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J H Allen, G M de Moore, R Heddle, J C Twartz
Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse
Gut 2004; 53: 1566-1570 [Abstract][Full text][PDF]

Electronic letters published:

[Read eLetter]Cannabinoid hyperemesis: normalization of gastric motility after cessation of use
NOEL R FAJARDO, YVONNE ROMERO   (22 July 2005)
[Read eLetter]Authors' Reply to Byrne et al.
James H Allen, Gregory De Moore, Richard Heddle, John Twartz   (5 May 2005)
[Read eLetter]'Cannabis hyperemesis' causation questioned
Andrew Byrne, Richard Hallinan, Alex Wodak   (26 April 2005)
[Read eLetter]Cannabinoid hyperemesis - Not just a problem in Adelaide Hills
Enrico Roche, Peter N. Foster   (12 November 2004)

Cannabinoid hyperemesis: normalization of gastric motility after cessation of use 22 July 2005
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NOEL R FAJARDO,
GI FELLOW
DIV. OF GASTROENTEROLOGY AND HEPATOLOGY MAYO CLINIC ROCHESTER MN,
YVONNE ROMERO

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Re: Cannabinoid hyperemesis: normalization of gastric motility after cessation of use

FAJARDO.NOEL{at}MAYO.EDU NOEL R FAJARDO, et al.

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.

Authors' Reply to Byrne et al. 5 May 2005
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James H Allen,
Medical Officer
Mt.Barker Hospital,Wellington Road,Mt.Barker .South Australia.,
Gregory De Moore, Richard Heddle, John Twartz

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Re: Authors' Reply to Byrne et al.

giballen{at}bigpond.com James H Allen, et al.

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]

'Cannabis hyperemesis' causation questioned 26 April 2005
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Andrew Byrne,
Dependency Physician
Private practice, Sydney, Australia,
Richard Hallinan, Alex Wodak

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Re: 'Cannabis hyperemesis' causation questioned

ajbyrne{at}ozemail.com.au Andrew Byrne, et al.

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.

Cannabinoid hyperemesis - Not just a problem in Adelaide Hills 12 November 2004
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Enrico Roche,
Consultant Gastroenterologist
Macclesfield District General Hospital, UK,
Peter N. Foster

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Re: Cannabinoid hyperemesis - Not just a problem in Adelaide Hills

enrico.roche{at}ntlworld.com Enrico Roche, et al.

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


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