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Case Report and Brief Review

Efficacy of Natural Honey Versus Fluticasone Propionate in Mild Psoriasis: A Case Study

Keywords
September 2017
1943-2704
Wounds 2017;29(9):E78–E83.

Abstract

Although many topical agents (including biologic products) are available for the treatment of psoriasis, clinicians may still be concerned about the side-effect profile, efficacy, and expected result of each of these therapies. Case Report. Herein, the authors suggest an alternative, cost-effective option that may help in the management of psoriatic plaques. The authors have investigated the efficacy of topical natural honey versus fluticasone propionate in a 28-year-old man with plaque psoriasis diagnosed previously by biopsy at the main dermatology clinic at Hamad General Hospital (Doha, Qatar). The patient was treated with topical preparation of coal tar and moderate topical corticosteroids intermittently over a 3-year time period prior to presentation; however, he was unsatisfied with the outcome. The purpose of this case report is to offer a primary care-based approach utilizing natural honey as a safe and effective alternative treatment for adult patients with chronic plaque psoriasis. To the best of the authors’ knowledge, this is the first report in the medical literature proposing the use of natural honey in the treatment of psoriasis. Conclusions. Although this case report demonstrates a successful outcome of topical application of honey in the management of mild psoriasis, randomized controlled trials will be needed to verify these results.

 

Introduction

Psoriasis is a common, chronic, inflammatory complex disease of the skin characterized by an interplay between innate immunity, adaptive immunity, and skin barrier defect. Psoriasis has many characteristic and even pathognomonic features presenting as erythematous papules and plaques with silver scaling.1 However, no agreed-upon or established diagnostic criteria. On occasion, evaluating dermatopathology is warranted to confirm the diagnosis of psoriasis. Treatment of psoriasis is based on its severity, including topical therapy, phototherapy, and systemic therapy. Globally, alternative and complimentary treatments, such as herbal and traditional Chinese medicine, may play an essential role.

Honey has multiple bioactivities: antioxidant activity due to its phenolic constituents, upregulation of angiogenesis linked to its prime molecular markers (vascular endothelial growth factor [VEGF] A, hypoxia-inducible factor-1 alpha, and VEGF receptor 21), antibacterial activity due to the enzymatic production of hydrogen peroxide, low pH, high osmolarity, and provision of adequate moisture in the wound, which is essential for wound repair without causing maceration. A systemic review assessing the effect of honey on treatment for chronic wounds by Ochoa Sosa2 compared with standard therapy concluded that natural honey was an effective wound management agent.

Natural honey has been demonstrated microscopically to decrease inflammatory cells in acute and chronic inflammation.3 It stimulates peripheral blood to draw T lymphocytes and B lymphocytes to the surface and stimulate phagocytes and monocytes to produce cytokines, tumor necrosis factor (TNF)-1, and interleukin (IL) 1 and IL-6.3 Reducing inflammation is essential in wound healing as it enhances circulation and delivers more nutrients and oxygen, thereby aiding tissue repair and healing.4

The case of a 28-year-old man with mild psoriasis is presented to highlight the potential of natural honey as an alternative therapy for psoriasis, which appears to be an efficacious, cost-effective, and acceptable option. 

Case Report

A 28-year-old man, with a known case of plaque psoriasis diagnosed 3 years prior at the Dermatology Clinic at Hamad General Hospital (Doha, Qatar) after taking biopsy, presented at Umgwailinah Primary Health Care Center, Doha, Qatar, with a chief complaint of persistent plaques. At time of presentation, psoriatic plaques were present on the extensor aspects of the elbows, scalp, and knees. The patient had not been on any recent topical or systemic treatment 6 months prior to presentation. His last treatment was a topical moderate-strength corticosteroid, which was prescribed 7 months prior to presentation. He continued using it for 1 week, and the scales disappeared but returned 1 month later. Review of systems was unremarkable for arthralgia, visual complaints (such as blurred vision and headache as a result of raised intraocular pressure), gastrointestinal upset, palpitations, or sweating. 

