Clinical Toxicology

ISSN: 1556-3650 (Print) 1556-9519 (Online) Journal homepage: http://www.tandfonline.com/loi/ictx20

Resolution of cannabis hyperemesis syndrome

with topical capsaicin in the emergency
department: a case series

Laurel Dezieck, Zachary Hafez, Albert Conicella, Eike Blohm, Mark J.

O’Connor, Evan S. Schwarz & Michael E. Mullins

To cite this article: Laurel Dezieck, Zachary Hafez, Albert Conicella, Eike Blohm, Mark J.
O’Connor, Evan S. Schwarz & Michael E. Mullins (2017): Resolution of cannabis hyperemesis
syndrome with topical capsaicin in the emergency department: a case series, Clinical Toxicology,
DOI: 10.1080/15563650.2017.1324166

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Published online: 11 May 2017.

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CLINICAL TOXICOLOGY, 2017
https://doi.org/10.1080/15563650.2017.1324166

CLINICAL RESEARCH

Resolution of cannabis hyperemesis syndrome with topical capsaicin in the

emergency department: a case series
Laurel Deziecka, Zachary Hafezb, Albert Conicellaa, Eike Blohma, Mark J. O’Connorc, Evan S. Schwarzb and
Michael E. Mullinsb
a
Department of Emergency Medicine, University of Massachusetts Medical School, Worcester, MA, USA; bDivision of Emergency Medicine,
Washington University School of Medicine, Saint Louis, MO, USA; cDepartment of Medicine, University of Massachusetts Medical School,
Worcester, MA, USA

ABSTRACT ARTICLE HISTORY

Background: Cannabinoid hyperemesis syndrome (CHS) is characterized by symptoms of cyclic Received 23 December 2016
abdominal pain, nausea, and vomiting in the setting of prolonged cannabis use. The transient receptor Revised 19 April 2017
potential vanilloid 1 (TRPV1) receptor may be involved in this syndrome. Topical capsaicin is a Accepted 21 April 2017
proposed treatment for CHS; it binds TRPV1 with high specificity, impairing substance P signaling in Published online 11 May
2017
the area postrema and nucleus tractus solitarius via overstimulation of TRPV1. This may explain its
apparent antiemetic effect in this syndrome. KEYWORDS
Purpose: We describe a series of thirteen cases of suspected cannabis hyperemesis syndrome treated GI; cannabis; marijuana;
with capsaicin in the emergency departments of two academic medical centers. capsaicin
Methods: A query of the electronic health record at both centers identified thirteen patients with
documented daily cannabis use and symptoms consistent with CHS who were administered topical
capsaicin cream for symptom management.
Results: All 13 patients experienced symptom relief after administration of capsaicin cream.
Conclusion: Topical capsaicin was associated with improvement in symptoms of CHS after other treat-
ments failed.

Introduction
Cannabinoid hyperemesis syndrome (CHS) is characterized by
symptoms of cyclic abdominal pain, nausea, and vomiting in
patients with frequent cannabis use over extended periods
of time. A unique hallmark of CHS is temporary relief of
symptoms with hot showers or baths, which often leads to
compulsive bathing, an impractical solution for management.
It is often refractory to treatment with common antiemetics.
The transient receptor potential vanilloid 1 (TRPV1) receptor
family may play a central role in the pathogenesis of CHS [1].
Capsaicin is known to activate the TRPV1 receptor [1,2].
The incidence of CHS is likely to increase as cannabis use
becomes more prevalent [3]. As the social or legal conse-
quences decrease, emergency physicians are likely to
encounter this condition more often. In the 2016 US elec-
tions, voters in eight states approved medical use of mari-
juana, which is now legal in 28 states and the District of
Columbia. Kim et al. [4] reported that emergency department
(ED) visits for cyclic vomiting doubled in two academic med-
ical centers in Colorado after liberalization of medical mari-
juana use.
We present a series of thirteen cases of successful treat-
ment of CHS with topical capsaicin cream.
Methods
We conducted our study at two academic medical centers:
University of Massachusetts Memorial Medical Center in
Worcester, Massachusetts, and Barnes-Jewish Hospital in St.
Louis, Missouri. Both institutions are tertiary care centers with
130,000 and 82,000 annual visits respectively. We retrospect-
ively identified patients who received topical capsaicin cream
after presenting to the ED with symptoms of CHS. We
searched pharmacy records to identify patients treated with
capsaicin cream during ED visits from 1 January 2015 to 31
December 2016 and then reviewed cases to determine
whether patients met criteria for CHS. Each chart underwent
review by one of the authors to confirm that patients
received capsaicin and met criteria for CHS. We defined CHS
using the criteria described by Simonetto et al. which include
“(A) long-term marijuana use before the start of symptoms,
(B) a history of recurrent vomiting, and (C) the absence of a
major illness that could explain the symptoms” [5]. These
parameters are consistent with Sorensen et al., who describe
CHS as: “a syndrome of cyclic vomiting in the setting of
chronic, high-dose cannabis use that is frequently associated
with compulsive hot baths/showers, used in an attempt to
control symptoms” [1].

