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PubMed1993

Double-blinded comparison of diphenhydramine versus lidocaine as a local anesthetic.

STUDY OBJECTIVE: To evaluate the efficacy, onset of action, duration of action, and side effects of 1% diphenhydramine compared with 1% lidocaine when used as a local anesthetic agent. DESIGN: Prospective, double-blinded, cross-over study. SETTING: Emergency medicine residency program, research section. PARTICIPANTS: Ten healthy male volunteers, aged 26 to 38 years old. INTERVENTIONS: Baseline levels of sensation to pinprick (18-gauge needle) within a 2.4-cm-diameter midvolar forearm area and levels of sedation were recorded on 10.2-cm visual analog scales. Subjects then underwent subcutaneous infiltration of 20 mg (2 mL) of the study agent using a 27-gauge needle. Visual analog scale sensation and sedation scores were recorded at five, ten, and 15 minutes and then every 15 minutes until return to baseline. Subjects were studied one week later with the alternate agent. Nonparametric data were analyzed using the Mann-Whitney U test with significance at P < .05. RESULTS: No significant differences in mean pinprick sensation were seen from baseline to 30 minutes. Significant differences were seen at 45 (P = .036) and 60 minutes (P = .036). The mean duration of effective anesthesia was significantly longer for lidocaine than diphenhydramine (81 versus 42 minutes, P = .028). No significant differences were seen in the sedation scores or in the frequencies of local reactions. One subject developed skin necrosis at the injection site with diphenhydramine. CONCLUSION: The duration of local anesthesia for 1% lidocaine was significantly longer and the depth of anesthesia after 30 minutes was significantly higher than that of 1% diphenhydramine. Diphenhydramine resulted in skin necrosis in one test subject.

Adult↗

PubMed1990

Comparison of cimetidine and diphenhydramine in the treatment of acute urticaria.

Recent case reports have suggested that H2-antihistamines used alone may be effective in the treatment of acute urticaria, a common complaint of patients presenting to the emergency department. This contradicts accepted doctrine on the treatment of acute urticaria. Based on theories of H1- and H2-receptor interaction at the cellular level, it has been stated that H2-blockade before H1-blockade may exacerbate symptoms. The purpose of our study was to compare diphenhydramine, an H1-blocker, with cimetidine, an H2-blocker, in a randomized, prospective, double-blind clinical trial. Ninety-three patients presenting to the ED with clinical evidence of acute urticaria were treated with either 50 mg diphenhydramine IM or 300 mg cimetidine IM. Patients' signs and symptoms were quantitated on a numeric scale before receiving medications and 30 minutes after treatment. Parameters measured included degree of itching, intensity and extent of wheals, degree of sedation, and perception of overall improvement. Each medication provided significant relief of itching and wheal intensity (P less than .0001). Sedation was caused by both diphenhydramine (P less than .0001) and cimetidine (P less than .0006). However, the degree of sedation caused by diphenhydramine was significantly greater than that caused by cimetidine (P = .0001). The perception of overall improvement was greater with cimetidine, with 87% of patients reporting improvement, whereas 76% of diphenhydramine-treated patients reported improvement. Our results indicate that cimetidine is efficacious as the initial treatment of acute urticaria and has less tendency toward sedation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1996

Effects of semprex-D and diphenhydramine on learning in young adults with seasonal allergic rhinitis.

OBJECTIVES: The purpose of this study was to test the hypothesis that learning ability is impaired in patients with seasonal allergic rhinitis relative to untreated individuals and to evaluate a combination compound (acrivastine 8 mg + pseudoephedrine 60 mg) for attenuation of the learning impairment in these patients. BACKGROUND: In a previous study employing the same method it was shown that young children (10 to 12 yrs) suffering from seasonal allergic rhinitis performed significantly worse on tests of learning and using knowledge after acute treatment with a sedating antihistamine (diphenhydramine 50 mg) or placebo as compared with nontreated healthy controls. This effect was partially reversed by treatment with loratadine. METHODS: Sixty-seven young adults suffering from seasonal allergic rhinitis and 28 matched controls were trained on didactic simulation for three consecutive days. Atopic subjects were treated differentially during training according to a double-blind, randomized, parallel group design with either diphenhydramine hydrochloride 50 mg, a combination compound (acrivastine 8 mg + pseudoephedrine 60 mg, A + P), or placebo, administered qd. After training, all atopic subjects were maintained on A + P treatment for 14 days at which time all groups returned for examination. RESULTS: Mean performance at the end of training was worse for all atopic subjects combined compared with normal subjects. Subjects treated with diphenhydramine performed significantly worse than either normals (P < .001) or those treated with A + P (P < .001). At the examination, the diphenhydramine group's performance differed significantly from those of the normal (P < .001) and A + P groups (P < .001). CONCLUSION: The study supports our previous finding that allergy symptoms reduce learning ability which is further reduced learning ability which is further reduced by diphenhydramine. Atopic subjects with allergies treated with acrivastine + pseudoephedrine learned as well as normal subjects.

