MJA 216 7 18 April cover

Issues

Volume 216 Issue 7

18 April 2022

News

18 April 2022 Free

News

How the gut communicates with the brain New research from Flinders University has discovered how specialised cells within the gut can communicate with both the brain and spinal cord, which up until now had remained a major mystery. The study, published in the American Journal of Physiology, reveals a breakthrough discovery regarding how enterochromaffin cells communicate with sensory nerve endings. “The gut–brain axis consists of bidirectional communication between the brain and the gut, which links emotional and cognitive centres of the brain with peripheral intestinal functions. Within the gut wall lie specialised cells called enterochromaffin [EC] cells that produce and release hormones and neurotransmitters in response to particular stimuli that are ingested when we eat,” said author Professor Nick Spencer. “These EC cells release the vast majority of serotonin into the body, so our study has uncovered a major clue into how the food we eat stimulates the release of serotonin, which then acts on the nerves to communicate with the brain. There is a direct connection between serotonin levels in our body and depression and how we feel. So, understanding how the gut EC cells communicate with the brain is of major importance.” The team made the discovery using a neuronal tracing technique developed in their lab, not used anywhere else in the world, allowing them to see the sensory nerve endings with clarity, for the first time, in the gut wall. The technique allowed the researchers to see that EC cells likely release substances by a process of diffusion, which then acts on the sensory nerves that communicate with the brain. No direct physical connection between the EC cells and sensory nerve endings were found, contrary to some suggestions. How does COVID‐19 affect people’s ability to smell? Olfactory dysfunction is a common symptom experienced by individuals with COVID‐19. In research published in The Laryngoscope, researchers searched the medical literature for studies reporting changes in olfactory structures detected through imaging tests of patients with COVID‐19. The prevalence of an olfactory cleft abnormality was nearly 16‐fold higher in patients with COVID‐19 and olfactory dysfunction (63%) compared with controls (4%). The olfactory clefts provide a crucial channel for airborne molecules to reach sensory olfactory neurons that connect to the brain to enable a person to perceive smells. “Before this study, most scientists thought that the loss of smell in COVID‐19 was mainly due to inflammation and damage to the olfactory nerves. Now, we have compiled evidence from medical imaging that COVID‐19 loss of smell is also due to swelling and blockage of the passages in the nose that conduct smells,” said senior author Neville Wei Yang Teo from Singapore General Hospital. “We think this is good news for patients who want to recover their sense of smell, since these blockages are expected to resolve with time, while nerve damage in comparison would likely be more difficult to recover from,” added co‐author Claire Jing‐Wen Tan, of the National University of Singapore. “These findings may not fully account for those who suffer from prolonged olfactory dysfunction, however, and further studies that evaluate patients in this group may provide more information.”

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Letters

Environmental health 18 April 2022 Free

Chemical analysis of fresh and aged Australian e‐cigarette liquids

To the Editor: In their recent article, Larcombe and colleagues1 describe the analysis of 65 electronic cigarette fluid samples. The gas chromatography mass spectrometry method, as described in the Supporting Information, used “the ratio between the peak area corresponding to the fragment with the highest signal‐to‐noise ratio … and the peak area of the internal standard” for quantification.1 Direct comparison of the peaks for the analyte of interest and the internal standard does not take into account differences in response factor and/or ionisation efficiency for the different molecules. For accurate quantification, individual calibration curves should be prepared for all molecules of interest. If the authors prepared calibration curves but did not include this information, then the methods section should be modified to reflect this, and additional validation should be provided for all analytes, including limits of detection, limits of quantification, and coefficients of determination for all curves. In addition, all samples should be analysed in triplicate and a standard deviation should be provided to further validate the analysis. Larcombe et al1 note in their article that the determined concentrations of benzaldehyde, menthol, 2‐chlorophenol and benzyl alcohol exceed inhalational LC50 (the median lethal concentrations that kill 50% of a test animal population) values for these compounds. This assertion, as written, is incorrect and should have been reworded to a less confident statement. As the authors themselves acknowledge, the e‐liquid concentration and the inhalational LC50 values are not comparable. Furthermore, the authors did not provide the LC50 values they were using nor a citation to their source for these values. For a more accurate comparison, the volume of e‐liquid vaporised per litre of inhaled vapour would need to be calculated. Assuming the consumption of 9.47 mg of e‐liquid per puff and a puff volume of 55 mL,2 the maximum concentration observed for both benzaldehyde (2.58 mg/m3) and menthol (30.5 mg/m3) would fall below their respective derived no‐effect level (DNEL) values of 9.8 mg/m3 and 132 mg/m3.3,4 We were unable to locate an inhalational DNEL or LC50 value for 2‐chlorophenol. The maximum concentration for benzyl alcohol (251 mg/m3) would exceed its DNEL value of 110 mg/m3 for acute exposure.5 This, along with the high prevalence of benzyl alcohol in e‐liquid samples, requires further investigation.