CONTACT Laurel Dezieck laurel.dezieck@umassmemorial.org Department of Emergency Medicine, University of Massachusetts Medical School, Worcester,
MA, USA
ß 2017 Informa UK Limited, trading as Taylor & Francis Group
2 L. DEZIECK ET AL.
Owing to the fact that this study is a retrospective chart
review, there is no standardization of dosing or application
method for the capsaicin. Anecdotally “one application” was
a thin layer of the capsaicin cream applied topically, often to
the abdomen of the patient, but dosing was likely varied and
at the discretion of the nurse administering the treatment.
The abdomen is frequently the site of topical application
because it provides a large surface area that is a safe dis-
tance away from sensitive mucous membranes. The back and
chest were also potential sites of application for the same
reason. The abdomen however, appeals cognitively to
patients because it is the site of their physical symptoms.
Our primary outcome of interest was success of capsaicin
treatment in patients with CHS. Indicators of treatment suc-
cess included the number of other treatments used before
and after capsaicin, the time to discharge after capsaicin
administration, ability to eat or drink after treatment, or
qualitative descriptions of how patients felt after receiving
capsaicin. This study received IRB approval at each
institution.
Results
We identified thirteen patients (nine men, four women) with
a median age of 34 years (19–47 years). These included six at
Barnes-Jewish Hospital and seven at University of
Massachusetts Memorial Medical Center. All thirteen subjects
acknowledged cannabis use for varying periods of time (usu-
ally for several years). Two patients explicitly mentioned that
hot showers provided temporary relief, and a third patient
covertly took three hot showers during the ED stay. Twelve
patients had previous ED visits or hospital admissions for the
same condition. During these previous visits, they underwent
repeated laboratory testing, radiographic studies, and special-
ist consultations to investigate the source of their symptoms.
Three patients had prior endoscopic studies, all of which
were non-diagnostic. All laboratory tests and radiographic
studies during each patient’s index visit were normal or non-
diagnostic. For those patients who had prior ED visits or hos-
pital admissions, none had an alternative diagnosis to explain
their symptoms.
Other treatment modalities administered before capsaicin
failed to relieve most patients’ symptoms. Ten patients had
little or no relief with intravenous antiemetics, most com-
monly ondansetron. Five received intravenous opioids.
Capsaicin was the first treatment provided to two patients
(cases two and six). Both received antiemetics after capsaicin.
One was a woman with insulin-dependent diabetes as a pos-
sible contributing cause of her cyclic vomiting (prior gastric
scintigraphy demonstrated normal gastric emptying eliminat-
ing gastroparesis as a cause), and the other was a man who
experienced relief from capsaicin but demanded intravenous
antiemetics because he feared the effect of the capsaicin
would wear off. Capsaicin was the first medication ordered
for one additional patient (case five), but he received two
doses of other antiemetics prior to capsaicin administration.
This was most likely due to the more immediate availability
of certain medications, including ondansetron and
metoclopramide in the ED. Capsaicin cream needed to be
ordered and obtained from the institution’s central pharmacy
and therefore took longer to procure. No patient required
hospital admission after capsaicin treatment.
Three patients had multiple ED visits within a three-day
period for similar symptoms prior to the visit in which capsa-
icin was administered; in all three cases the patients received
varying antiemetics and IV fluids before discharge from the
ED. Only one patient returned to the ED within three days
after receiving capsaicin for similar gastrointestinal symp-
toms. This patient again first received antiemetics and then
received capsaicin cream. He improved after capsaicin admin-
istration and was subsequently discharged without receiving
any further antiemetics.
Table 1 details each patient’s clinical presentation and
course. Figure 1 illustrates the time course for each patient’s
index ED visit and shows the times of other treatments
occurring before and after application of capsaicin.
Discussion
The pathophysiology of CHS is incompletely understood. Two
commonly recognized cannabinoid receptors, CB1 and CB2,
exist. Both are G-protein-coupled receptors (GPCRs) that
inhibit adenylyl cyclase upon activation. CB1 is highly con-
centrated in certain areas of the brain, and CB1 stimulation
may decrease serotonin release [6,7]. However, cannabinoids
also have direct or indirect effects mediated through other
receptors, including other GPCRs and TRPV1.
The TRPV1 receptor is located peripherally as well as in
the select parts of the central nervous system, including the
emesis center in the area postrema and nucleus tractus soli-
tarius (NTS) [8]. It is a non-selective cation channel with cal-
cium preference, which opens to ligand binding or thermal
stimulation. Endocannabionoids (anandamide) and exogen-
ous cannabinoids (cannabidiol, cannabidivarin) are known
agonists of TRPV1 [9,10]. It appears that agonism at TRPV1 is
pro-emetic under low ligand concentration, but anti-emetic
under high ligand concentration. Significant stimulation leads
to TRPV1 desensitization [11]. This may be the result of
altered substance P and calcitonin gene-related peptide
(CGRP) signaling, likely due to reduced substance P receptor
density in the NTS [11–13]. The TRPV1 ion channel opens at
temperatures above 43  C and provides the noxious sensa-
tion of heat [14]. Hot bathing may therefore lead to TRPV1
desensitization and an antiemetic effect in the setting of
CHS. Capsaicin binds TRPV1 with high specificity [15]. It fol-
lows that capsaicin, similar to resiniferatoxin and hot water,
may impair substance P signaling in the area postrema and
NTS by over stimulating TRPV1, thereby exerting antiemetic
properties.
It is plausible that Delta-9 tetrahydrocannabinol (D9 THC)
is anti-emetic in high central nervous system concentration
by means of reduced substance P signaling, as is the case
during active consumption of marijuana. Lipophilic cannabi-
noids deposit in adipose tissue, however, and are gradually
released between episodes of marijuana administration. After
prolonged and heavy marijuana use, cannabinoids released
 CLINICAL TOXICOLOGY 3

