eMJA: In Other Journals, 4 February 2008

Platelet-activating factor (PAF) and PAF acetylhydrolase have been identified as important mediators of anaphylaxis in humans, according to Canadian researcher Vadas and colleagues. PAF is a proinflammatory phospholipid secreted by mast cells, monocytes and fixed tissue macrophages; PAF acetylhydrolase is the enzyme that inactivates PAF. In a two-part study, they found that: (1) mean serum PAF levels were not only higher in 41 patients with anaphylaxis than in 23 healthy volunteers but were also correlated with the severity of anaphylaxis; and (2) that serum PAF acetylhydrolase activity was lower in nine patients with fatal peanut anaphylaxis than patients in any of several control groups. They suggested that failure of PAF acetylhydrolase to inactivate PAF may contribute to the severity of anaphylaxis.

The researchers said further studies will be needed to assess the usefulness of PAF acetylhydrolase as a biochemical marker of risk for anaphylaxis. They also said that their data provide a rationale for the development of drugs to selectively block the actions of PAF — both as rescue therapy in cases of acute anaphylaxis and, potentially, as long-term preventive treatment for those at highest risk for fatal anaphylaxis.

Facing up

The world’s first full facial transplant could finally happen in the United Kingdom this year, according to a feature article in the BMJ. Adopting an evidence-based research strategy, pioneering plastic surgeon Peter Butler’s London-based team has now gained approval to conduct a clinical series of four full facial transplants. A small group of recipients have been identified, including casualties from the armed forces injured on duty in Iraq. The next phase is to look for a suitable well matched donor face, so that the donor is not “seen” in the recipient. Each transplant operation will involve about 35 professionals, and will be funded by Butler’s charity, the Face Trust.

BMJ 2008; 336: 18-19

Fallout follows deluge

When Hurricane Katrina hit New Orleans on 29 August 2005, the city’s hospital staff struggled to care for patients for several days afterwards, without power (and air-conditioning), fresh water or functional sanitation. Now, an article reports that one of the doctors who “stayed behind” to help faces three civil suits after reportedly administering morphine and midazolam to several critically ill patients who subsequently died. Due to the litigation, details have not been publicly discussed; however, as it stands, the incomplete story suggests that civilian doctors were expected to make difficult triage, evacuation and other decisions when working with limited resources in conditions more closely resembling those of a battlefield than a hospital; miscommunication may also have played a part in events.

Although a grand jury has previously refused to indict the doctor involved, there has been at least one prediction that efforts to prosecute the doctor will have a chilling effect on the willingness of medical professionals to volunteer during disasters. It is suggested that expanded training and public debate about triage, communication and decision making in disasters could help all of us to better prepare for any ordeals of the future.

N Engl J Med 2008; 358: 1-5

Be a doctor in 3 years?

How long does it take to become a doctor? How long should it take? For about 30 years, two universities in Canada — McMaster University in Hamilton, Ontario and the University of Calgary — have been training people to become doctors in just 3 years, whereas all the other medical schools in Canada offer a 4-year program. Given the high professional and social costs of a further year of study, CMAJ editors say that it is time to formally examine whether the “extra” fourth year is really needed. They suggest comparing the 3-year and 4-year programs in terms of, first, short-term outcomes — particularly medical licensing examination scores — and second, long-term outcomes — such as the proportion of graduates in leadership roles, the proportion serving areas of greatest need, and the proportion subject to licence restrictions or disciplinary actions.

CMAJ 2008; 178: 11

Obesity and gum disease

Researchers in the United States have shown that obesity interferes with the ability of the immune system to respond to bacterial infection. In animal research, Amar and colleagues infected (diet-induced) obese mice and lean control mice with live Porphyromonas gingivalis, an organism strongly associated with periodontitis in people. The mice were infected with the P. gingivalis either orally or systemically; in both cases, the obese mice developed a blunted systemic inflammatory response, including reduced levels of pro-inflammatory cytokines. The researchers suggested that strong antimicrobials rather than anti-inflammatory agents should be used in individuals with diet-induced obesity and severe infection.

Proc Natl Acad Sci U S A 2007; 104: 20466-20471

Dr Ann Gregory, MJA

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