Jody Morgan · Alison Jones · Celine Kelso

Respiratory disease 18 April 2022 Free

E‐cigarette or vaping product use‐associated lung injury in an adolescent

To the Editor: Chan and colleagues1 recently reported a case of putative e‐cigarette or vaping product use‐associated lung injury (EVALI) in a 15 year‐old girl who was a low level user of vaporised nicotine (without adulterants). We believe that, rather than EVALI, her presentation is better explained by urosepsis‐related acute lung injury. Current guidance from the United States Centers for Disease Control and Prevention (CDC)2 emphasises the role of adulterants, especially vitamin E acetate, in EVALI. In a US study completed before the widespread adoption of e‐cigarettes, the incidence of acute lung injury in 15–19‐year‐olds was 16 per 100 000 patient‐years, with many cases stemming from non‐pulmonary sepsis.3 In February 2020, only 2807 cases of vaping lung injury had been reported in the US, representing an incidence of well under one case per 100 000 patient‐years.1 Given these rates, as well as the patient’s prominent dysuria, polyuria, back pain and worsening pyrexia, we think urosepsis triggered the acute lung injury in this case. The authors say that sepsis was ruled out due to negative blood and urine cultures. However, if samples were collected after the initiation of antibiotics, false negative cultures are common in sepsis. The patient met the accepted criteria for sepsis, with suspected infection, a systemic inflammatory response syndrome and acute end‐organ failure,4 and was treated for this condition with antibiotics and corticosteroids for the acute lung injury. The CDC criteria for EVALI emphasise that the diagnosis should only be made where there is “no evidence in [the] medical record of alternative plausible diagnoses”.5 Dysuria, polyuria and back pain are not known symptoms of EVALI, and the authors have not explained how EVALI could account for this aspect of her presentation nor why these symptoms preceded the respiratory symptoms. In conclusion, the evidence to support a diagnosis of EVALI is insufficient in this case, and an alternative explanation is far more likely. Therefore, this case report should not be regarded as evidence for a case of EVALI occurring in Australia.

Cameron RL McKenzie · Joshua Davis · Adrian J Dunlop

Careers

Next Issue Volume 216 Issue 8

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MJA 216 8 2 May cover
News 2 May 2022 Free

News briefs

Perspectives 18 April 2022 Open Access

Practical recommendations to communicate with patients about health‐related conspiracy theories

Mathew D Marques · Karen M Douglas · Daniel Jolley

Perspectives 2 May 2022 Open Access

Emerging evidence for the use of colchicine for secondary prevention of coronary heart disease

Stefan M Nidorf · Jamie Layland · Philip C Robinson · Sanjay Patel · Peter J Psaltis · Peter L Thompson

Perspectives 2 May 2022 Open Access

The need for improved Australian data on social determinants of health inequities

Joanne Flavel · Martin McKee · Toby Freeman · Connie Musolino · Helen Eyk · Fisaha H Tesfay · Fran Baum

Previous Issue Volume 216 Issue 6

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MJA 216 6 4 April cover
News 4 April 2022 Free

News briefs

Perspectives 4 April 2022 Free

Concussion in Aboriginal and Torres Strait Islander peoples: what is the true epidemiology?

Jonathan Bullen · Trish Hill‐Wall · Elizabeth Thomas · Richard Norman · Gill Cowen

Perspectives 4 April 2022 Free

Realising the potential: leveraging clinical quality registries for real world clinical research

Susannah Ahern · Belinda J Gabbe · Sally Green · Carol L Hodgson · Erica M Wood · John R Zalcberg OAM · Tsharni Zazryn

Perspectives 4 April 2022 Open Access

Population DNA screening for medically actionable disease risk in adults

For the DNA Screen Investigator Group†

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