Histologic report showed acanthosis, parakeratosis and orthokeratosis, loss of granular cell layer, and formation of spongiform pustules and parakeratotic microabscesses. In the epidermis, narrow rete ridges were discovered with neutrophils found in the thinned superficial epidermis forming a Munro’s microabscess, and mitotic activity was evident in the basal cells. During the initial assessment, a complete history and examination was carried out.  Although ideally pretreatment and posttreatment biopsy should be taken, this privilege is not available to the primary health care setting in Qatar where the treatment of this patient took place. 

Patient had no past medical or surgical history other than psoriasis, which was diagnosed 3 years prior to presentation; he had fragmented follow-up with numerous private physicians since that time. Past treatments included coal tar preparations, various steroid ointments, anthralin, and a few other unknown preparations by private physicians. No systemic or ultraviolet therapy was performed.

In the treating clinic, the patient consented to partaking in a trial comparing the effect of topical honey treatment on the right knee and fluticasone ointment on the left. The honey used in the authors’ clinic was a food-grade honey purchased from a specialized local honey shop. Prior to its usage, the honey was sent to the main laboratory of the Ministry of Public Health (Doha, Qatar) and was found to be pure and sterile5,6; it had no clostridium spores or fungi. The honey was homogenous, thick, and white in color and produced by Apis mellifera bees, native to the Primorsky Krai region in Russia. 

About 4 g of natural honey was topically applied to the right knee, and 2 g of 0.005% fluticasone propionate ointment was applied to the left. Both knees were covered with Tegaderm (3M, St Paul, MN), a waterproof transparent dressing, and were changed with a reapplication of honey and ointment daily at the clinic for a period of 1 week. This treatment is an alternative to classical, expensive topical antipsoriasis medications and photochemotherapy.

The patient displayed improved response to both treatments with disappearance of scales and dryness 1 week after treatment was initiated (Figures 1, 2). He reported no burning, itching, or other side effect from the natural honey treatment. Unfortunately, 2 weeks posttreatment he was lost to follow-up, preventing a longer observation of the course of his plaques.

Discussion

Psoriasis is a common, chronic, inflammatory skin disorder that usually presents as erythematous papules and plaques with silver scaling. Treatment options for mild-moderate disease typically involve topical steroids and ultraviolet therapy. The focus in this case presentation is on honey as an alternative therapy for psoriasis, which appears to be an efficacious, cost-effective, and acceptable option. 

Psoriasis affects about 2% of the US population with a predominant skin and joint manifestation.2 As a result of chronic inflammation and excessive skin cell proliferation, patients clinically present with scaling, disfiguring, and erythematous plaques. Psoriasis is classified by skin lesion morphology into plaque, pustular, inverse, erythrodermic, and guttate forms. Impacting about 80% to 90% of patients, plaque psoriasis is by far the most common.2 Its severity can be determined by calculating the involved body surface area (BSA): BSA < 3% = mild, BSA 3% to 10% = moderate, and BSA > 10% = severe. The case presented herein is a mild-moderate case (BSA < 5%). The first-line treatment for these mild cases is high-potency topical corticosteroid, which often shows immediate improvement in the psoriatic wound.3 Interestingly, the topical white honey applied to the other knee in the present case generated a similar result after 1 week of treatment, suggesting that further trials on patients may be warranted.

Several studies7-9 in the past have highlighted the potential therapeutic use of natural honey in chronic wounds such as diabetic foot ulcers and atopic dermatitis. Surahio et al10 demonstrated the potential therapeutic use of honey in the treatment of patients with mild-moderate psoriasis, but data on the application for psoriatic patients are currently very limited. A trial by Al Waili11 on 18 patients with psoriasis treated with natural honey showed that 50% of the subjects responded with significant improvement in their lesions over the 2-week course of therapy. However, honey was not used on its own as in the present case but rather mixed with olive oil and bees wax.

