Possible Case Report of Furosemide-Induced Psoriasis

Purpose: After reviewing PubMed, drug-induced psoriasis has been previously reported. This case is believed to be the first furosemide-induced psoriasis reported and includes a summarization of antihypertensive-induced psoriasis on some of the previously published literature. Summary: A 32-year-old African American female with hypertension secondary to edema was noted to have developed psoriasis 3.3 years after the initiation of furosemide 20 mg orally once daily. She initially had a new-onset rash to hydrochlorothiazide 25 mg orally once daily after 1 week prior to switching to furosemide. After presenting with her psoriatic-like skin lesions all throughout her body while on furosemide for 3.3 years, dermatologic biopsy confirmed the psoriasis diagnosis. After discontinuation of furosemide and initiation of topical and oral supportive medications, the patient’s psoriasis resolved after 4 weeks. She was changed to lisinopril 10 mg orally once daily then finally switched to losartan 50 mg orally once daily with spironolactone 50 mg orally twice daily. Conclusion: Using the scale of Naranjo et al. it was determined that furosemide use was the possible cause of the patient’s psoriasis. This report can contribute to the literature by describing another druginduced psoriasis and provide a possible first case report of furosemideinduced psoriasis. Introduction Psoriasis is a chronic, inflammatory condition, commonly affecting either the joints, skin, or both [1]. Plaque psoriasis is the most common type of psoriasis, affecting approximately 2% of Americans [1]. This type of psoriasis is defined as a dermatologic condition, causing well-defined, erythematosus plaques on hands, feet, and extremities [1]. Plaque psoriasis can be induced by certain medications, such as beta-blockers, lithium, indomethacin, and tetracycline [2,3]. Furosemide is one of four high-ceiling or loop diuretics that has been available for nearly fifty years. Structurally, it retains similarities to the thiazide diuretic, hydrochlorothiazide (HCTZ), but would be better classified as an open-chain analogue. The thiazide ring within hydrochlorothiazide possesses a weakly acidic proton, which is required for activity. As an open-chain analogue, furosemide substitutes the acidic thiazide with a more acidic carboxylic acid (Figure 1). A furanylmethyl functional group is attached to the other amine nitrogen. These structural differences alter the mechanistic binding activity, as well as serving to increase the overall saliuretic efficacy [4]. Furosemide has a saliuretic effect 8 to 10 times that of the thiazide diuretics, but with a much shorter half-life, whereas HCTZ acts by inhibiting the Na+/Clsymporter located in the distal convoluted tubule. Furosemide acts by inhibiting the luminal Na+ / K+ / 2Clsymporter in the thick ascending loop of henle. The oral absorption and bioavailability for furosemide ranges between 50 to 70% [5]. The half-life of furosemide ranges from 0.33 to 1.17 hours in healthy subjects, and from 4.9 to 9.7 hours in patients with advanced renal failure [5]. Although furosemide is generally considered to be safe and effective at normal therapeutic doses, it has been associated with a number of potential adverse effects attributable to idiosyncratic metabolism [6,7]. Objective In clinical practice, furosemide is commonly used for symptomatic management of heart failure and blood pressure management. The effect of furosemide causing psoriasis has not been published in the literature. We summarize a possibly case report of furosemideinduced psoriasis. In addition, we conducted a PubMed search and reviewed literature regarding antihypertensive medications and psoriasis. Case Report The patient is a 32-year-old African American female, who became a new patient to the rural-health, family medicine clinic in August 2010. Family history included father and mother alive and well; the patient did not have a significant social history as she denied smoking any tobacco products and drinking alcohol. She did not Jennifer Clements1*, Kristopher G. Virga2 and Aida R. Bickley1 1Department of Pharmacy Practice, Presbyterian College School of Pharmacy, South Carolina, USA 2Department of Pharmaceutical Sciences, Presbyterian College School of Pharmacy, South Carolina, USA Address for Correspondence Jennifer Clements, Pharm.D, BCPS, CDE, BCACP, Department of Pharmacy Practice, Presbyterian College School of Pharmacy, 307 N, Broad Street Clinton, South Carolina 29325, USA, Tel: 8649383870; E-mail: jclements@presby.edu Submission: 13 October 2015 Accepted: 05 November 2015 Published: 10 November 2015 Copyright: © 2015 Clements J et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Reviewed & Approved by: Dr. Rutesh H. Dave, Associate Professor, Division of Pharmaceutical Sciences, Arnold and Marie Schwartz College of Pharmacy and Health sciences, Long Island University, USA Case Report Open Access Journal of Pharmaceutics & Pharmacology