ライフサイエンスコーパス: antihistamine

1 3F8 was given with an opiate and an antihistamine.

2 agonist drug astemizole, a widely prescribed antihistamine.

3 l corticosteroid in combination with an oral antihistamine.

4 ination therapy with a glucocorticoid and an antihistamine.

5 medications in addition to standard dose of antihistamine.

6 rtisements for Zyrtec (McNeil), a competitor antihistamine.

7 ponded to treatment with corticosteroids and antihistamines.

8 ly responsive to standard therapy, including antihistamines.

9 hey disappeared after oral administration of antihistamines.

10 al, and systemic diseases is unresponsive to antihistamines.

11 ptly with intramuscular epinephrine and oral antihistamines.

12 a (PBD-ZrO2) phase was used to separate nine antihistamines.

13 manner after subjects were premedicated with antihistamines.

14 known cardiotoxic effects of other, related antihistamines.

15 h angioedema refractory to high doses of H1 -antihistamines.

16 x, health care use because of AR, and use of antihistamines.

17 despite treatment with approved doses of H1 antihistamines.

18 blished medications, notably scopolamine and antihistamines.

19 be delayed if receiving systemic steroids or antihistamines.

20 matic despite the use of approved doses of H-antihistamines.

21 went to the hospital, 27% self-treated with antihistamines, 10% called 911, 11% self-administered ep

22 e), antidepressants (2.3-fold increase), and antihistamines (2.1-fold increase).

23 lower fill rates for the respiratory agents (antihistamines: -23%, 95% confidence interval [CI]: -10%

24 ing NSAIDs (27%) and allergy patients taking antihistamines (31%).

25 l anti-inflammatory drugs (NSAIDs) (45%) and antihistamines (44%).

26 rofessionals included corticoids (60.4%) and antihistamines (52.8%).

27 atients receiving SCF were premedicated with antihistamines, albuterol, and pseudoephedrine.

28 atopic diseases, a known allergy, the use of antihistamines (all P < 0.001), depression (P = 0.003),

29 e receiving standard-of-care therapy with H1-antihistamines along with 1 or more add-on therapies.

30 s defined as the association between an oral antihistamine and a local anti-allergic drug on the same

31 When used in lower doses and with antihistamine and beta-agonist premedication, stem cell

32 ector, prior improvement with use of an oral antihistamine and immediate visit to a hospital emergenc

33 hylaxis could be blocked by a combination of antihistamine and platelet-activating factor antagonist

34 molecule that was initially developed as an antihistamine and subsequently was shown to stabilize mi

35 d treatment for likely related AEs, 59% with antihistamines and 12% with epinephrine.

36 t but improved pruritus controlled with oral antihistamines and 23 remained asymptomatic, with only 2

37 e use of antidepressants, phenothiazines, or antihistamines and breast cancer.

38 phylaxis; second-line medications (including antihistamines and glucocorticoids) are not.

39 and the use of intranasal steroids and both antihistamines and intranasal steroids were more common

40 nctivitis, and treatment consists of topical antihistamines and mast cell inhibitors.

41 Treatment with antihistamines and mast cell stabilizers alleviates the

42 Oral and intranasal antihistamines and nasal corticosteroids are both approp

43 The use of medications such as antihistamines and NSAIDs, which are taken intermittentl

44 ic delay of many years and do not respond to antihistamines and other treatments of urticaria.

45 Common medications such as antihistamines and steroids can have undesirable long-te

46 ck, shoulder, and arm, resistant to systemic antihistamines and topical corticosteroids.

47 ufficiently controlled by a standard dose of antihistamine, and revisited from 2003 to 2009.

48 Premedication included analgesics, antihistamines, and 5-minute infusions of HM3F8.

49 7% of patients received adrenaline, 85% oral antihistamines, and 89% received IV glucocorticosteroids

50 elf-administration: 67% corticosteroids, 83% antihistamines, and 9% intramuscular adrenaline.

51 Dexamethasone, 5HT3 receptor antagonists, antihistamines, and anticholinergics reduce the incidenc

52 t containing an adrenaline autoinjector, H1 -antihistamines, and corticosteroids depending on the sev

53 ion of topical and systemic corticosteroids, antihistamines, and immunosuppressants was unsuccessful.

