ライフサイエンスコーパス: antihistamine

1 e, often refractory to standard therapy (ie, antihistamines).

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

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

4 agonist drug astemizole, a widely prescribed antihistamine.

5 r alone or in combination with an intranasal antihistamine.

6 The patient received H 1-antihistamine.

7 l corticosteroid in combination with an oral antihistamine.

8 ination therapy with a glucocorticoid and an antihistamine.

9 medications in addition to standard dose of antihistamine.

10 blished medications, notably scopolamine and antihistamines.

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

12 ly responsive to standard therapy, including antihistamines.

13 al, and systemic diseases is unresponsive to antihistamines.

14 ptly with intramuscular epinephrine and oral antihistamines.

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

16 manner after subjects were premedicated with antihistamines.

17 known cardiotoxic effects of other, related antihistamines.

18 ective for patients with ColdU refractory to antihistamines.

19 quality of life and is often unresponsive to antihistamines.

20 t efficacy of classical drugs such as H(1) R-antihistamines.

21 f nasal corticosteroids with or without oral antihistamines.

22 SU who have had an inadequate response to H1 antihistamines.

23 bers of adverse events than first-generation antihistamines.

24 ponded to treatment with corticosteroids and antihistamines.

25 d highly divergent MoAs for two FDA-approved antihistamines.

26 be delayed if receiving systemic steroids or antihistamines.

27 hey disappeared after oral administration of antihistamines.

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

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

30 despite treatment with approved doses of H1 antihistamines.

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

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

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

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

35 the Italian market is dominated by systemic antihistamines (41.4%) followed by intranasal corticoste

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

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

38 bed drugs with anticholinergic activity were antihistamines (68.9%), gastrointestinal antispasmodics

39 idated these effects, demonstrating that one antihistamine activates autophagy, while the other targe

40 elated analogues through N-oxidation affects antihistamine activity in an enantiomer-dependent fashio

41 cal notes (OR, 3.21; 95% CI, 1.27-8.08); and antihistamine administration alone or in combination (OR

42 asibility of this approach, we have used the antihistamine agent loratadine (1).

43 H1-antihistamines (AHs) may exert protective effects agains

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

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

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

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

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

49 Subsets of subjects were premedicated with antihistamine and corticosteroid.

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

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

52 tion (as per EAACI definition), treated with antihistamine and steroids.

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

54 laxis, although evidence supports a role for antihistamine and/or glucocorticoid premedication in spe

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

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

57 Antihistamines and benzodiazepines are frequently prescr

58 Larger randomized trials comparing both antihistamines and benzodiazepines with placebo could be

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

60 Patients with skin symptoms received more antihistamines and corticosteroids in the acute treatmen

61 ds or a fixed combination of intranasal H(1)-antihistamines and corticosteroids.

62 management of acute allergic reactions with antihistamines and epinephrine autoinjectors.

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

64 The ability to demonstrate the impact of antihistamines and immunomodulation from peanut oral imm

65 onditions improved after treatment with oral antihistamines and instruction to dry their underwear in

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

67 ic chronic urticaria, which was treated with antihistamines and leukotriene receptor antagonists.

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

69 Treatment with antihistamines and mast cell stabilizers alleviates the

70 Oral and intranasal antihistamines and nasal corticosteroids are both approp

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

72 Antihistamines and omalizumab, an anti-IgE mAb, are the

73 nts who do not respond to the combination of antihistamines and omalizumab.

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

75 Antihistamines and second-line therapies such as omalizu

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

77 o prevent IR include the prophylactic use of antihistamines and steroids, but they cannot ensure tota

78 ld avoidance, the regular use of nonsedating antihistamines and the off-label use of omalizumab.

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

80 Evidence is lacking to support the role of antihistamines and/or glucocorticoid routine premedicati

81 Antihistamines and/or glucocorticoids are not reliable i

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

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

84 7% of patients received adrenaline, 85% oral antihistamines, and 89% received IV glucocorticosteroids

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

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

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

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

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

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

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

92 and other opioids, amphetamines, cathinones, antihistamines, and tetracyclic antidepressants.