Adolescent↗

PubMed1996

Effect of cimetidine on the pharmacokinetics and pharmacodynamics of chlorpheniramine and diphenhydramine in rabbits.

PURPOSE: The effects of concomitant administration of the H2-receptor antagonist cimetidine on the pharmacokinetics and pharmacodynamics of the H1-receptor antagonists chlorpheniramine and diphenhydramine were studied in rabbits. METHOD: A single dose of chlorpheniramine 10 mg (Group A) or diphenhydramine 10 mg (Group B) was given intravenously on three different study days as follows: 2 weeks before cimetidine administration, after giving cimetidine 100 mg/kg intravenously every 12 hours for one week, and two weeks after discontinuing the cimetidine. Serum chlorpheniramine and diphenhydramine concentrations were measured by HPLC. Histamine H1-blockade was assessed by measuring suppression of the histamine-induced wheals in the skin. RESULTS: The chlorpheniramine and diphenhydramine terminal elimination half-life values and area under the curve values were significantly increased, and the systemic clearance rates were significantly decreased, during concomitant administration of cimetidine. For each H1-receptor antagonist, pharmacokinetic parameters were similar before cimetidine was co-administered and two weeks after cimetidine was discontinued. Wheal suppression produced by chlorpheniramine or diphenhydramine was increased and prolonged when cimetidine was administered concomitantly. CONCLUSION: Any enhanced peripheral H1-blockade observed could be attributed, at least in part, to a pharmacokinetic interaction.

Alanine Transaminase↗

PubMed1980

Diphenhydramine in Orientals and Caucasians.

The kinetics and psychomotor effects of diphenhydramine were investigated in Orientals and Caucasians. Each of 5 Oriental and 5 Caucasian young adults received on 1 of 3 occasions diphenhydramine 50 mg/70 kg body weight either intravenously or orally, or placebo. Plasma levels of diphenhydramine were measured hourly for 8 hr at each session. Tests of subjective sedation and psychomotor performance were performed at hourly intervals. The results showed that after both intravenous and oral diphenhydramine, at all times Orientals had plasma levels approximately half those of Caucasians. With the assumption of linear kinetics and a 1-compartment open model, analysis of the data showed that the volume of distribution (VD) and plasma clearance (Cl) but not plasma half-life (t 1/2) were higher in Orientals than Caucasians: [VD = 480 +/- 24 (SEM) and 292 +/- 36 1/70 kg; Cl = 79 +/- 7 and 51 +/- 7 1/70 kg/hr; t 1/2 = 4.1 +/- 0.4 and 4.3 +/- 0.4 hr]. Unbound diphenhydramine in fresh plasma was higher in Orientals than Caucasians [24.0 +/- 1.9% (SEM) and 14.8 +/- 1.5%] and probably explains the increased VD in Orientals. Orientals had significantly less sedation and deterioration in psychomotor performance.

Adult↗

PubMed1988

Oral metoclopramide with or without diphenhydramine: potential for prevention of late nausea and vomiting induced by cisplatin.

Late nausea and vomiting lasting 2-7 days occurs in 20%-68% of patients receiving cisplatin. We therefore studied the effects of oral metoclopramide given at doses of 20, 50, or 100 mg four times a day for 25 doses (7 days) beginning after cisplatin to determine the maximum tolerated dose (MTD) for prophylactic oral antiemetic regimens. Patients were stratified into younger (less than or equal to 30 yr old) and older (greater than 30 yr old) groups. Dose escalation was performed without or with concomitant oral diphenhydramine. For the younger group, the MTD for metoclopramide without diphenhydramine was less than 20 mg, and the MTD with diphenhydramine was 20 mg. For the older group, the MTD without diphenhydramine was 20 mg, and the MTD with diphenhydramine was 50 mg. Extrapyramidal reactions in the younger group and agitated depression in the older group were the major dose-terminating toxic effects. Patient acceptance of these regimens was excellent.