54 and emesis of pregnancy, ginger, pyridoxine, antihistamines, and metoclopramide were associated with

55 with placebo, two compared two different H1 -antihistamines, and one study compared H1 - and H2 -anti

56 lcium or vitamin D supplements, antibiotics, antihistamines, and prednisolone significantly more ofte

57 similar for nonantiarrhythmic drugs such as antihistamines, antibiotics, and antipsychotics.

58 ve a number of enantiomeric pairs, including antihistamines, antidepressants and phenylhydantoins, us

59 rhythmics, antidepressants, anticonvulsants, antihistamines, antihypertensives, antimalarials, relaxa

60 First-generation antihistamines are associated with sedation, psychomotor

61 ere significantly higher in nonresponders to antihistamines as compared to responders (P < .001).

62 rsistent CIU/CSU despite treatment with H(1)-antihistamines at up to 4 times the approved dose plus H

63 derations: avoid the eliciting food, take an antihistamine before any situation with a possible risk

64 20% when CPN1(-/-) mice were treated with an antihistamine before C5a challenge.

65 Antihistamines, benzodiazepines, and antipsychotics may

66 s response(s) to ALA-PDT, the impact of H(1) antihistamine blockade, and measured dermal histamine re

67 Pretreatment of the skin with an antihistamine blocked the itch produced by histamine but

68 t frequently given drugs were corticoids and antihistamines, but not adrenaline.

69 Several forms of itch can be blocked using antihistamines, but others cannot and these constitute a

70 The second-generation antihistamines cetirizine and ketotifen, which have eosi

71 Initial treatment included a combination of antihistamines, colchicine, and dapsone.

72 metabolites of astemizole and those of other antihistamine compounds have not been implicated as caus

73 will respond to conventional treatment with antihistamines, corticosteroids or epinephrine.

74 s indicated that histamines and, conversely, antihistamines could potentially modulate sebocyte funct

75 Pretreatment of the tested skin with an antihistamine cream (doxepin) inhibited histamine-induce

76 uently, clinicians need to use the best H(1)-antihistamines currently available and the pharmaceutica

77 mate, disodium valproate, levetiracetam, the antihistamine cyproheptadine, and the antidepressant ami

78 All three antihistamines did not affect NT-mediated hypothermia.

79 e inhibitor alpha-methylparatyrosine and the antihistamine diphenhydramine hydrochloride were adminis

80 tes norfluoxetine and norsertraline) and the antihistamine diphenhydramine.

81 re randomly allocated to receive intravenous antihistamines (diphenhydramine, 1 mg/kg, and cimetidine

82 The treatment of choice is nonsedating antihistamines, dosages of which may be increased up to

83 mercial formulations of the over-the-counter antihistamine drug cetirizine dihydrochloride.

84 A formal synthesis of carbinoxamine, an antihistamine drug used for the treatment of seasonal al

85 However, current antihistamine drugs are not effective in controlling the

86 ia) do not have a response to therapy with H-antihistamines, even at high doses.

87 lipids, and metabolites were identified, and antihistamine excretion was followed via the direct anal

88 vestigations need to determine whether early antihistamine exposure is a major risk factor for ADHD o

89 intranasal corticosteroid and an intranasal antihistamine for initial treatment.

90 inhibitors, nonbenzodiazepine hypnotics, and antihistamines for more than 4 weeks was associated with

91 has replaced older less specific drugs (e.g. antihistamines) for the treatment of adverse effects cau

92 nd flare responses which are abrogated by H1-antihistamines giving rise to the hypothesis that PAF-in

93 There is very limited evidence that antihistamines improve olfactory function.

94 t indicator we have of effectiveness of H(1)-antihistamines in clinical practice.

95 a biomarker of severity and resistance to H1-antihistamines in CU patients.

96 profile, and (iii) the sales of prescription antihistamines in The Netherlands.

97 iveness, and safety of second-generation H1 -antihistamines in treatment of primary MCAS.

