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By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.
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 dermati-tis (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 adminis-tration 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 insult usually 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.