Adolescent↗

PubMed2006

Characterizing impaired functional alertness from diphenhydramine in the elderly with performance and neurophysiologic measures.

STUDY OBJECTIVES: Psychometric task performance measures can be highly sensitive to manipulations that impair functional alertness in young adults; such measures have been shown to be less sensitive to reduced alertness in older adults. The purpose of this study is to determine whether neurophysiologic measures can aid in the detection and characterization of impairments in functional alertness in the elderly. DESIGN: Double-blind, placebo-controlled, counter-balanced, crossover study. SETTING: Research laboratory. PARTICIPANTS: Twelve healthy older adults (62-75 years of age). INTERVENTIONS: Diphenhydramine, 50 mg. MEASUREMENTS AND RESULTS: Behavioral performance and electroencephalogram measures were obtained while participants completed spatial working memory and word recognition episodic memory tasks in a baseline interval before drug ingestion and in 4 hourly test intervals following drug ingestion. Relative to placebo, diphenhydramine had marginal effects on task performance yet was effective in reducing alertness, as evidenced by subjective ratings and objective neurophysiologic (electroencephalogram) markers. Diphenhydramine significantly reduced the amplitude of alertness-sensitive event-related potentials recorded during working memory task performance, including the N160 and P300. It also affected neurophysiologic processes underlying episodic memory, as evidenced by a reduction in the difference in event-related potentials between old and new words in the word recognition task. Discriminant analyses incorporating neurophysiologic measures showed that the time course of the central effects of diphenhydramine in older subjects was similar to that previously observed in young adults. CONCLUSIONS: These results demonstrate that diphenhydramine has adverse neurocognitive effects in elderly individuals and highlights the utility of incorporating direct measures of brain function into assessments of functional alertness.

Aged↗

PubMed2003

Acute pharmacological effects of temazepam, diphenhydramine, and valerian in healthy elderly subjects.

Elderly insomniacs are often treated pharmacologically with benzodiazepines, antihistamines, or natural products. A double-blind, randomized, crossover, placebo-controlled study was performed to assess the comparative pharmacodynamics of single doses of temazepam (15 and 30 mg), diphenhydramine (50 and 75 mg), and valerian (400 and 800 mg) in 14 healthy elderly volunteers (mean age, 71.6 years; range, 65-89). Assessments were made at 0, 0.5, 1, 2, 3, 4, 6, and 8 hours postdosing with use of validated measures of subjective sedation and mood (visual analogue scales, Tufts University Benzodiazepine scale) and psychomotor performance (manual tracking and digit symbol substitution tests). Temazepam had dose-dependent effects on sedation and psychomotor ability with a distinct time course. Temazepam 30 mg had the most detrimental effect on psychomotor ability (p < 0.001 compared with all other treatments). Temazepam 30 mg and both doses of diphenhydramine elicited significantly greater sedation than placebo (p < 0.05, all), and temazepam had the greatest effect. There was no difference in sedation scores between 50 and 75 mg diphenhydramine. Sedative effects were slightly lesser with 15 mg temazepam and were not significant in comparison with placebo. Psychomotor impairment was evident after administration of 75 mg diphenhydramine in comparison with placebo on the manual tracking test (p < 0.05); this was less than the impairment with 30 mg temazepam (p < 0.001) but similar to that with 15 mg temazepam (NS). No psychomotor impairment was detected with 50 mg diphenhydramine. Valerian was not different from placebo on any measure of psychomotor performance or sedation.

Aged↗

PubMed2006

Oral sedation with midazolam and diphenhydramine compared with midazolam alone in children undergoing magnetic resonance imaging.