98 ns on children with urticaria and the use of antihistamines in women who are pregnant or breastfeedin

99 es, pruritus is not effectively treated with antihistamines, indicating the involvement of nonhistami

100 lar adrenaline injection, corticosteroid and antihistamine infusions, volume resuscitation, and salbu

101 he same treatment as allergic patients using antihistamines, inhaled corticosteroids and IgE antagoni

102 th intranasal corticosteroid plus intranasal antihistamine is more effective than either alone and pr

103 Supportive treatment with steroids and antihistamines is not very effective.

104 teroids (INCS) (daily or on demand) and oral antihistamines, it remains unclear which treatment provi

105 Our study evaluated acupuncture and antihistamine itch therapy (cetirizine) on type I hypers

106 Antihistamines lack efficacy in treating itch in AD, sug

107 (up to 4 times the approved dose) plus H(2)-antihistamines, leukotriene receptor antagonists, or bot

108 at up to 4 times the approved dose plus H(2)-antihistamines, leukotriene receptor antagonists, or bot

109 , we examined the effects of the nonsedating antihistamine loratadine on a rapidly activating delayed

110 einyl leukotriene antagonist montelukast and antihistamine loratadine or two matched placebos were ad

111 e degrees of allergic conjunctivitis include antihistamines, mast cell stabilizers, and nonsteroidal

112 H1-antihistamines may be of benefit, but this evidence was

113 Sedating antihistamines may impair driving performance as serious

114 The use of nonsedating antihistamines may, on rare occasions, be associated wit

115 indicator of the in vitro potency of an H(1)-antihistamine, may help in the initial selection of cand

116 effect of Claritin (Merck & Co.), a leading antihistamine medication, across subjects randomized to

117 k of bias indicated that ginger, vitamin B6, antihistamines, metoclopramide (for mild symptoms), pyri

118 ere significantly improved compared with the antihistamine monotherapy group.

119 S on demand (fluticasone propionate) or oral antihistamine on demand (levocetirizine) for 3 months du

120 ily was not superior to INCS on demand or to antihistamine on demand regarding the number of symptom-

121 otoxicity of terfenadine, the effect of this antihistamine on L-type Ca2+ channel current (ICa,L) was

122 The antihistamine on-demand group had 15% symptom-free days,

123 e studies suggested possible effects of oral antihistamines on asthma and sleep-disordered breathing.

124 INCS is superior to on-demand use or to oral antihistamines on demand.

125 ors, tricyclic antidepressants, opioids, and antihistamines on the risk of motor vehicle crashes in 1

126 an a mild reaction, 4 of the 8 received oral antihistamines only, and none received epinephrine.

127 s not respond to conventional agents such as antihistamines or corticosteroids.

128 therapeutically by, for example, H1- and H2-antihistamines or cysteinyl leukotriene receptor antagon

129 No risk data were available for nasal antihistamines or montelukast sodium.

130 Pretreatment with intravenous H1 and H2 antihistamines permitted rapid vancomycin administration

131 rcyclizine (CCZ, Rac-2), an over-the-counter antihistamine piperazine drug, possesses in vitro and in

132 cells, where it can serve as a vasodilator, antihistamine, platelet aggregation inhibitor, and antic

133 during 30 minutes without corticosteroid or antihistamine premedications on days 1, 8, and 15 of a 2

134 The oral antihistamines pyrilamine and ranitidine were administer

135 In vivo, treatment with antihistamines pyrilamine or cimetidine decreased lung w

136 Analogues of the known H(1)-antihistamine R-dimethindene were profiled as potential

137 lizumab treatment in patients with severe H1-antihistamine-refractory CSU with angioedema.

138 Although antihistamines remain a cornerstone of therapy, particul

139 urticarias (CIndUs), which are frequently H1-antihistamine resistant.

140 effective treatment option for patients with antihistamine-resistant chronic urticaria.