Table 1. Case reports.

ED visits/admissions Treatment
Marijuana within one year Arrival Discharge
Case Age Gender frequency Co-morbidities of index time Medication Dose Route Time time
1 28 M Daily Peptic ulcer disease 2/1 16:06 Normal saline 1000 mL IV 16:55
Splenectomy Ondansetron 4 mg IV 17:00
Maalox 20 mL PO 17:05
Viscous lidocaine 10 mL PO 17:05
Ondansetron 4 mg IV 17:23
Fentanyl 100 mcg IV 17:30
Normal saline 1000 mL IV 18:12
Fentanyl 50 mcg IV 18:12
Metoclopramide 10 mg IV 18:27
Lorazepam 1 mg IV 19:00
Fentanyl 50 mcg IV 21:16
Capsaicin 0.25% Topical 21:46 22:53
2 47 M Daily Hiatal hernia 7/4 6:45 Capsaicin 0.25% Topical 7:33
Irritable bowel syndrome Viscous lidocaine 10 mL PO 8:08
Polysubstance abuse Maalox 20 mL PO 8:08
Ondansetron 4 mg IM 9:16
Ketorolac 60 mg IM 10:36 11:12
3 29 M Daily Gastroesophageal reflux 3/0 13:35 Ondansetron 4 mg IV 14:35
Normal saline 1000 mL IV 14:36
Capsaicin 0.25% Topical 16:59 17:42
4 38 M Daily Asthma 4/0 13:52 Fentanyl 100 mcg IV 14:48
Hepatitis C Ondansetron 4 mg IV 14:48
Chronic low back pain Capsaicin 0.25% Topical 16:14
Ondanestron 4 mg IV 16:45
Capsaicin 1.5% Topical 16:49
Metoclopramide 10 mg IV 17:13 22:20
5 19 M Daily Polysubstance abuse 3/0 19:36 Normal Saline 1000 ml IV 20:00
Anxiety Normal Saline 1000 ml IV 21:00
Conversion disorder Ondansetron 4 mg IV 21:00
Metoclopramide 10 mg IV 22:30
Capsaicin 0.25% Topical 23:00 02:11
6 26 F Twice daily Type 1 Diabetes 22/16 13:18 Capsaicin 0.25% Topical 13:30
Gastroesophageal reflux Diphenhydramine 25 mg IV 14:18
Ondansetron 4 mg IV 14:19
Normal Saline 1000 ml IV 14:20
Lorazepam 1 mg IV 14:27
Phenergan 12.5 mg IV 15:42
Diphenhydramine 25 mg IV 16:36
Lorazepam 1 mg IV 16:36
Normal Saline 1000 ml IV 16:45
Ondansetron 4 mg IV 16:52
Normal Saline 1000 ml IV 19:56
Ondansetron 4 mg IV 21:37 22:55
7 27 F Daily None 2/1 21:51 Ondansetron 4 mg IM 01:09
Capsaicin 0.25% Topical 03:55 09:27
8 34 M Daily None 10/3 20:16 Prochlorperazine 5 mg IV 22:50
