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Do Topical Steroids Lead to Glaucoma or Cataract?
Source: Haeck IM, et al. Topical corticosteroids in atopic dermatitis and the risk of glaucoma and cataracts. J Am Acad Dermatol 2011;64:275-281.
The treatment of atopic dermatitis (ATD) usually is initiated with topical steroids (TPS). Because ATD is a chronic remitting and relapsing disorder and may occupy a large cutaneous area, exposure to TPS can be extensive. Since both glaucoma and cataracts are associated with ophthalmic TPS, and ATD may require periocular application of TPS, it is important to learn whether non-ophthalmic utilization of TPS could lead to increased intraocular pressure. The use of inhaled steroids for asthma has been associated with development of cataracts, but not glaucoma.
To study the impact of TPS in ATD upon glaucoma and cataract, 88 adults with chronic ATD were evaluated. For each study subject, data on total amount of TPS prescribed over the last 2-5 years was available. Two-thirds of the study subjects had applied TPS in the periocular region, since they suffered from ATD on the eyelids and periorbital region. The authors cite the average amount of periocular TPS use within this group as "3.9 days/week, 6.4 months/yr, for 4.8 years."
There was no sign of increased incidence of glaucoma among TPS users. Corticosteroid-induced cataract was seen in 2 of the 88 subjects, both of whom had received courses of systemic steroids in addition to TPS. These data are reassuring that TPS application does not appear related to the development of glaucoma or cataracts, even when TPS needs to be applied in the periorbital region.
Can Exenatide Prevent Glucocorticoid-Induced Hyperglycemia?
Source: Van Raalte DH, et al. Glucagon-like peptide-1 receptor agonist treatment prevents glucocorticoid-induced glucose intolerance and islet-cell dysfunction in humans. Diabetes Care 2011;34:412-417.
Clinicians anticipate that administration of systemic glucocorticoids, such as prednisone (PRED), to persons with diabetes worsen hyperglycemia. PRED reduces insulin sensitivity and impairs beta-cell function, resulting in hyperglycemia.
Chronic PRED administration is associated with increased risk for osteoporosis and peptic ulcer; preventive strategies for each of these adverse effects has been developed. To date, no such plan for mollifying exaggerated glucose excursions due to PRED has been offered.
The glucose dysregulation secondary to PRED appears to be primarily postprandial, rather than fasting. Clinical trials of metformin failed to confirm efficacy in preventing glucocorticoid-induced hyperglycemia (GIH). Because exenatide (EXE) has prominent effects specifically on postprandial glucose, it was logical to investigate whether EXE might favorably impact GIH.
Healthy adult men (n = 8) received a PRED load of 80 mg orally for two days (prednisolone, actually, but prednisone and prednisolone are mg-for-mg equivalent). They were randomized to also receive placebo or EXE. GIH was prevented by concomitant EXE administration.
This proof-of-concept trial should stimulate further investigation to determine whether the demonstrated ability of EXE to prevent GIH is similarly favorable in diabetics.
COPD: Beyond Pulmocentricity
Source: Nussbaumer-Ochsner Y, Rabe KF. Systemic manifestations of COPD. Chest 2011;139:165-173.
Chronic obstructive pulmonary disease (COPD) generally is regarded as a pulmonary process induced by toxic insultusually cigarettes, but sometimes other environmental exposures. Why only a small subset of chronic smokers develops COPD (20-25%) remains a mystery. Progressive loss of pulmonary function continues even after smoking cessation, suggesting that some inflammatory process, once set in gear in susceptible individuals, becomes self-perpetuating.
Experts recognize other non-pulmonary tissue compartments are involved in COPD. Musculoskeletal wasting, metabolic syndrome, and depression are disproportionately comorbid with COPD. Biopsy studies have found increased inflammatory cytokines in intercostal muscles, providing an explanation for dyspnea that goes beyond simple damage to alveolar capacity for gas exchange.
Both diabetes and chronic kidney disease have been found to be associated with COPD. In the absence of a visible etiologic link, systemic inflammation is a suspected culprit. Indeed, early data indicate that smoking cessation slows progression of renal failure. In reference to diabetes, smoking cessation is associated with short-term worsening of diabetes risk, attributed to the weight gain commonly seen after smoking cessation. COPD is increasingly viewed as part of a systemic process.
