Antiretroviral-Drug Resistance among Newly HIV-Infected Patients

In a study of 377 patients with newly acquired human immunodeficiency virus (HIV) infection in 10 cities in North America, the prevalence of antiretroviral-drug resistance increased from 3.4 percent in 1995 through 1998 to 12.4 percent in 1999 through 2000. The frequency of multidrug resistance at presentation also increased, from 1.1 percent to 6.2 percent. After initial antiretroviral therapy was administered, it took longer to achieve viral suppression in those who were infected with resistant virus, and the time to virologic failure in these patients was shorter.

The frequency of drug-resistant virus is increasing among patients with newly diagnosed HIV infections, reflecting a higher rate of transmission of resistant virus. Drug-resistance testing before treatment is now indicated even for patients who are newly infected and have never received antiretroviral therapy.

Related Editorial

Intramuscular Injection of Botulinum Toxin for Wrist and Finger Spasticity after a Stroke

Intramuscular injection of botulinum toxin type A has been used to treat patients with spasticity after a stroke, but its efficacy remains uncertain. In this randomized, double-blind, placebo-controlled trial involving patients with spasticity after a stroke, one-time injections of botulinum toxin A into wrist and finger muscles with high flexor tone reduced muscle tone and improved functional disability over a 12-week period. There were no major adverse effects of botulinum toxin injections.

Treatment with injections of botulinum toxin A in wrist and finger muscles appears to be safe and effective in the short term, reducing disability and improving the quality of life in patients with upper-limb spasticity after a stroke.

Related Perspective

Variant Cystic Fibrosis Phenotypes in the Absence of CFTR Mutations

Classic cystic fibrosis is an autosomal recessive disorder that is caused by loss-of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Clinical manifestations in the airways, pancreas, male reproductive tract, and sweat glands that resemble those occurring in classic cystic fibrosis have been observed in patients with mutations that reduce, but do not eliminate, the function of CFTR protein. This study included 30 patients who had no identifiable CFTR mutations and who had some features of cystic fibrosis but did not meet a clinical definition of classic cystic fibrosis. The authors conclude that this variant phenotype derives from factors other than mutations in the CFTR gene.

If reproducible, these findings suggest that a syndrome with many aspects of cystic fibrosis can arise from mutations in genes other than CFTR.

Related Editorial

Voriconazole for Invasive Aspergillosis

Invasive aspergillosis is a major infectious complication in patients with prolonged neutropenia and in transplant recipients, and for decades, amphotericin has been the standard treatment. This randomized, unblinded trial involving 391 patients compared voriconazole with amphotericin as the initial treatment for invasive aspergillosis. Those treated with voriconazole had a significantly better response rate and improved survival at 12 weeks (70.8 percent vs. 57.9 percent, P=0.02).

Voriconazole represents a major advance in the treatment of invasive aspergillosis. In this randomized trial, treatment with voriconazole, a broad-spectrum triazole, led to improved survival and was better tolerated than amphotericin, with fewer severe adverse reactions.

Medical Progress: Inflammatory Bowel Disease

Clinical experience has suggested that Crohn's disease and ulcerative colitis constitute distinct, if not discrete, entities. However, whether these conditions are fundamentally different or are part of a mechanistic continuum is a question with both conceptual and practical implications for management. This review summarizes current understanding of the mechanisms underlying the major forms of inflammatory bowel disease and discusses approaches to therapy.

Inflammatory bowel disease is the result of inappropriate and ongoing activation of the mucosal immune system fueled by the presence of normal luminal flora. This aberrant response appears to be facilitated by defects in both the barrier function of the intestinal epithelium and the mucosal immune system.

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