Is enough attention being given to the adverse effects of corticosteroid therapy?

Background: Although the corticosteroids are valuable anti-inflammatory and immunosuppressive agents, they also possess many potential adverse effects, especially with continued use. In particular, long-term corticosteroid exposure carries a significant risk of osteoporosis. Aim: To review the use of corticosteroids in patients presenting to the major teaching hospital in Tasmania, Australia; principally to determine whether patients receiving long-term corticosteroid therapy were being monitored for loss of bone mineral density and offered preventive therapy for osteoporosis. Methods: A retrospective review of the medical records for 212 consecutive patients admitted to the medical wards of the hospital over a 5-month period and receiving treatment with either oral or inhaled corticosteroids, was performed. An extensive range of demographic and clinical variables was recorded for each patient. Patients were also questioned about diet and exercise, and whether they had undergone tests for measuring bone mineral density or blood glucose. Results: The median age of the patients was 69 years (range: 15-90 years) and 58% were female. Over half (53%) of the patients were on oral corticosteroids only, with 26% using inhaled corticosteroids only, and 21% on both oral and inhaled corticosteroid therapy. The most common conditions for which patients were receiving corticosteroid therapy were asthma (37% of patients), chronic obstructive pulmonary disease (33%) and rheumatoid arthritis (17%). The most commonly used oral corticosteroid was prednisolone (93%), the median daily dose was 10 mg prednisolone equivalent, and the median duration of oral corticosteroid treatment was 50 weeks. Disregarding short courses, the median duration of oral corticosteroid treatment was 104 weeks. Almost one-third (31%) of the patients receiving oral corticosteroid treatment had been taking the equivalent of 7.5 mg prednisolone daily for at least 6 months. Only 11% of all patients on oral corticosteroids and 21% of those who had been taking oral corticosteroids for at least one year had documented evidence of bone mineral density testing being performed in the past in the hospital. Only 21% of all patients on oral corticosteroids and 31% of those who had been taking oral corticosteroids for at least one year were receiving medication for osteoporosis prevention, and only 15% of women over 45 years of age and on oral corticosteroid therapy were taking hormone replacement therapy. Only about half of the patients on long-term systemic corticosteroid therapy had either documented evidence in their hospital medical records, or were aware, of having undergone blood glucose testing in the preceding 12 months. Conclusions: More attention to the prevention and monitoring of possible adverse effects of long-term corticosteroid therapy is warranted. Guidelines covering preventive measures and treatment options for corticosteroid-induced osteoporosis need to be considered routinely when using these agents

Multifaceted educational program increases prescribing of preventive medication for corticosteroid induced osteoporosis

Objective. Despite evidence that oral corticosteroids increase fracture risk and the existence of guidelines for the prevention of corticosteroid induced osteoporosis, few patients prescribed longterm corticosteroids receive osteoporosis prevention. We performed a controlled trial of a comprehensive educational program aimed at increasing the use of osteoporosis preventive therapy in patients prescribed longterm oral corticosteroids. Methods. The intervention was conducted in Southern Tasmania, Australia, using Northern Tasmania as a control area. All general practitioners and community pharmacies were sent educational material and locally produced guidelines on the prevention of corticosteroid induced osteoporosis. This was followed by academic detailing visits and reminders. Pharmacists were provided with supplies of an educational refrigerator magnet, intended for patients. Outcomes were measured using evaluation feedback from the general practitioners and pharmacists, and drug utilization data provided by (1) a series of patients presenting to hospital and taking oral corticosteroids for at least 3 consecutive months; and (2) dispensing of osteoporosis preventive therapy under the Australian Pharmaceutical Benefits Scheme. Results. The prevalence of osteoporosis preventive therapy increased from 31% of admitted hospital patients taking longterm oral corticosteroids to 57% postintervention (p < 0.0001). The use of bisphosphonates (6% to 24% of patients), calcium (5% to 19%), and vitamin D (3% to 11%) all increased significantly. Prescription data also indicated a significant (p < 0.01) increase in the use of osteoporosis preventive therapy in the intervention region. Conclusion. A multifaceted education program, incorporating academic detailing of general practitioners and community pharmacists, increased the use of osteoporosis prevention strategies in longterm oral corticosteroid users