BACKGROUND: The purpose of this study was to compare the safety and efficacy of oral midazolam and midazolam-diphenhydramine combination to sedate children undergoing magnetic resonance imaging (MRI). METHODS: We performed a prospective randomized double-blind study in 96 children who were randomly allocated into two groups. Group D received oral diphenhydramine (1.25 mg x kg(-1)) with midazolam (0.5 mg x kg(-1)), and Group P received oral placebo with midazolam (0.5 mg x kg(-1)) alone. Sedation scores, onset and duration of sleep were evaluated. Adverse effects, including hypoxemia, failed sedation, and the return of baseline activity, were documented. RESULTS: Diphenhydramine facilitated an earlier onset of midazolam sedation (P < 0.01), and higher sedation scores (P < 0.01). In children who received midazolam alone, 20 (41%) were inadequately sedated, compared with 9 (18%) children who received midazolam and diphenhydramine combination (P < 0.01). Time to complete recovery was not significantly different between the two groups. CONCLUSIONS: Our study indicates that the combination of oral diphenhydramine with oral midazolam resulted in safe and effective sedation for children undergoing MRI. The use of this combination might be more advantageous compared with midazolam alone, resulting in less sedation failure during MRI.

Administration, Oral↗

PubMed2005

Sensitivity of late-latency auditory and somatosensory evoked potentials to threat of electric shock and the sedative drugs diazepam and diphenhydramine in human volunteers.

Late-latency auditory and somatosensory evoked potentials are sensitive to some centrally acting drugs and to certain psychological interventions. In this experiment we compared the effects of acute doses of a benzodiazepine, diazepam and an H(1) histamine receptor-blocking sedative, diphenhydramine, on auditory and somatosensory evoked potentials within the latency range 100-500 ms in a fear conditioning paradigm. Twelve healthy males (18-30 years) participated in three sessions at weekly intervals in which they received diazepam 10mg, diphenhydramine 75 mg and placebo in a balanced, double-blind, crossover protocol. One hundred and twenty min after diphenhydramine or 60 min after diazepam, they underwent an 8 min recording period in which auditory evoked potentials elicited by 40 ms, 95 dB[A], 1 kHz tones, and somatosensory evoked potentials elicited by a mildly painful electric shock (1.8 mA, 50 ms) were recorded at Cz (vertex). Each session consisted of four blocks of trials in which either the sound pulse or the shock was presented. Alternate blocks were designated SAFE or THREAT ('context' conditions); in THREAT blocks subjects were warned that shocks would be delivered via electrodes placed on the wrist (electrodes were removed during SAFE blocks). In one SAFE and one THREAT block, the sound stimuli and shocks (shocks were delivered only in the THREAT block) were preceded by a 2 s conditioned stimulus (CS: a red light) ('cue' condition). Diazepam, but not diphenhydramine, reduced the amplitude of the P2 auditory evoked potential. The THREAT context was associated with increased N1 and reduced N2 potential amplitudes. The CS had no effect on the amplitudes, but markedly reduced the latencies of the N1, P2 and N2 potentials under the THREAT condition. Diazepam reduced the amplitudes of the somatosensory potential evoked by the shock; the CS shortened the latencies of the later components of the response. Diazepam and diphenhydramine were approximately equi-sedative in the doses used in this experiment, as judged by visual analogue self-rating scales. The results indicate that the suppression of late-latency auditory and somatosensory evoked potentials by diazepam is not simply a reflection of sedation. Late-latency evoked potentials can be modified by an aversive CS, but the components that are sensitive to the CS are different from those that are sensitive to diazepam.

Acoustic Stimulation↗

PubMed2000

Inhibition of Na(+) current by diphenhydramine and other diphenyl compounds: molecular determinants of selective binding to the inactivated channels.

Diphenhydramine is an H1 histamine receptor antagonist, yet it also has a clinically useful local anesthetic effect. We found that diphenhydramine inhibits the neuronal Na(+) current, and the inhibition is stronger with more positive holding potentials. The dissociation constant between diphenhydramine and the inactivated Na(+) channel is approximately 10 microM, whereas the dissociation constant between diphenhydramine and the resting channel is more than 300 microM. The local anesthetic effect of diphenhydramine thus is ascribable to inhibition of Na(+) current by selective binding of the drug to the inactivated channels. Most interestingly, many other compounds, such as the anti-inflammatory drug diclofenac, the anticonvulsant drug phenytoin, the antidepressant drug imipramine, and the anticholinergic drug benztropine, have similar effects on neuronal Na(+) current. There is no apparent common motif in the chemical structure of these compounds, except that they all contain two phenyl groups. Molecular modeling further shows that the two benzene rings in all these drugs have very similar spatial orientations (stem bond angle, approximately 110 degrees; center-center distance, approximately 5 A). In contrast, the two phenyl groups in phenylbutazone, a drug that has only a slight effect on Na(+) current, are oriented in quite a different way. These findings strongly suggest that the two phenyl groups are the key ligands interacting with the channel. Because the binding counterpart of a benzene ring usually is also a benzene ring, some aromatic side chain groups of the Na(+) channel presumably are realigned during the gating process to make the very different affinity to the aforementioned drugs between the inactivated and the resting channels.