Aspirin and Risk of Death from Cancer
Source: Rothwell PM, et al. Effect of daily aspirin on long-term risk of death due to cancer: Analysis of individual patient data from randomized trials. Lancet 2011;377:31-41.
In animal models, aspirin (asa) has favorable effects on the incidence and/or growth rate of some cancers (CA). Most clinical trials of ASA have been for primary or secondary prevention of cardiovascular disease. Rothwell et al analyzed data from three UK clinical trials that included CA mortality outcomes, although none of the trials was designed specifically to study the impact of ASA upon CA as a primary or secondary endpoint. Their data set of almost 24,000 adult men and women divided treatment groups by duration of follow-up: 0-5 years of treatment, and > 5 years of ASA treatment.
ASA was associated with an 18% relative risk reduction in deaths due to cancer; risk reduction was greatest in subjects treated for more than 5 years. Gastrointestinal (GI) cancer deaths were reduced most prominently, but other cancers (e.g., lung) also showed favorable impact from ASA treatment. Although bleeding induced by ASA typically is viewed as an adverse effect, it has been suggested that ASA treatment also makes GI tumors more likely to bleed, facilitating their discovery. There appears to be a "latent period" of at least 5 years before the effects of ASA impact esophageal, pancreatic, brain, and lung cancer.
When evaluating the risk-benefit of ASA for cardiovascular risk reduction, the favorable impact of ASA upon cancer mortality also should be considered.
Reducing Incontinence After Prostatectomy
Source: Goode PS, et al. Behavioral therapy with or without biofeedback and pelvic floor electrical stimulation for persistent postprostatectomy incontinence: A randomized controlled trial. JAMA 2011;305:151-159.
When prostate cancer (pca) was diagnosed primarily at the later stages of disease, post-surgical adverse effects such as incontinence or erectile dysfunction weighed less heavily on the risk-benefit scale, since without surgery outcomes were poor. In an era when most PCA is diagnosed at a stage of localized disease, much of which would be destined to never evolve to clinical relevance, balancing adverse surgical consequences, becomes more complex.
Incontinence occurs and persists in the majority of men after radical prostatectomy. Two-thirds of men have persistent incontinence 5 years postoperatively. Encouraging results have been seen in trials that incorporate behavioral and physical therapies promptly after surgery. Little insight is available about the success of intervention for persistent incontinence distant from surgery.
Goode et al enrolled 208 men who had undergone prostatectomy and continued to suffer incontinence 4-5 years later. Participants were randomized to behavioral therapy (pelvic floor exercises, bladder control methods, fluid management) plus biofeedback and/or pelvic floor electrical stimulation versus control.
The reduction in incontinence was significantly greater in treatment groups (55% reduction) than in the control group (24% reduction). Neither biofeedback nor pelvic floor electrical stimulation added effectiveness to behavioral therapy alone. Clinicians should be encouraged that even late employment of behavioral therapies can provide substantial incontinence improvement.
Real-life Efficacy of Herpes Zoster Vaccine
Source: Tseng HF, et al. Herpes zoster vaccine in older adults and the risk of subsequent herpes zoster disease. JAMA 2011;305:160-166.
Herpes zoster vaccine (zostavax) was licensed in the United States in 2006 subsequent to the publication of the Shingles Prevention Study, a large (n = 38,546) prospective trial that demonstrated a 51% reduction in zoster and a 67% reduction in postherpetic neuralgia in vaccines compared to controls. Clinicians may wonder whether the favorable results seen in a major clinical trial would be replicated in their private clinical settings. According to this report by Tseng et al, that may very well be the case.
Enrollees in the Southern California Kaiser Permanente health plan older than 60 years of age who had received zoster vaccine (n = 75,761) were compared with age-matched controls (n = 227,283) in this retrospective analysis. The Kaiser Permanente study population was comprised of healthy, immunocompetent, community-dwelling adults. The primary outcome of interest was incidence of zoster.
The rate of zoster in the vaccine recipients (6.4/1000 person-years) was significantly less than the rate in unvaccinated study subjects (13.0/1000 person-years). This 55% relative risk reduction is highly concordant with the reductions seen in the Shingles Prevention Study, confirming the generalizability of their results.