Bariatric Surgery and Its Effects on the Skin and Skin Diseases

In light of the increasing prevalence of obesity worldwide, the popularity of bariatric surgery is on the rise. As with any other invasive procedure, these surgeries, especially with the obesity risk factor, carry the risk of direct cutaneous complications following the penetration and manipulation of tissues. In addition, bariatric surgery has an effect on skin structure and function. It also appears to be affiliated with several dermatoses. Some of these represent preexisting diseases the course of which is altered by the procedure, such as psoriasis. On the other hand, other skin disorders are triggered by the surgery itself. This article reviews and summarizes these cutaneous effects and complications. © 2013 Springer Science+Business Media New York.Alasfar F, 2010, OBES SURG, V20, P168, DOI 10.1007-s11695-008-9708-3; Araco A, 2007, OBES SURG, V17, P828, DOI 10.1007-s11695-007-9126-y; Ashourian N, 2006, NEW ENGL J MED, V354, P1614, DOI 10.1056-NEJMicm050641; Ballinger S, 2003, CURR OPIN RHEUMATOL, V15, P591, DOI 10.1097-00002281-200309000-00012; BARR DJ, 1984, ARCH DERMATOL, V120, P919, DOI 10.1001-archderm.120.7.919; Biorserud C, 2011, OBES SURG, V21, P273, DOI 10.1007-s11695-009-9849-z; Bleasel NR, 1999, J AM ACAD DERMATOL, V41, P322, DOI 10.1016-S0190-9622(99)70375-0; Bobowicz M, 2011, OBES SURG, V21, P1843, DOI 10.1007-s11695-011-0403-4; Brolin RE, 1996, AM J SURG, V172, P328, DOI 10.1016-S0002-9610(96)00194-8; Brouard MC, 2004, J EUR ACAD DERMATOL, V18, P89, DOI 10.1111-j.1468-3083.2004.00712.x; Bussolaro RA, 2012, OBES SURG, V22, P353, DOI 10.1007-s11695-011-0485-z; Callen JP, 2002, DERMATOL CLIN, V20, P409, DOI 10.1016-S0733-8635(02)00006-2; Cone LA, 2004, OBES SURG, V14, P690, DOI 10.1381-096089204323093507; Danese C, 2011, CLIN TER, V162, pE89; de Jongh RT, 2008, MICROVASC RES, V75, P256, DOI 10.1016-j.mvr.2007.08.001; D'Ettorre M, 2010, OBES SURG, V20, P1552, DOI 10.1007-s11695-010-0224-x; DICKEN CH, 1986, J AM ACAD DERMATOL, V14, P792, DOI 10.1016-S0190-9622(86)70095-9; Dumon KR, 2011, SURG CLIN N AM, V91, P1313, DOI 10.1016-j.suc.2011.08.014; ELY PH, 1980, J AM ACAD DERMATOL, V2, P473; Ettinger JEMTM, 2006, OBES SURG, V16, P94; Farias MM, 2012, OBES SURG, V22, P877, DOI 10.1007-s11695-012-0646-8; Faurschou A, 2011, MED HYPOTHESES, V77, P1098, DOI 10.1016-j.mehy.2011.09.011; Fisch C, 2001, RHEUMATOLOGY, V40, P351, DOI 10.1093-rheumatology-40.3.351; Folope V, 2007, GASTROEN CLIN BIOL, V31, P369, DOI 10.1016-S0399-8320(07)89395-X; Freeman JT, 2011, OBES SURG, V21, P836, DOI 10.1007-s11695-010-0105-3; GAMBLE CN, 1982, AM J CLIN PATHOL, V77, P347; Garcia H. L., 2002, AM J CLIN DERMATOL, V3, P497; Girard C, 2006, PEDIATR DERMATOL, V23, P346, DOI 10.1111-j.1525-1470.2006.00261.x; Goldberg LJ, 2010, CLIN DERMATOL, V28, P412, DOI 10.1016-j.clindermatol.2010.03.038; GOLDMAN JA, 1979, ARCH DERMATOL, V115, P725, DOI 10.1001-archderm.115.6.725; Hamminga EA, 2006, MED HYPOTHESES, V67, P768, DOI 10.1016-j.mehy.2005.11.050; Herron MD, 2005, ARCH DERMATOL, V141, P1527, DOI 10.1001-archderm.141.12.1527; Higa-Sansone G, 2004, OBES SURG, V14, P1132, DOI 10.1381-0960892041975569; Hossler EW, 2011, J AM ACAD DERMATOL, V65, P198, DOI 10.1016-j.jaad.2010.01.001; Hossler EW, 2013, BRIT J DERMATOL, V168, P660, DOI 10.1111-j.1365-2133.2012.11211.x; Jonk AM, 