Anesthetics, Local↗

PubMedDate not supplied

Sedative-hypnotic use of diphenhydramine in a rural, older adult, community-based cohort: effects on cognition.

OBJECTIVE: The authors sought to identify patterns and associations of prescription and over-the-counter sedative-hypnotic use in an older, rural, blue-collar, community-based cohort in southwestern Pennsylvania over 10 years. METHODS: A group of 1,627 individuals age 65 and over were recruited and assessed during 1987-1989 and re-assessed during approximately biennial waves. Data included sleep medications, demographics, depressive symptoms, sleep complaints, and cognitive functioning (Mini-Mental State Exam [MMSE]). RESULTS: At Waves 1 through 5, the mean age of the cohort increased from 73.4 to 80.5 years. Use of prescription sedative-hypnotics (primarily benzodiazepines) increased from 1.8% to 3.1%, and over-the-counter sedative-hypnotic use (primarily diphenhydramine) increased from 0.4% to 7.6%. At Wave 5 (1996-1998), 8.17% of the sample reported using diphenhydramine as a sleep aid. After adjusting for age and sex, diphenhydramine use was associated with higher education and more depressive symptoms, the latter becoming nonsignificant after controlling for initial insomnia. MMSE became significantly associated with diphenhydramine use when 143 subjects with dementia were excluded from the analysis. CONCLUSION: As the cohort aged, prescription sedative-hypnotic use remained relatively stable, whereas over-the-counter sedative use, principally diphenhydramine, increased substantially. The association of this drug with cognitive impairment in persons without dementia highlights its potential for causing adverse reactions in older adults.

Aged↗

PubMed2003

Fatal diphenhydramine intoxication in infants.

Diphenhydramine is an antihistamine available in numerous over-the-counter preparations. Often used for its sedative effects in adults, it can cause paradoxical central nervous system stimulation in children, with effects ranging from excitation to seizures and death. Reports of fatal intoxications in young children are rare. We present five cases of fatal intoxication in infants 6, 8, 9, 12, and 12 weeks old. Postmortem blood diphenhydramine levels in the cases were 1.6, 1.5, 1.6, 1.1 and 1.1 mg/L, respectively. Anatomic findings in each case were normal. In one case the child's father admitted giving the infant diphenhydramine in an attempt to induce the infant to sleep; in another case, a daycare provider admitted putting diphenhydramine in a baby bottle. Two cases remain unsolved; one case remains under investigation. The postmortem drug levels in these cases are lower than seen in adult fatalities. We review the literature on diphenhydramine toxicity, particularly as it pertains to small children, and discuss the rationale for treating these cases as fatal intoxications.

Diphenhydramine↗

PubMed1992

Diminished mephobarbital anticonvulsant action following diphenhydramine pretreatment.

Diphenhydramine and other antihistamines produce biphasic effects on drug disposition and lower seizure threshold, thereby potentially diminishing the efficacy of anticonvulsants such as mephobarbital. Accordingly, the influence of diphenhydramine (50 mg/kg, IP) pretreatment on the anticonvulsant activity of mephobarbital (50 mg/kg, IP) was determined in adult female Swiss-Webster mice given pentylenetetrazol (SC). Diphenhydramine lowered the pentylenetetrazol convulsive dose (CD50) by 60%. Administration of diphenhydramine in combination with mephobarbital produced a 65% decrease in the CD50 of pentylenetetrazol in comparison with that of animals given mephobarbital plus pentylenetetrazol. Pharmacokinetic evaluation of mephobarbital blood level data indicates that the mechanism responsible for the observed interaction between diphenhydramine and mephobarbital involves a decrease in mephobarbital uptake from the administration site.

Animals↗

PubMed1979

Diphenhydramine protection of the failing myocardium during gram-negative endotoxemia.

