Mortality From Sexually Transmitted Diseases in Reproductive-Aged Women: United States, 1999–2010

Objectives. I estimated the sexually transmitted disease–related mortality among US reproductive-aged women from 1999 to 2010.Methods. I estimated mortality from National Center for Health Statistics’ Multiple Cause of Death data. I defined reproductive age as 15 to 44 years. For diseases partially caused by sexual transmission, I estimated the proportion attributable to sexual transmission from the literature. To calculate mortality rates, I estimated number of deaths from each disease and Census Bureau population for reproductive-aged women for 1999 to 2010.Results. From 1999 to 2010, the cumulative sexually transmitted disease–related mortality rate decreased by 49%, from 5.3 to 2.7 deaths per 100 000. The primary contributors were HIV and human papilloma virus infections. Mortality from sexually transmitted HIV infection decreased by 62%, from 3.4 to 1.3 deaths per 100 000. Mortality from human papilloma virus–associated gynecologic cancers decreased by 19%, from 1.6 deaths per 100 000 in 1999 to 1.3 deaths per 100 000 in 2010.Conclusions. Screening and treatment for sexually transmitted diseases may reduce mortality. Research is needed to determine whether sexually transmitted disease–related morbidity among reproductive-aged women has decreased over the past decade.Deaths from sexually transmitted diseases (STDs) often occur long after acute infection, making their incidence difficult to estimate.1–3 Some infections, such as syphilis, may directly result in death. By contrast, human papilloma virus (HPV), HIV, and hepatitis more commonly cause death because of secondary sequelae. Genital herpes, gonorrheal infection, and chlamydial infection may cause death from primary infection (e.g., disseminated herpes simplex virus or pelvic inflammatory disease [PID]) or secondary sequelae (e.g., ectopic pregnancy). Because death certificates usually list only the prevalent conditions, STDs are often not recorded on death certificates. In addition, some causes of death, such as liver cancer, may or may not be STD related. STD-related deaths cannot always be counted directly; therefore, direct and indirect methods of estimation must be used.The methodology for estimating STD-related mortality in women in the United States has evolved. Early estimates used measures of reproductive health mortality.1 Subsequently, a more comprehensive approach used direct and indirect measures of deaths from all STD-related diseases.2 Most recently, disability-adjusted life-years lost because of sexual behaviors were found to be threefold higher in the United States than in other developed countries. Women carry a disproportionately high proportion of the health burden.3Between 1955 and 1975, STDs such as syphilis and PID were responsible for 20% to 30% of reproductive mortality among women aged 15 to 44 years.1 Since then, mortality from syphilis and PID has decreased. Cervical carcinoma, HIV, and viral hepatitis infection were the top 3 contributors to STD-related mortality among all women older than 15 years as of 1992.2 I have updated the estimated annual STD-related mortality among reproductive-aged women in the United States for 1999 to 2010.     

Cell surface IL-1α trafficking is specifically inhibited by interferon-γ, and associates with the membrane via IL-1R2 and GPI anchors

IL-1 is a powerful cytokine that drives inflammation and modulates adaptive immunity. Both IL-1α and IL-1β are translated as proforms that require cleavage for full cytokine activity and release, while IL-1α is reported to occur as an alternative plasma membrane-associated form on many cell types. However, the existence of cell surface IL-1α (csIL-1α) is contested, how IL-1α tethers to the membrane is unknown, and signaling pathways controlling trafficking are not specified. Using a robust and fully validated system, we show that macrophages present bona fide csIL-1α after ligation of TLRs. Pro-IL-1α tethers to the plasma membrane in part through IL-1R2 or via association with a glycosylphosphatidylinositol-anchored protein, and can be cleaved, activated, and released by proteases. csIL-1α requires de novo protein synthesis and its trafficking to the plasma membrane is exquisitely sensitive to inhibition by IFN-γ, independent of expression level. We also reveal how prior csIL-1α detection could occur through inadvertent cell permeabilisation, and that senescent cells do not drive the senescent-associated secretory phenotype via csIL-1α, but rather via soluble IL-1α. We believe these data are important for determining the local or systemic context in which IL-1α can contribute to disease and/or physiological processes.     

Comparison of tissue disruption caused by excimer and midinfrared lasers in clinical simulation

Laser coronary angioplasty is a useful therapy for selected complex coronary lesions. Laser-induced acoustic trauma is postulated to be a cause of dissection and acute vessel occlusion. Controversy exists regarding the relative degree of photoacoustic effects of midinfrared and excimer lasers in clinical practice. To date, these systems have not been compared at clinical energy doses and with clinical pulsing strategies. Therefore, we studied the photoacoustic effects of both midinfrared and excimer lasing at clinically accepted doses. Human atherosclerotic iliofemoral artery segments were obtained at autopsy (n = 36) and placed lumen side up in a saline bath. Clinical laser catheters were advanced over an 0.018′ guide wire, perpendicular to the tissue. A 10-g down force was applied to the catheter for full-thickness lasing. Pulsing strategies were, for midinfrared laser: 5 pulses, 1-sec pause, 5 pulses, 1-sec pause, 5 pulses, withdraw; for excimer: 5 sec of pulses, wait 10 sec, 5 sec of pulses. Several clinically acceptable energy levels were used; for excimer: 25 mJ/mm², 40 mJ/mm², 60 mJ/mm²; for midinfrared: 3 W (400 mJ/mm²), 3.5 W (467 mJ/mm²). Photoacoustic effect was assessed histologically by determining the number of lateral cleavage planes (dissections) arising from the lased crater border and extending into the surrounding tissue. In normal tissue, midinfrared lasing produced less acoustic damage than excimer lasing (2.79 ± 0.78 vs. 5.27 ± 0.75 cleavage planes, mean ± SD, P < 0.05, data for lowest energy for each system). The same was true in noncalcified atheroma (2.48 ± 0.71 vs. 6.43 ± 1.09, P < 0.05) and calcified atheroma (2.47 ± 1.21 vs. 6.27 ± 1.13, P < 0.05). This effect was similar at all energy levels, with a trend for more damage at higher energies in both systems. This study demonstrates that midinfrared lasing causes less acoustic damage than excimer lasing when using clinical catheters, energy levels, and pulsing strategies. This effect is independent of tissue-type but tends to be dose-related. These findings may explain, in part, the differences in dissection rates seen clinically. © 1996 Wiley-Liss, Inc.