2007, PHYSIOLOGY, V22, P252, DOI 10.1152-physiol.00012.2007; JORIZZO JL, 1983, ARCH INTERN MED, V143, P457, DOI 10.1001-archinte.143.3.457; Karmali S, 2010, CAN FAM PHYSICIAN, V56, P873; Katsuki A, 1998, J CLIN ENDOCR METAB, V83, P859, DOI 10.1210-jc.83.3.859; Katugampola RP, 2004, CLIN EXP DERMATOL, V29, P261, DOI 10.1111-j.1365-2230.2004.01476.x; Kovaleski CR, 1997, ARCH DERMATOL, V133, P113; Lewandowski Helen, 2007, Endocr Pract, V13, P277; Light D, 2010, PLAST RECONSTR SURG, V125, P343, DOI 10.1097-PRS.0b013e3181c2a657; LINDEGARD B, 1986, DERMATOLOGICA, V172, P298; Lopez JF, 2000, ANN CHIR, V125, P297, DOI 10.1016-S0001-4001(00)00135-5; Maronn M, 2005, PEDIATR DERMATOL, V22, P60, DOI 10.1111-j.1525-1470.2005.22113.x; Mason EE, 1992, AM J CLIN NUTR, V55, p537S; Maverakis Emanual, 2007, Dermatol Online J, V13, P11; Michaels J, 2011, PLAST RECONSTR SURG, V127, P1693, DOI 10.1097-PRS.0b013e31820a649f; Moreira Mde A, 2010, ACTA GASTROENTEROL L, V40, P244; Nadler EP, 2007, J PEDIATR SURG, V42, P137, DOI 10.1016-j.jpedsurg.2006.09.014; Naldi L, 2005, J INVEST DERMATOL, V125, P61, DOI 10.1111-j.0022-202X.2005.23681.x; National Institutes of Health, 2012, GASTR SURG SEV OB; Neve HJ, 1996, OBES SURG, V6, P63, DOI 10.1381-096089296765557295; Ocon J, 2012, JPEN-PARENTER ENTER, V36, P361, DOI 10.1177-0148607111422067; Orpheu SC, 2010, OBES SURG, V20, P480, DOI 10.1007-s11695-009-0019-0; Papavramidis ST, 1999, OBES SURG, V9, P535, DOI 10.1381-096089299765552620; Patton Timothy, 2009, Dermatol Online J, V15, P3; Perez-Perez L, 2009, CLIN EXP DERMATOL, V34, pe421, DOI 10.1111-j.1365-2230.2009.03406.x; PORRES JM, 1977, ARCH DERMATOL, V113, P983; Quigley S, 2011, CLIN RADIOL, V66, P903, DOI 10.1016-j.crad.2011.04.017; Raychaudhuri SP, 2000, CUTIS, V66, P348; Reoch J, 2011, ARCH SURG-CHICAGO, V146, P1314, DOI 10.1001-archsurg.2011.270; Robinson MR, 2011, J AM ACAD DERMATOL, V65, P448, DOI 10.1016-j.jaad.2010.03.004; Rojas P, 2011, NUTR HOSP, V26, P856, DOI [10.1590-S0212-16112011000400028, 10.3305-nh.2011.26.4.5199]; Rossi M, 2011, OBES SURG, V21, P87, DOI 10.1007-s11695-010-0286-9; Rubin M, 2001, OBES SURG, V11, P315, DOI 10.1381-096089201321336674; Setty AR, 2007, ARCH INTERN MED, V167, P1670, DOI 10.1001-archinte.167.15.1670; Shipman AR, 2011, BRIT J DERMATOL, V165, P743, DOI 10.1111-j.1365-2133.2011.10393.x; Shon W, 2011, J CUTAN PATHOL, V38, P560, DOI 10.1111-j.1600-0560.2011.01703.x; Shope TR, 2003, OBES SURG, V13, P355, DOI 10.1381-096089203765887651; Skroubis G, 2011, WORLD J SURG, V35, P93, DOI 10.1007-s00268-010-0816-6; Slater GH, 2004, J GASTROINTEST SURG, V8, P48, DOI 10.1016-j.gassur.2003.09.020; Slater GH, 2004, OBES SURG, V14, P133, DOI 10.1381-096089204772787446; Snow JM, 2011, SURG CLIN N AM, V91, P1249, DOI 10.1016-j.suc.2011.08.008; Stapleton Phoebe A, 2008, Pathophysiology, V15, P79, DOI 10.1016-j.pathophys.2008.04.007; Tu J, 2011, AUSTRALAS J DERMATOL, V52, pE5, DOI 10.1111-j.1440-0960.2009.00614.x; WECHSLER HL, 1979, ARCH DERMATOL, V115, P73, DOI 10.1001-archderm.115.1.73; Wellen KE, 2003, J CLIN INVEST, V112, P1785, DOI 10.1172-JCI200320514; WILLIAMS HJ, 1979, ARCH DERMATOL, V115, P1091, DOI 10.1001-archderm.115.9.1091; World Health Organisation (WHO), OB OV; Xanthakos SA, 2009, PEDIATR CLIN N AM, V56, P1105, DOI 10.1016-j.pcl.2009.07.002; Young RJ, 2010, LANCET ONCOL, V11, P983, DOI 10.1016-S1470-2045(10)70023-114