

Imipenem-cilastatin was given in doses of 1 g intravenously every 6 h to 31 patients. Twenty-five patients, with 27 infections, were clinically evaluable and received 20 to 210 g of imipenem for a duration of 5 to 56 days (average 16.3 days). Infections included seven cases of osteomyelitis, seven of bacteremia, five of cellulitis, two of pneumonia, three of pelvic cellulitis, two of intraabdominal abscess, and one each of empyema, mediastinitis, and endometritis. Fifty-five percent of the infections were caused by gram-negative bacilli, 33% were due to gram-positive organisms, and 10% were caused by anaerobes. Twenty-two patients (81%) were cured, three improved, one relapsed, and one became superinfected with a resistant organism. In 5 of 11 cases with Pseudomonas aeruginosa, the imipenem MIC for organisms isolated by the end of treatment was higher than it was initially, raising concern that imipenem should not be used alone to treat Pseudomonas aeruginosa infections. Twenty-one patients had no adverse reaction; of the remaining 10 patients, 4 had nausea, 1 had urticaria, and 6 had mild abnormalities in hepatic function; three episodes of diarrhea included two with Clostridium difficile toxin in stool and one with pseudomembranous colitis, as determined by sigmoidoscopy. Levels of creatinine, hemoglobin, leukocytes, platelets, prothrombin, and urine components were unchanged. Imipenem-cilastatin is a clinically effective antibiotic with freedom from nephrotoxicity and hematological abnormalities in the large doses used in this study.
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PMID:Safety and efficacy of high-dose treatment with imipenem-cilastatin in seriously ill patients. 386 Jan 87

Basic and clinical studies on cefotetan (CTT) were carried out and the results were as follows: Absorption and excretion Two patients were given 10 mg/kg of CTT by one shot intravenous injection. At 30 minutes after injection, mean serum level was 76.5 micrograms/ml and the half-life time was 2.3 hours. Mean 6-hour urinary recovery in same patients was 57.5%. Clinical evaluation Forty-two patients were treated with CTT, in doses of 19.2-102.9 mg/kg divided 2-4 times per day for 3-10 days intravenously. Responses were excellent in 14, good in 23, fair in 1, poor in 4, and the overall efficacy rate was 88.1%. As to adverse reaction, urticaria was observed in 1 patient. Abnormal laboratory data noted were elevation of GOT in 1, GOT and GPT in 2, creatinine in 1, and eosinophilia in 3 patients.
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PMID:[Experimental and clinical evaluation of cefotetan in pediatrics]. 658 25

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report]. 807 26

In a retrospective analysis, 79 allogeneic bone marrow recipients treated with AmBisome prophylactically or because of proven or suspected invasive fungal infection (IFI) were evaluated in 92 episodes. The median duration of treatment was 14 (range 1-112) days. The mean maximum dose given was 1.64 +/- 0.8 mg kg-1 day-1 and the mean total dose was 1.29 +/- 2.28 g. The overall incidence of reported adverse events was 194, of which none had a serious outcome. In six cases, the drug was withdrawn as a result of toxic or allergic reactions: dyspnoea and flush (3), urticaria (1), cholecystitis (1) and disorientation (one case, probably not related to AmBisome). No anaphylactoid reactions were seen. Laboratory findings, including low serum potassium (48% of the episodes), increased serum creatinine (38%) and increased serum sodium levels (7%), caused no major clinical problems. Thirteen cases of verified IFI were evaluated regarding the efficacy of AmBisome. Survival or cure of the mycotic infection occurred in 5/13 patients (38%). Two patients were treated with AmBisome (3.6 and 3.3 mg kg-1 day-1) because of verified IFI before BMT. One died of IFI. The other died of venoocclusive disease of the liver (VOD) without histological evidence of active IFI. We found a significant (P < 0.05) reduction in autopsy-proven IFI, 12/199 (6%) compared to the period when only conventional doses of amphotericin B were used, 26/227 (11%).
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PMID:Safety and efficacy of liposomal amphotericin B in allogeneic bone marrow transplant recipients. 890 28