141 a, nerve growth, leukocyte infiltration, and antihistamine-resistant scratching behavior in mice expo

142 nt to consider in patients who are seen with antihistamine-resistant urticaria in combination with sy

143 , other antidepressants, phenothiazines, and antihistamines; results were very similar using both con

144 of treatment with the second-generation H1 -antihistamine rupatadine, compared with placebo, resulte

145 While second generation antihistamines (sgAHs) are the first line therapeutic st

146 ERG block is relevant to the toxicity of the antihistamine, since the clinical terfenadine concentrat

147 mainly cutaneous) and 49 patients used oral antihistamine, six inhaled adrenaline, and ten took no t

148 nnic acid and tea extracts), phenothiazines, antihistamines, statins, and antimalarial compounds.

149 -generation humanized recombinant anti-CEA x antihistamine-succinyl-glycine (HSG) trivalent BsMAb TF2

150 ffectiveness of adrenaline (epinephrine), H1-antihistamines, systemic glucocorticosteroids or methylx

151 Administration of the antihistamine terfenadine (Seldane) to patients may resu

152 The antihistamine terfenadine and a gastrointestinal prokine

153 A high-throughput screen identified the antihistamine terfenadine to possess, previously unrepor

154 ical industries need to keep developing H(1)-antihistamines that are more effective than the ones we

155 urticaria who remained symptomatic despite H-antihistamine therapy (licensed doses).

156 d its Impact on Asthma group's call for oral antihistamines to exhibit additive anti-allergic/anti-in

157 management plan, as well as epinephrine and antihistamines to have on hand at all times.

158 ghly sensitive persons may want to take oral antihistamines to minimize cutaneous reactions to mosqui

159 empirical treatments, including antibiotics, antihistamines, topical and oral corticosteroids, and ep

160 Each patient received a combination of antihistamines, topical corticosteroids, and thick emoll

161 recipients and will require epinephrine and antihistamine treatment and, possibly, intensive care.

162 CIU/CSU) who remained symptomatic despite H1 antihistamine treatment at licensed doses.

163 y cases, pathological itch is insensitive to antihistamine treatment.

164 gic and systemic disorders that often resist antihistamine treatment.

165 (CIU/CSU) who remain symptomatic despite H1 -antihistamine treatment.

166 and angioedema unresponsive to high doses of antihistamine treatment.

167 uffering a severely active CSU refractory to antihistamine treatment.

168 Oral antihistamine treatments do not disrupt the development

169 Oral antihistamine treatments with pyrilamine or ranitidine d

170 remained symptomatic despite the use of H(1)-antihistamines (up to 4 times the approved dose) plus H(

171 yroid disease (OR, 1.43; 95% CI, 1.02-1.99), antihistamine use (OR, 1.54; 95% CI, 1.18-2.02), and ste

172 ents in disease-specific quality of life and antihistamine use measures after 8 weeks of treatment co

173 IgE reduction and nasal symptoms and rescue antihistamine use.

174 ine (a long-acting and nonsedating tricyclic antihistamine) using an ion trap mass spectrometer (LCQ)

175 ese results could shift current paradigms of antihistamine utilization from a predominantly systemic

176 ria that was treated with a standard dose of antihistamine was lower than that treated with additiona

177 ffer concentration on retention of the basic antihistamines was also studied.

178 in an USH2C patient was that oral intake of antihistamines was associated with temporary resolution

179 The efficacy of second-generation antihistamines was evaluated on the day of blood collect

180 Premedication with corticosteroids and antihistamines was not used.

181 In children with AD-only, previous use of antihistamines was significantly associated with increas

182 The nine antihistamines were baseline separated on the tandem col

183 s unit leading to inflammatory acne lesions, antihistamines were investigated for their effect on seb

184 For therapeutic agents, antihistamines were most prescribed, and the combination

185 despite treatment with approved doses of H1 antihistamines were randomized (1:1:1:1) in a double-bli

186 lergy treatment (CAT; nasal steroids or oral antihistamines) were compared with regard to mortality a

187 tments for allergies include epinephrine and antihistamines, which treat the symptoms after an allerg

188 gency medication allocated accordingly: oral antihistamine with or without inhaled or injected epinep

189 Two studies compared an H1 -antihistamine with placebo, two compared two different H

190 tamines, and one study compared H1 - and H2 -antihistamines with oral cromolyn sodium.

191 008, the primary focus was on its role as an antihistamine, with a thorough evaluation of its pharmac