Honey is a natural substance known to have both pro- inflammatory and anti-inflammatory properties in wound healing. Current knowledge suggests honey stimulates TNF-α from monocytes in the skin during states of low inflammation and also has anti-inflammatory properties in states of active inflammation.12,13 This property serves to modulate the transition from the inflammatory and proliferative stages of wound healing to the recovery phase. This is a possible explanation as to why honey may treat psoriasis, a condition characterized by excessive wound healing and keratinocyte hyperproliferation. Topical honey also has other properties to promote wound healing, such as wound debridement action, antimicrobial activity, and antioxidant properties14-17 

The pathophysiology of the inflammatory component of psoriasis is not fully understood. The current understanding is that in addition to the old concept of keratinocyte hyperproliferation, psoriasis is more significantly caused by a dysregulation of the immune system.2 Key cellular components include dendritic cells, macrophages, and neutrophils. Dendritic cells are of 2 key components: plasmacytoid, which produce interferon-alpha; and myeloid antigen presenting cells, which produce TNF-α, IL-23, and IL-12.18-20 These cytokines serve to promote an inflammatory state through the T-cell immune system. One study21 also found in vitro that TNF-α plays a role in upregulating N-methyl D-aspartate (NMDA)-2RC receptors in skin cells after reaching a confluent state, which in turn allows TNF-α to exert a growth-inhibitory effect. This same study found that psoriatic skin cells lack the ability to express NMDA-2RC in response to the action of TNF-α, thus leading to uncontrolled proliferation and inflammation. In addition to actions on cell migration and proliferation, TNF-α also has the effects of increased vascularity through nitric oxide and VEGF release, T-cell proliferation, helper T 1 cytokine production, and cell apoptosis. It seems paradoxical that TNF-α increases apoptosis when psoriasis is in a state of keratinocyte hyperproliferation with increased TNF-α levels22; however, other complex factors play a role in preventing apoptosis and increasing cell proliferation, such as nuclear factor-kappa B production and increased nitric oxide production. 

Psoriasis topical corticosteroids are multifaceted and include broad-spectrum action on skin barrier and immune function (although their mechanism of action is not well understood). Despite their demonstrated efficacy, topical corticosteroids are associated with potential adverse effects such as stria, atrophy, telangiectasia, and purpura as well as hypopigmentation. In addition, long-term use can result in cumulative increases in percutaneous absorption, with the possibility of rare but systemic adverse events (adrenal suppression, hypertension, insulin resistance, hyperglycemia, and cataracts).23 The authors have used topical steroids in favor of systemic corticosteroids due to the fact that systemic corticosteroid use is associated with insulin resistance and hyperglycemia in patients with preexisting and new-onset diabetes. The effects of systemic steroid intake on blood glucose levels are seen within hours of steroid intake24 and seems to be dose-dependent.25 Bone loss and increased bone fragility is related partially to the inhibitory effects of corticosteroids on osteoblast activity. Corticosteroids reduce intestinal calcium absorption and increase renal calcium excretion. This may contribute to hyperparathyroidism and bone loss as determined by bone densitometry. 

Fluticasone propionate is classified as a potent anti-inflammatory drug. It is available as 0.05% ointment and 0.005% cream formulations for acute and maintenance treatment of patients with psoriasis, dermatitis, and vitiligo. Several clinical trials26-28 have documented its safety since there was a low potential for cutaneous and systemic side effects, including areas such as the eyelids and the face. 

The mechanism by which topical honey exerts its anti-inflammatory action has yet to be established; however, it has been proposed that honey inhibits prostaglandin synthesis, which is often responsible for the observed characteristics of heat, itchiness, and pain associated with inflammation.29 It is hypothesized that antioxidants in honey were responsible for inhibition of reactive oxygen species production by activated human plymorphonuclear cells,30 thereby partially responsible for the anti-inflammatory action of honey. Tumor necrosis factor-alpha most commonly acts as an inflammatory cytokine that binds to the TNF receptor. Honey has a modulating effect by exerting some of its anti-inflammatory activity via stimulation of the production of anti-inflammatory cytokines, which, in turn, cause a decrease in TNF-α expression through various feedback loops.