Standard prophylaxis and treatment of malignancy-associated hyperuricemia in the USA has been allopurinol with vigorous hydration, urinary alkalinization and osmotic diuresis. Urate oxidase, the enzyme that converts uric acid to allantoin (a readily excreted metabolite that has 5- to 10-fold higher solubility than uric acid), is an alternative therapy; however, few published findings support this practice. Between February 1994 and December 1996, we administered non-recombinant urate oxidase (Uricozyme) to 126 children with newly diagnosed non-B cell acute lymphoblastic leukemia (ALL) during the first 5 days of chemotherapy with methotrexate, 6-mercaptopurine or both. Their blood levels of uric acid and other indicators of tumor lysis were measured at diagnosis and during treatment and then compared with findings in 129 similarly treated historical controls who had received allopurinol to control hyperuricemia. Clinical responses to urate oxidase were also determined in eight patients with newly diagnosed B cell ALL or advanced-stage non-Hodgkin lymphoma. Patients treated with urate oxidase had rapid and significantly greater decreases in their blood uric acid levels than did the historical controls (median maximal level during treatment, 2.3 vs 3.9 mg/dl, P < 0.001). They also had lower creatinine (0.6 vs 0.7 mg/dl, P = 0.01) and blood urea nitrogen (11 vs 24 mg/dl, P < 0.001) levels. Similar findings were made in the eight cases of B cell ALL or non-Hodgkin lymphoma. None of the patients required dialysis for acute renal failure. Six (4.5%) of the 134 children given urate oxidase had allergic reactions, manifested primarily by urticaria, bronchospasm and hypoxemia. Thus, non-recombinant urate oxidase is a more effective uricolytic agent than allopurinol but is associated with acute hypersensitivity reactions, even in patients without a history of allergy.
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PMID:Urate oxidase in prevention and treatment of hyperuricemia associated with lymphoid malignancies. 936 11

In diabetic nephropathy, heparan sulfate glycosaminoglycan side chains are reduced in glomerular basement membranes proportionally to the degree of proteinuria. Recently, it was demonstrated that additional therapy with danaparoid sodium, a mixture of sulfated glycosaminoglycans with mainly heparan sulfate, lowered proteinuria in type 1 diabetes patients with diabetic nephropathy. A randomized placebo-controlled parallel study was performed with 750 anti-Xa units of danaparoid sodium once daily in type 2 diabetes patients with severe proteinuria. The aim of the study was to evaluate the possible effects of danaparoid sodium on proteinuria, endothelial dysfunction, and hard exudates in the retina and to determine the safety/tolerability of this drug. Twenty-two patients completed the study, and one patient had to stop prematurely after 6 wk of danaparoid sodium treatment because of urticaria at the injection sites. Apart from a small decrease of hemoglobin and minor skin hematomas at the injection site in five patients in the danaparoid sodium group, no other safety parameters showed any clinically or statistically significant difference between and within groups. The relative change in time of both the urinary albumin and protein excretion rate corrected for creatinine did not differ between both treatment arms (P = 0.2 and 0.49, respectively). No retinal complications or changes of hard exudates occurred. von Willebrand factor was elevated in both groups, but was not influenced by either treatment modality. Contrary to the beneficial effects that occurred in type 1 diabetes patients with diabetic nephropathy, treatment for 8 wk with 750 anti-Xa units of danaparoid sodium gave no reduction of proteinuria, hard exudates, and von Willebrand factor.
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PMID:Effect of danaparoid sodium on proteinuria, von Willebrand factor, and hard exudates in patients with diabetes mellitus type 2. 1036 73

