Updates-By Carol A. Kemper, MD, FACP
September 1, 2000 4 minutes read
Updates-By Carol A. Kemper, MD, FACP
Flu Vaccine Shortage
Source: Med Lett Drugs Ther 2000;42: 79-80.
Because of a delay in the availability of this year’s influenza vaccine, physicians are being advised to focus on those highest risk patients such as nursing home residents; people with chronic heart, lung, or kidney disease; people with immunodeficiency; pregnant women who will be in their second and third trimester during the flu season; and children and teens on long-term aspirin therapy. Health care workers should also preferentially receive the vaccine. Production problems with several vaccine products in the United States have delayed their shipment. Immunization of low-risk patients should be deferred until later in the season, although it is not yet known whether sufficient vaccine will be produced in time for this year’s flu season. The optimal time for vaccination is now through mid-November, although anytime during the flu season is appropriate.
Poor Response in Primary HIV
Source: Tamalet C, et al. J Med Virol 2000;61:181-186.
Data suggest that the administration of highly active antiretroviral (HAART) is beneficial for patients presenting with acute, primary HIV-1 infection. The desire to hit the virus "early and hard" in this circumstance begs the question of what to choose for optimal therapy, especially given the increasingly common transmission of drug-resistant mutants. Tamalet and colleagues examined the genotypic resistance patterns of isolates obtained from 48 patients presenting with primary HIV infection in Marseille and Toulouse between 1995 and 1998, to determine whether the presence of significant nucleoside-reverse transcriptase (NRTI) mutations affected the virological response to therapy. Primary infection was defined as exposure to infection with documented seroconversion within three months.
Major mutations associated with resistance to NRTIs were found in eight of 48 (17%) patients, including 215F/Y (10%), K70R (6%), and M184v (2%), as well as others. Major protease mutations were detected in only one patient (2%), who had a D30N amino acid substitution. D30N has been associated with ~70% of nelfinavir failures but is not necessarily associated with cross-resistance to other PIs. Forty-one patients received "triple therapy," with or without a protease inhibitor, including the use of AZT in all but one patient without AZT resistance. An additional five patients, all of whom had no evidence of AZT resistance, received two NRTIs.
There was no apparent difference in the mean change in HIV RNA or CD4 cell counts at six and 12 months of therapy between the seven patients with significant AZT-associated resistance mutations and those patients with wild-type virus. The proportion of patients with undetectable viremia (< 20 copies/mL) was 43% vs. 38% at six months, and 26% vs. 52% at 12 months. The single patient with the D30N mutation had a complete response to an indinavir-containing regimen. While these data suggest that patients with acquired NRTI-resistant mutants may respond to therapy, this data looks fairly discouraging. However, recent data from Johns Hopkins found that only ~17% of treatment-naïve patients maintained an undetectable viral load during their first 14 months of HAART therapy, which is not much better.
Nevertheless, the use of AZT in patients with known major AZT-resistance mutations seems inappropriate if other alternatives are available. More than half of patients with primary HIV infection in this study failed their first regimen within 6-12 months, placing them at risk for additional resistance mutations, despite their early stage disease. This study did not assess whether the use of genotypic information in the selection of initial therapy would have improved the response rates. Updated guidelines in HIV care recommend the use of genotypes in the assessment of treatment-naïve patients, including those with primary HIV. This seems much more feasible now that genotypic data can be obtained in many patients within a few days.
GI Specialists at Risk for H. pylori
Source: Hildebrand P, et al. BMJ 2000; 321:149.
To determine whether gi specialists are at greater risk for Helicobacter pylori infection, Hildebrand and colleagues identified 56 gastroenterologists and 104 healthy age and race-matched control subjects who were negative for H. pylori based on the results of a 13C urea breath test. Subjects were recruited between 1989 and 1991 at the annual meeting of the Swiss Society of Gastroenterology and Hepatology. Persons who had received antibiotics or proton pump inhibitors within three months of testing were excluded from participation. In 1996 through 1998, repeat 13C urea breath tests in those available for testing were positive in seven of 54 (12.9%) gastroenterologists and one of 103 (1.0%) control subjects. Based on years of follow-up, H. pylori infection occurred in gastroenterologists at a rate of 2.6% per year vs. 0.14% per year of controls. All seven infected gastroenterologists indicated they routinely wore gloves for all endoscopic procedures. Hildebrand et al raise the question of whether micro-aerosolization of gastric juice during endoscopy may increase the risk of transmission of H. pylori, and suggested that face masks may provide additional protection.
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