Normal Saline 1000 mL IV 23:16
Ondansetron 4 mg IV 23:16
Capsaicin 0.075% Topical 23:16
Pyridoxine 50 mg IV 23:17
Normal saline 1000 mL IV 0:14
Ondansetron 4 mg IV 4:41
Prochlorperazine 5 mg IV 4:41 10:33
9 34 M Daily Irritable bowel syndrome 10/3 18:42 Normal Saline 1000 mL IV 19:31
Morphine 4 mg IV 19:31
Ondansetron 4 mg IV 19:31
Normal Saline 1000 mL IV 20:28
Prochlorperazine 10 mg IV 20:39
Ondansetron 4 mg IV 21:46
Pyridoxine 50 mg IV 23:44
Ondansetron 4 mg IV 23:46
Normal Saline 1000 mL IV 23:46
Sumatriptan 100 mg PO 0:35
Morphine 4 mg IV 1:02
Morphine 4 mg IV 6:19
Chlopromazine 25 mg IV 9:50
Capsaicin 0.075% Topical 9:50
Hydromorphone 1 mg IV 12:47 13:53
10 43 F Twice weekly Irritable bowel syndrome 4/0 7:12 Ondansetron 4 mg IV 8:17
Hypertension Morphine 4 mg IV 8:17
Normal Saline 1000 mL IV 8:17
Capsaicin 0.075% Topical 15:12 17:52
(continued)
4 L. DEZIECK ET AL.

Table 1. Continued
ED visits/admissions Treatment
Marijuana within one year Arrival Discharge
Case Age Gender frequency Co-morbidities of index time Medication Dose Route Time time
11 39 M Daily None 2/0 20:54 Ondansetron 4 mg PO 22:55
Normal Saline 1000 mL IV 22:55
Capsaicin 0.075% Topical 00:32 2:00
12 35 M Daily Chronic abdominal pain 0/0 01:54 Ondansetron 4 mg IV 03:20
Normal Saline 1000 mL IV 03:21
Prochlorperazine 10 mg IV 04:20
Normal Saline 1000 mL IV 05:46
Haldol 5 mg IV 07:15
Ondansetron 4 mg IV 10:50
D5 normal saline 1000 mL IV 10:53
Famotidine 20 mg IV 10:53
Capsaicin 0.075% Topical 16:10 18:36
13 24 F Daily None 4/0 10:22 Normal Saline 1000 mL IV 11:23
Ondansetron 4 mg IV 11:23
Normal Saline 1000 mL IV 12:44
Maalox 30 mL PO 12:48
Viscous lidocaine 10 mL PO 12:48
Maalox 30 mL PO 13:28
Viscous lidocaine 10 mL PO 13:28
Ondansetron 4 mg IV 14:25
Morphine 4 mg IV 16:10
Capsaicin 0.075% Topical 16:56 18:16
a
D5 normal saline refers to dextose-5%-normal saline.
Doses of capsaicin are indicated in bold.