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

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

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

96 First-generation antihistamines are associated with sedation, psychomotor

97 Second-generation H1 antihistamines are first-line treatment, omalizumab is s

98 Second-generation H1 antihistamines are first-line treatment; partial or comp

99 mast-cell-associated itch disorders in which antihistamines are ineffective.

100 Although antihistamines are still widely prescribed for the treat

101 Second-generation H1 antihistamines are the mainstay of management, with refr

102 Histamine H1 receptor antagonists (antihistamines) are recommended as adjunctive therapy fo

103 nallergic rhinitis consists of an intranasal antihistamine as monotherapy or in combination with an i

104 esponses and warrant prospectively exploring antihistamines as adjuvant agents for combinatorial immu

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

106 two groups, the percentage of patients using antihistamines at 3 years was significantly lower in the

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

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

109 20% when CPN1(-/-) mice were treated with an antihistamine before C5a challenge.

110 Antihistamines, benzodiazepines, and antipsychotics may

111 Drugs like antihistamines, beta-blockers, antipsychotics, antidepre

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

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

114 More IgE-sensitized patients used antihistamines but fewer inhaled corticosteroids than no

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

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

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

118 The antihistamine clemastine inhibits multiple stages of the

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

120 %-62% lower incidence of AD versus an active antihistamine comparator (adjusted hazard ratio 0.38; in

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

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

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

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

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

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

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

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

129 tes norfluoxetine and norsertraline) and the antihistamine diphenhydramine.

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

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

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

133 The antihistamine drug fexofenadine inputs were greater duri

134 e was incorporated into the structure of the antihistamine drug Rupatidine instead of the pyridine ri

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

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

137 lyses revealed that cancer patients who took antihistamines during immunotherapy treatment had signif

138 desloratadine, loratadine) or an intranasal antihistamine (eg, azelastine, olopatadine), whereas pat

139 rhinitis may include a second-generation H1 antihistamine (eg, cetirizine, fexofenadine, desloratadi

140 eg, quetiapine) or off-label use of sedative antihistamines (eg, promethazine).

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

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

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

144 Epinephrine and antihistamines followed by systemic corticosteroids are

145 intranasal corticosteroid and an intranasal antihistamine for initial treatment.

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

147 cyclic antidepressants, and first-generation antihistamines) for at least 3 consecutive months.

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

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

150 roved urticaria symptoms in patients with H1-antihistamine (H1-AH) refractory CSU.

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

152 mbination treatment with INCS and intranasal antihistamines in both AR and NAR.

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

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

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

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

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

158 Intranasal antihistamines (INAH), corticosteroids (INCS), and their

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

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

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

162 stent across key drug classes including oral antihistamine, intranasal corticosteroids, short-acting

163 ents include oral, intranasal or ocular H(1)-antihistamines, intranasal corticosteroids or a fixed co

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

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

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

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

168 l stabilizers (including cromolyn and the H1-antihistamine ketotifen), suplatast tosilate which is a

169 Antihistamines lack efficacy in treating itch in AD, sug

170 naged with an array of options, including H2 antihistamines, leukotriene receptor antagonists, glucoc

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

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

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

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

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

176 Topical antihistamines, mast cell stabilizers, or double-action

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

178 Sedating antihistamines may impair driving performance as serious

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

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

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

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

183 rs, opioids, antiemetics, antivertiginosa or antihistamines, metoclopramide, domperidone, anticholine

184 ere significantly improved compared with the antihistamine monotherapy group.

185 H(1)-antihistamines, montelukast, danazol, H(2)-antihistamine

186 e safe for breastfeeding patients, including antihistamines, mucolytics, antitussives, antifungals, a

187 n/N = 26/112) patients on non-sedating H(1) -antihistamines (nsAH) and 41.9% (n/N = 44/105) patients

188 Non-sedating H(1) -antihistamines (nsAH) are the most commonly used treatme

189 owed that nonsedating second-generation H(1)-antihistamines (nsAHs) are effective in the treatment of

190 drug-target network analysis suggested that antihistamine of promethaziney and dietary supplement of

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

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

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

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

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

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

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

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

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

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

201 Either intranasal antihistamines or INCS may be offered as first-line mono

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

203 cologic treatment (omalizumab, cyclosporine, antihistamines, or systemic corticosteroids).