A random population-based sample of 131 subjects was used to assess the value of serum eosinophil cationic protein (ECP), serum myeloperioxidase (MPO), and urinary leukotriene E4 (LTE4) in predicting bronchial hyper-responsiveness measured by methacholine challenge. Special interest was focused on the history of aspirin intolerance and on smoking as contributing factors. The mean serum ECP and MPO were higher in hyper-reactive [provocational dose causing a 20% fall in forced expiratory volume in 1 sec. (PD20) < or = 6900 micrograms] than in non-hyper-reactive subjects (22.3 vs. 13.2 micrograms l-1, P < 0.001 and 377 vs. 278 micrograms l-1, P = 0.001, respectively). This was also seen in current smokers vs. never smokers (17.2 vs. 12.9 micrograms l-1, P = 0.03 and 372 vs. 286 micrograms l-1, P = 0.04, respectively). There were no differences in baseline urinary excretion of LTE4 between hyper-reactive and non-hyper-reactive subjects. During the 2 h after methacholine challenge, urinary LTE4 excretion increased from 53.8 and 69.0 ng mmol-1 creatinine in non-hyper-reactive subjects, but there was no change in hyper-reactive subjects (non-hyper-reactive vs. hyper-reactive, P = 0.06). The increase was greatest in subjects with aspirin intolerance causing urticaria or angioedema but not aggravation of asthma (from 58.5 to 87.2 ng mmol-1 creatinine), probably due to extrapulmonary leukotriene production. Our results indicate that serum ECP and MPO, but not urinary LTE4 (even in subjects with a history of aspirin intolerance), predict bronchial hyper-responsiveness to methacholine. The subject's smoking history must be taken into account when these parameters are considered.
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PMID:Serum ECP and MPO, but not urinary LTE4, are associated with bronchial hyper-responsiveness. 1054 94

Mizolastine is a new histamine H1 receptor antagonist. Mizolastine 10 mg/day is effective in allergic rhinitis and chronic idiopathic urticaria. In young healthy volunteers, absorption of mizolastine is rapid with time (tmax) to peak concentration (Cmax) of about 1 hour. The absolute bioavailability of mizolastine 10mg tablets is about 65%. Distribution is rapid with a mean distribution half-life of 1.5 to 1.9 hours. Mizolastine is >98% bound to serum albumin and the apparent volume of distribution is between I and 1.4 L/kg. Mizolastine is extensively metabolised by hepatic glucuronidation and sulphation, with no major active metabolite, and excreted in faeces. The terminal elimination half-life (t1/2beta) is 7.3 to 17.1 hours. The apparent oral clearance after a repeated oral dose of 10mg is 6.02 L/h, with steady state reached from day 3 and no accumulation between days 1 and 7. Cmax and area under the concentration-time curve (AUC) are linearly related to dose. Mizolastine appears in vivo to be a relatively weak inhibitor of cytochrome P450 2E1, 2C9, 2D6 and 3A4. In vivo, no interactions were observed between mizolastine and lorazepam or ethanol. A significant increase in Cmax and trough plasma concentration (Cmin) of digoxin occurred after coadministration with mizolastine, without change in AUC, tmax or clinical parameters. Significant increases in theophylline Cmin and AUC were observed after coadministration with mizolastine. Mizolastine Cmax and AUC were increased when coadministered with erythromycin, with no change in t1/2beta. Concomitant administration of mizolastine and ketoconazole increased mizolastine AUC values with no change in t1/2beta. In a population analysis of the pharmacokinetics of mizolastine in patients with allergies, parameter values were close to those in healthy volunteers, except for duration of absorption, which was almost doubled in the patients. Bodyweight and creatinine clearance were found to have little influence on oral clearance, and no influence of liver transaminases was found on clearance and distribution. Pharmacokinetic parameters of mizolastine in elderly individuals were similar to those observed in healthy young volunteers. In patients with chronic renal insufficiency, t1/2beta was prolonged by 47% compared with young healthy volunteers. In patients with cirrhosis, tmax was longer, Cmax was lower, distribution half-life was prolonged and AUC was 50% higher than in healthy volunteers. In pharmacodynamic-pharmacokinetic trials, the percentage of wheal and flare inhibition was found to correlate with mizolastine Cmin values. No direct relationship was found between drug concentrations in skin blister fluid and antihistamine activity.
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PMID:Clinical pharmacokinetics of mizolastine. 1151 Jun 27


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