Figure 1. Clinical courses.

from the adipose tissue may reach low but sufficient CNS
concentrations to stimulate TRPV1 past the emetic threshold.
We propose that the signal disappears with abstinence and
CHS resolves.
Cannabinoid hyperemesis syndrome itself is triphasic: pro-
dromal, hyperemetic, and recovery. Phases occur in a cyclical
fashion. The characteristic prodromal phase includes nausea
and abdominal discomfort, which are typically worse in the
morning. This precedes the hyperemesis phase, in which the
patient experiences severe, often debilitating vomiting, as
well as diffuse abdominal pain. In this phase, patients can
experience dangerous volume depletion, with documented
cases of acute renal failure and electrolyte abnormalities [16].
It is during the hyperemesis phase that the patient often
develops compulsive bathing, a learned behavior after inci-
dental discovery of symptomatic relief. The recovery phase
can last anywhere from days to months.
The current approach to care is supportive treatment and
allowing for hot showers or baths. Allowing the patient to
bathe can be unwieldy in the ED and offers only temporary
relief of symptoms. Some case reports and case series
suggest haloperidol may be effective in CHS [17–20].

Another case series described seven patients with suspected
CHS, all seven of whom had little or no relief with intraven-
ous granisitron and metoclopramide but subsequently had
rapid relief with topical capsaicin [21]. Additionally, three
abstracts presented in 2014 suggest capsaicin as a treatment
for CHS [2,22,23]. Our findings are consistent with these
reports.
The most common adverse effect (AE) of topical capsaicin
is burning sensation, which some patients found intolerable
and resulted in refusal of further dosing. Other common AEs
include localized erythema and nonproductive cough. Less
common documented AEs include diarrhea, nausea, vomit-
ing, nasopharyngitis, sinusitis, back pain, dizziness, headache,
hypertension, and neuropathy exacerbation [24]. In a recent
Cochrane review article of capsaicin used for neuropathy or
arthritis, localized AEs such as burning sensation and ery-
thema were common but mild; systemic AEs occurred in
3.5% of interventional subjects in multiple RCTs and in 3.2%
of control subjects. AEs requiring withdrawal from the
reviewed studies were 0.8% [25].
Aside from AEs, another limitation to capsaicin adminis-
tration is patient insight and compliance with a topical
medication for their CHS symptoms. While effective long-
term treatment is to cease further marijuana use, multiple
patients in this series refused to believe that their cannabis
use contributed to their symptoms or that the capsaicin
cream was the source of their symptom relief and therefore
refused to continue taking capsaicin cream. Additionally,
they were seldom receptive to cannabis cessation
counseling.
Limitations to this case series include small sample size,
presence of medical comorbidities, discrepancy in treatment
modalities, and lack of an objective means of measuring
positive outcome. Because this study is a retrospective case
series, supportive treatments such as antiemetics and nar-
cotic pain medications varied among patients.
Conclusions
Capsaicin is a non-invasive, low-risk treatment for CHS.
Capsaicin use has a temporal association with relief of CHS
symptoms. Future research should evaluate the relative utility
of capsaicin and other high potency antiemetics such as
haloperidol.
Acknowledgements
The authors would like to thank Dr. Kavita Babu and Dr. Andrew Monte
for their constructive feedback on the revision of this manuscript.
This manuscript includes data presented as poster abstracts at the
37th International Congress of the European Association of Poisons
Centers and Clinical Toxicologists (EAPCCT) 16–19 May 2017, Basel,
Switzerland, and at the 21st New England Regional Society for Academic
Emergency Medicine Regional Meeting 29 March 2017, Worcester, MA,
United States.
Disclosure statement
The authors report no conflicts of interest. The authors alone are respon-
sible for the content and writing of this article.
CLINICAL TOXICOLOGY 5
ORCID
Michael E. Mullins http://orcid.org/0000-0001-8605-0217
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