Idcp Snapshots

December 2001

Statins Decrease Mortality Rate in Bacteremia

The statin drugs are widely used to reduce cholesterol levels. They work by inhibiting the rate-limiting enzyme (often abbreviated as HMG-CoA) involved in cholesterol biosynthesis. There is also some evidence from studies done in vitro and in animals that the statins may reduce the inflammatory reaction within atherosclerotic plaques, possibly through reducing leukocyte migration or the production of tumor necrosis factor. The mortality of bacteremic infections is thought to be due in part to the inflammatory response and cytokine production. Therefore, Liappis et al. (Clin Infect Dis 2001;33:1352-7) examined the effect of statins on mortality in bacteremic infections. They carried out a retrospective review of 388 infections with bacteremia either from Staphylococcus aureus or gram-negative bacilli, with the endpoints being death from any cause during hospitalization or death from infection, as inferred by the investigators on the basis of chart review. Patients receiving statins were similar to those not receiving the drugs in most demographic and baseline laboratory tests. Both overall mortality (6% vs 28%, p = .002) and attributable mortality (3% vs 20%, p = .01) were sharply lower in patients taking statins than those not taking the drugs. This reduction persisted in a multivariate analysis. These results are certainly interesting and merit study in other populations.

The First Nucleotide RTI Approved for HIV

As noted in Prescriber's Letter (December, 2001, pg 70), a new antiretroviral drug called Viread (pronounced VEER-ee-ad) has been approved by the FDA for the treatment of HIV. It is the first nucleotide reverse transcriptase inhibitor (RTI) and may be somewhat more potent than the various nucleoside RTIs now available. It also seems to have fewer side effects and fewer drug interactions than other RTIs. It is taken once a day, which is another advantage. Because it is renally excreted, the dosage may have to be adjusted in patients with renal impairment.

Anthrax . . . Not Easy to Infect Massively

A commentary in The Lancet (Ala'Aldeen, A. 2001;358:1386-8) makes some interesting points about the difficulty perpetrators would have in causing widespread inhalational anthrax infection. Like most biological weapons, anthrax is used more to terrify than to kill. In modern warfare, soldiers fight in protective suits and most have been immunized against anthrax. Although the LD₅₀ for inhalational anthrax is thought to be a few thousand spores, huge quantities would need to be aerosolized to cause widespread infection. The World Health Organization has suggested that 50 kg of spores (which would require huge fermenters and months of work) released over a city of 5 million people would cause 250,000 cases. The Japanese cult that poisoned underground commuters in Tokyo with sarin gas reportedly tried repeatedly to deliver anthrax around the city without success. These points are not made to suggest that inhalational anthrax is not a cause for concern, but simply to illustrate that it would not be easy for terrorists to cause huge numbers of infections.

Helicobacter pylori and Angioneurotic Edema

There is some evidence that H. pylori infection may be a cause of various dermatological conditions including rosacea, urticaria, angioneurotic edema and atopic dermatitis and, in particular, refractory angioneurotic edema. Farkas H, et al. (The Lancet 2001;358:1695-6) documented H. pylori infection in 19 of 65 patients with hereditary angioneurotic edema, using serological diagnosis and the carbon-14-urease breath test. All 19 of the infected patients (but only 11 of 46 without infection) had a history of recurrent abdominal crises. The frequency of crises was greater in those with infection than in the uninfected. Elimination of H. pylori infection in 18 patients was followed by a sustained decrease in the number of episodes of abdominal pain. In a subset of patients with dyspepsia and unusually frequent episodes of angioedema, cure of the H. pylori infection resulted in a decrease of abdominal episodes from 28 before treatment to 1 after treatment. Other manifestations of angioedema also disappeared. The authors postulate that immune responses to H. pylori infection trigger complement activation and angioneurotic edema episodes. The picture is reminiscent of the putative role of Chlamydia pneumoniae in arteriosclerotic disease. This will be an interesting field to follow.