Cannabinoid
hyperemesis - Not just a problem in Adelaide Hills 12
November 2004
Enrico Roche,
Peter N. Foster Dear
Editor
We read the article by Allen et al[1] with interest and would like to report
a case of probable cannabinoid hyperemesis seen in a district general hospital
in the UK.
A 21-year-old chef was admitted to our hospital on seven occasions during a two
year period (April 2001 to December 2002) with profuse vomiting. Apart from a
history of migraine as a child he was fit and well. He smoked cannabis. Physical
examination was unremarkable. The observation that the patient wanted to take
regular baths because he had found that bathing eased the sickness was documented
in the nursing notes but its significance was not appreciated. Investigations
during attacks disclosed neutrophilia but blood urea, electrolytes, liver biochemistry
and serum amylase were normal. Abdominal X-ray was also normal. Upper GI endoscopy
showed grade I oesophagitis and gastritis. Gastric biopsies were histologically
normal. An abdominal ultrasound scan and small bowel barium follow through examination
were normal. Additional normal or negative investigations included: autoantibodies
and immunoglobulins, C-reactive protein and urinary porphyrin screen. A CT scan
of the brain was also normal.
During his last admission, the patient’s girlfriend showed us an article
published in an Australian newsletter, which she had obtained via the internet,
in which Dr JH Allen had raised the possibility of a link between recurrent vomiting
and cannabis abuse. With the aid of the internet we traced and contacted Dr Allen
who shared his experience of this condition with us.
Reviewing the patient’s history, he freely admitted to smoking cannabis
and experiencing the compulsive desire to bathe during the bouts of vomiting.
Following his last admission in December 2002 our patient stopped smoking cannabis
and has remained free of symptoms. The clinical presentation which is almost identical
to the cases described by Allen et al together with the response to cessation
of smoking cannabis supports the view that our patient was suffering from cannabinoid
hyperemesis and that this condition is international. Reference
1. Allen JH, de Moore, GM Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical
hyperemesis in association with chronic cannabis abuse. Gut 2004; 53: 1566-1570
'Cannabis
hyperemesis' causation questioned 26
April 2005
Andrew Byrne, Richard Hallinan, Alex Wodak
Dear Editor,
These authors describe a number of cases of a bizarre syndrome of severe vomiting,
abdominal symptoms leading to dehydration in combination with repetitive bathing
behaviour. They have concluded that these symptoms are due to cannabis use.
Cannabis has been consumed for many centuries and is currently used by millions
of people in many countries. It is hard to believe that a distinctive syndrome
caused by cannabis has never been noted before by users or clinicians.
The authors assert that cannabis laws are particularly liberal in South Australia.
Four Australian jurisdictions now have a cannabis expiation notice system which
South Australia first introduced in 1986. The other four Australian jurisdictions
have variations on a bond system. Several European countries have far more lenient
legislative arrangements. After over a generation of liberalisation of cannabis
laws in many countries around the world, there is little evidence of a subsequent
increase in cannabis use.
In a comparative study using the same methodology, the prevalence of cannabis
use in more 'liberal' Amsterdam was lower than in more 'punitive' San Francisco
[1].
The title of the paper, 'Cannabinoid hyperemesis' is unduly presumptive. Some
of these cases appeared to improve with abstinence and then relapsed when patients
were 'rechallenged' with cannabis, however neither the patients nor the authors
appear to have been blinded in the rechallenge. The proposed biological explanation
is weak.
We suggest that alternative explanations need to be sought for these cases. This
syndrome should not be accepted as being caused by cannabis without additional
reports and other evidence.
Yours faithfully,
Andrew Byrne
Richard Hallinan
Alex Wodak References
1.
Reinarman C, Cohen PDA, Kaal HL. The Limited Relevance of Drug Policy: Cannabis
in Amsterdam and in San Francisco. Am J Public Health. (2004) 94:836 842.
Authors'
Reply to Byrne et al. 5
May 2005
James H Allen, Gregory De Moore, Richard Heddle, John Twartz
Dear Editor, We
would like to thank Byrne et al. for their interest in our Paper.[1] It should
be noted that we undertook an observational study by necessity. Cannabis is an
illegal drug and double blind control trials with illicit substances are prohibited
and unethical. The assertion that cannabis has been “consumed for many centuries”
needs to be tempered with the fact that cannabis has been grossly nder-researched
clinically and, as we have shown with this syndrome, nowhere near fully understood
in its neuropharmacology or paradoxical actions. Since publication of our article
other authors have published similar findings and drawn the same conclusions.[2]
References
1.
JH Allen, GM De Moore, R Heddle, JC Twartz. Cannabinoid hyperemesis: cyclical
hyperemesis in association with chronic cannabis abuse. Gut 2004 Nov;53(11):1566-70.
[MEDLINE] 2.
Roche E, Foster PN. Cannabinoid hyperemesis: not just a problem in Adelaide Hills.
Gut 2005 May;54(5):731.[MEDLINE]
Cannabinoid
hyperemesis: normalization of gastric motility after cessation of use
22
July 2005
Noel R Fajardo, Yvonne Romero
Dear Editor,
We have been following the case of a 41 year old male with spontaneous and recurrent
episodes of vomiting occurring regularly in a cycle every 4-6 months, separated
by symptom-free intervals, which started 5 years ago. Endoscopy and imaging studies
were negative for disease. He is healthy and does not have any other active medical
problems. He admitted to be a daily marijuana user for the past 20 years. A scintigraphic
gastric emptying study performed last November 2004 revealed delayed emptying
at the 2nd and 4th hour (39% [40-78%] and 64% [84-98%] respectively [normal range
in brackets]).
Allen et al.[1] suggested the association of cannabis use and hyperemesis. We
advised our patient to cease from marijuana use. After 2 weeks of abstention,
a repeat gastric emptying study was performed, and showed normal 2nd and 4th hour
emptying (58% and 94% respectively). Clinically, it is still too premature at
this point to make a statement whether he will be free from his cyclic vomiting
episodes.
The mechanism of cannabinoid hyperemesis and cyclic vomiting syndrome is unknown.
To date, cyclic vomiting has not been shown to be associated with any GI functional
testing abnormality. Clinical studies on the effect of cannabis showed delayed
gastric emptying in healthy volunteers.[2] The case series of Allen et al. suggested
the association of chronic cannabis use and hyperemesis but the physiologic explanation
of the phenomena was not fully elucidated.
The presentation of this case was not an attempt to explain the neuropharmacology
of chronic marijuana use and its role in cyclic vomiting syndrome. Rather, we
are more intrigued by the observation that chronic marijuana use may lead to gastric
dysmotility resulting in hyperemesis, and that the dysmotility may normalize after
a period of cessation. It is apparent that further studies are needed to determine
marijuana-associated toxicity. Also, the association between marijuana use and
cyclic vomiting syndrome should further be explored with longitudinal, population
based studies.
We do, however, reiterate the views of Allen et al. that in the management of
patients presenting with hyperemesis, marijuana use should be ascertained, and
its cessation should be recommended. References:
1.Allen, J.H., G.M. de Moore, R. Heddle, et al., Cannabinoid hyperemesis: cyclical
hyperemesis in association with chronic cannabis abuse. Gut, 2004. 53(11): p.
1566-70.
2.McCallum, R.W., I. Soykan, K.R. Sridhar, et al., Delta-9- tetrahydrocannabinol
delays the gastric emptying of solid food in humans: a double-blind, randomized
study. Alimentary Pharmacology & Therapeutics, 1999. 13(1): p. 77-80.
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