Clinical Briefs

By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville, Associate Editor, Internal Medicine Alert.

Morphine, Gabapentin for Neuropathic Pain

The management of neuropathic pain (NPP) presents a challenge to clinicians of all specialties, since disorders associated with NPP span the gamut of medical disciplines. Opioid analgesics such as morphine (MOR) and gabapentin (GBPT) are 2 of the agents commonly used to manage NPP from diverse etiologies, although adverse effects or a ceiling dose for efficacy ultimately limit successful pain control in some patients. In several pharmacologic scenarios, it has been feasible to capitalize upon the beneficial effects of different classes of medications by using modest doses of complementary (ie, having potentially additive positive effects) agents, thereby minimizing their respective adverse effect profiles, without approaching their inherent therapeutic ceiling.

This randomized, double-blind trial assessed patients with NPP (n = 57) who were randomized to 5-week crossover periods of MOR (specifically, sustained release morphine), GBPT, GBPT + MOR, or active placebo (ie, lorazepam). The primary outcome was mean daily pain intensity. Baseline pain intensity was 5.72 on a 0-10 scale. The mean pain at 4-weeks treatment was statistically significantly different from placebo and baseline in persons treated with GBPT (pain = 4.15), MOR (pain = 3.7), and GBP + MOR (pain = 3.06). Lower doses of GBPT and MOR were required in combination to achieve a similar or superior therapeutic effect than the maximum dose of either single agent alone. Adverse effects of combination therapy were similar to those of monotherapy with MOR, although dry mouth with GBPT + MOR was considerably more frequent than either GBPT or MOR alone.

Gilron I, et al. N Engl J Med. 2005;352:1324-1334.

Correlation of Decreased Androgen Levels and Female Sexual Function Index

Low libido (LLB) is one of the most distressing female sexual dysfunctions, and is the most commonly reported female sexual dysfunction in epidemiologic surveys. Studies with androgen replacement or supplementation have suggested that amplification of androgens has an enhancing effect on libido.

Turna and colleagues compared levels of various androgenic and non-androgenic hormones in premenopausal (n = 40) and postmenopausal (n = 40) women equally divided between those with and without LLB. Women who reported LLB reported symptoms for at least 6 months, and were in stable relationships were included. Measurements of psychological status (ie, Beck Depression Inventory) and the Female Sexual Function Index (FSFI)were coupled with laboratory analysis including total testosterone (tTST), free testosterone (fTST), estradiol, dehydroepiandrosterone sulfate (DHEA-S), and sex hormone binding globulin (SHBG).

There was a positive correlation between androgens and scores on the FSFI in both premenopausal and post-menopausal women. Similarly, lower androgen levels were associated with lower levels of arousal, lubrication, and orgasm as measured on the FSFI (P <0.05). Additionally, women with LLB had statistically significantly lower androgen levels than their menopausal-status-matched comparators. These correlations were consistent across tTST, fTST, and DHEA-S.

The role of androgen supplementation in women remains highly controversial. If androgen supplementation is desired, the best method is similarly indeterminate. Nonetheless, such data suggest that attention to the androgen status of women with LLB may merit consideration.

Turna B, et al. Int J Impot Res. 2005; 17:148-153.

Smoking and ED

It is increasingly recognized in the clinical community that erectile dysfunction (ED) most commonly represents endothelial dysfunction associated with any of the risk factors for vasculopathy: eg, diabetes, dyslipidemia, and hypertension. Cigarette smoking (CIG) is also recognized as a potent inducer of vasculopathy, but there are not much data specifically addressing the relationship between CIG and ED. Critical questions for elucidation include the relative risk effects of CIG upon ED, the prognostic effect of CIG upon established ED, and whether ED elicits any modifications in smoking behavior.

This population study included residents from communities around Tampere, Finland aged 50-70 years (n = 2198). Information was obtained at baseline and 5 years later, and included questions on presence, absence, and severity of ED, and smoking status.

There was a trend for increased incidence of ED (OR = 1.4; CI, 0.9-2.3) with smoking; among men who subsequently recovered their erectile function, the rate of recovery was less in those who continued to smoke than those who quit.

Curiously, men who incurred ED more often then began to smoke, so that "smoking causes ED and ED causes smoking." These data support the deleterious relationship of smoking to erectile function. Smokers who continue to smoke are less likely to recover erectile function.

Shiri R, et al. Int J Impot Res. 2005;17:164-169.