204 )-antihistamines, montelukast, danazol, H(2)-antihistamines, pentoxifylline, doxepin, and tranexamic

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

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

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

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

209 ly strong evidence suggests that single-dose antihistamines provide greater vertigo relief at 2 hours

210 The oral antihistamines pyrilamine and ranitidine were administer

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

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

213 2727) >=18 years of age diagnosed with H(1) -antihistamine-refractory chronic spontaneous urticaria (

214 The biologic omalizumab, 300 mg, for H1 antihistamine-refractory chronic spontaneous urticaria (

215 and harms of all available treatments for H1 antihistamine-refractory chronic spontaneous urticaria (

216 AWARE (A World-wide Antihistamine-Refractory chronic urticaria patient Evalu

217 ria activity score over 7 days [UAS7] >= 16) antihistamine-refractory CSU treated with intravenous ba

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

219 diminished disease activity in patients with antihistamine-refractory CSU, including more patients wi

220 imab demonstrated activity across 3 forms of antihistamine-refractory CU.

221 Although antihistamines remain a cornerstone of therapy, particul

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

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

224 sulted in a marked reduction of CTTs in H(1)-antihistamine-resistant patients.

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

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

227 the primary outcome of interest: single-dose antihistamines resulted in significantly more improvemen

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

229 Antihistamines reverse these effects and improve the eff

230 TCAs (RR = 2.23, 95% C.I. = 1.83-2.72), and antihistamines (RR = 2.18, 95% C.I. = 1.83-2.59) outperf

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

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

233 ment escalation from second-generation H(1) -antihistamines (sgAHs) to omalizumab and cyclosporine un

234 Furthermore, we find that clemastine, an antihistamine shown to increase oligodendrocyte precurso

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

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

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

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

239 Antihistamines suppressed histamine-induced contraction

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

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

242 The antihistamine terfenadine and a gastrointestinal prokine

243 The antihistamine terfenadine decreased cell proliferation a

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

245 For the antihistamine terfenadine, drug-induced disruption of co

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

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

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

249 ep-up administration of second-generation H1-antihistamines to four-fold the approved dose, followed

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

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

252 ine administration of glucocorticoids and/or antihistamines to prevent anaphylaxis with prior ICM hyp

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

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

255 0001) and omalizumab-treated patients versus antihistamine-treated patients (0.7% vs 2.6%; HR 3.99, P

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

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

258 Patients were off antihistamine treatment for at least 3 days before testi

259 ow-up experiments testing the impact of oral antihistamine treatment on mosquito feeding parameters f

260 HRH1 knockout or antihistamine treatment reverted macrophage immunosuppre

261 Side effects requiring antihistamine treatment were uncommon (0.21%), and no ep

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

263 gic and systemic disorders that often resist antihistamine treatment.

264 xis, presence of skin lesions, and long-term antihistamine treatment.

265 uffering a severely active CSU refractory to antihistamine treatment.

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

267 and angioedema unresponsive to high doses of antihistamine treatment.

268 Oral antihistamine treatments do not disrupt the development

269 Oral antihistamine treatments with pyrilamine or ranitidine d

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

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

272 Other evidence suggested that daily antihistamine use may not benefit patients with acute ve

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

274 (fluticasone propionate or its equivalent), antihistamine use, leukotriene antagonist use and intran

275 IgE reduction and nasal symptoms and rescue antihistamine use.

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

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

278 ing the use of intranasal corticosteroids or antihistamines versus placebo.

279 patients treated with second-generation H(1) antihistamines versus untreated patients (1.0% vs 2.3%;

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

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

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

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

284 Premedication with corticosteroids and antihistamines was not used.

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

286 The nine antihistamines were baseline separated on the tandem col

287 Differences between oral H(1)-antihistamines were found.

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

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

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

291 d 1 month, neither daily benzodiazepines nor antihistamines were reported to be superior to placebo.

292 ith CSU who had an inadequate response to H1 antihistamines were screened for inclusion independently

293 g intranasal corticosteroids and 8 oral H(1)-antihistamines were studied.

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

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

296 Meclizine, an antihistamine with anticholinergic properties, is the mo

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

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

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

300 008, the primary focus was on its role as an antihistamine, with a thorough evaluation of its pharmac