Gram-negative endotoxin (Escherichia coli, 4 mg/kg) was found to produce a sustained fall in systemic arterial pressure, left ventricular pressure, and cardiac output that could be blocked by the histamine antagonist diphenhydramine. Histamine infusion was found to produce a parallel depression of systemic arterial pressure. Further, endotoxemia was found to produce a significant depression of myocardial contractility (dP/dt max) that could also be blocked by diphenhydramine. Cardiac myofibrillar adenosine triphosphatase (ATPase) activity from endotoxin-shocked hearts was found to be depressed, ATPase activity from subendocardial myofibrils being more depressed than that from subepicardial myofibrils. Myofibrillar ATPase activity was significantly protected by pretreating the animals with diphenhydramine. It is concluded that the initial hemodynamic phase of endotoxin shock is histamine-mediated and that this hemodynamic depression can be blocked with diphenhydramine. Further, it appears that endotoxin is capable of depressing myocardial contractility by depressing contractile protein function (myofibrillar ATPase activity)--the subendocardial surface more so than the subepicardial surface--and this depression of myocardial contractility can be blocked with diphenhydramine.

Adenosine Triphosphatases↗

PubMed1991

Compatibility of dexamethasone sodium phosphate with hydromorphone hydrochloride or diphenhydramine hydrochloride.

The stability and compatibility of dexamethasone sodium phosphate and hydromorphone hydrochloride or diphenhydramine hydrochloride at various concentrations at room temperature was studied. Solutions containing equal volumes in the following ranges of concentrations were prepared: dexamethasone sodium phosphate 0-10 mg/mL, diphenhydramine hydrochloride 0-50 mg/mL, and hydromorphone hydrochloride 0-40 mg/mL. Samples of each combination were analyzed immediately after mixing and at 7 and 24 hours using a stability-indicating high-performance liquid chromatographic assay. The pH of each solution was measured, and each combination was visually inspected. Precipitation occurred in solutions containing dexamethasone and hydromorphone hydrochloride or diphenhydramine hydrochloride when equal volumes of the most concentrated solutions were mixed. Some of the combinations at lower concentrations were visually compatible, and more than 90% of the initial concentrations of both drugs (i.e., dexamethasone-hydromorphone and dexamethasone-diphenhydramine) remained in these compatible solutions. Dexamethasone is visually compatible with diphenhydramine or hydromorphone but only within specific concentration ranges. In visually compatible solutions, both drug combinations are stable for up to 24 hours at room temperature.

Chromatography, High Pressure Liquid↗

PubMed1986

Determination of diphenhydramine in biological fluids by capillary gas chromatography using nitrogen-phosphorus detection. Application to placental transfer studies in pregnant sheep.

A nitrogen-phosphorus detection-gas chromatographic method, which provides improved sensitivity and selectivity for diphenhydramine, is reported. A 25 m X 0.31 mm cross-linked, 5% phenylmethyl silicone-coated fused-silica capillary column (film thickness 0.52 micron) was used for all analyses. The splitless capillary injection mode was employed with a 2-microliter sample being introduced by an automatic liquid sampler. Standard curves, using orphenadrine as an internal standard, were linear in the range 2-320 ng of diphenhydramine per 0.5 ml of sheep plasma. This represents an amount of diphenhydramine from ca. 40 pg to 6.4 ng at the detector. Chromatographic separation of diphenhydramine and orphenadrine was excellent, with no interference from endogenous plasma constituents. Applicability of the method was demonstrated by a placental transfer study in a chronically instrumented pregnant sheep following a 100 mg intravenous injection of diphenhydramine to the ewe.

Animals↗

PubMed1976

Allergic and photoallergic dermatitis from diphenhydramine.

A 52-year-old man developed contact and photoallergic dermatitis caused by diphenhydramine hydrochloride as well as contact dermatitis from paraphenylenediamine. The diphenhydramine photoallergy was elicited by long-wave ultraviolet light. The action spectrum differs from that noted in a recent report in which wavelengths shorter than 320 nm were responsible for eliciting diphenhydramine photoallergy. To the best of my knowledge, this is the third case of diphenhydramine photosensitivity reported in the English literature. The combination of both contact and photosensitivity to diphenhydramine has not previously been described.

Dermatitis, Contact↗