Furthermore, honey significantly increases the expression of IL-1 receptor antagonist and IL-10, allowing monocytes/macrophages to recruit more immune cells to the affected site yet suppressing the inflammatory response of these recruited cells; as a result, inflammation is dampened, leading to the healing of affected sites.31

Although there is a possibility that the right knee receiving topical fluticasone did better because of a combination effect from possible systemic absorption, the low level of absorption of topically applied fluticasone propionate makes this assumption unlikely; however, it does not rule it out completely. Consequently, ideally speaking, a crossover design or spaced treatment plan would negate this question.

Conclusions

This case report demonstrates a successful outcome of topical application of honey in the management of mild psoriasis, thereby offering a natural alternative treatment and avoiding the systemic side effects of corticosteroids. This is quite promising, especially in Third World countries where health care resources are limited. However, randomized controlled trials are needed to verify these results and to determine the optimal frequency, contact time, and duration of natural honey application as well as efficacy of different floral honey.

Acknowledgments

Affiliations: Weill Cornell Medical College in Qatar, Doha, Ar-Rayyan, Qatar; and Primary Health Care Corporation, Doha, Qatar
 
Correspondence:
Hashim Mohamed, MD
20 Sahar Bin Ayash Street
PO Box 7452
Doha, Qatar
fmcc2000@gmail.com
 
Disclosure: The authors disclose no financial or other conflicts of interest.

References

  1. Barui A, Banerjee P, Chaudhary A, et al. Evaluation of angiogenesis in diabetic lower limb wound healing using a natural medicine: a quantitative approach. Wound Med. 2014;6:26–33. 2. Ochoa Sosa S. The Effect of Honey on Treatment for Chronic Wounds Compared to Standard Therapy: A Systematic Review [dissertation]. Forest Grove, OR: Pacific University School Physician Assistant Studies; 2010.  3. Abuharfeil N, Al-Oran R, Abo-Shehada M. The effect of bee honey on the proliferative activity of human B- and T-lymphocytes and the activity of phagocytes. Food Agric Immunol. 1999;11(2):169–177. 4. Molan P, Rhodes T. Honey: a biologic wound dressing. Wounds. 2015;27(6):141–151. 5. Al-Lenjawi B, Mohamed H, Abu Salma M, Abo Gouda Z. Natural honey in the management of thermal burn of the foot in a type 2 diabetic patient: a case report. Dermatol Open J. 2016;1(1):14–18.   6. Mohamed H, Salma MA, Al Lenjawi B, et al. The efficacy and safety of natural honey on the healing of foot ulcers: a case series. Wounds. 2015;27(4):103–114. 7. Pieper B. Honey-based dressings and wound care: an option for care in the United States. J Wound Ostomy Continence Nurs. 2009;36(1):60–66. 8. Menter A, Korman NJ, Elmets CA, et al; American Academy of Dermatology Work Group. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: case-based presentations and evidence-based conclusions [published online ahead of print February 8, 2011]. J Am Acad Dermatol. 2011;65(1):137–174. 9. Raychaudhuri SK, Maverakis E, Raychaudhuri SP. Diagnosis and classification of psoriasis [published online ahead of print January 13, 2014]. Autoimmun Rev. 2014;13(4-5):490–495. 10. Surahio AR, Khan AA, Farooq M, Fatima I. Role of honey in wound dressing in diabetic foot ulcer. J Ayub Med Coll Abbottabad. 2014;26(3):304–306. 11. Al-Waili NS. Topical application of natural honey, beeswax and olive oil mixture for atopic dermatitis or psoriasis: partially controlled, single-blinded study. Complement Ther Med. 2003;11(4):226–234. 12. Tonks A, Cooper RA, Price AJ, Molan PC, Jones KP. Stimulation of TNF-alpha release in monocytes by honey. Cytokine. 2001;14(4):240–242. 13. Oryan A, Alemzadeh E, Moshiri A. Biological properties and therapeutic activities of honey in wound healing: a narrative review and meta-analysis [published online ahead of print January 23, 2016]. J Tissue Viability. 2016;25(2):98–118. 14. Mohamed H. Successful healing of diabetic foot ulcers and various etiology ulcers with natural honey: an alternative paradigm in wound healing. J Diab Rel Dis. 2016;1(1):107. 15. Al-Lenjawi B, Mohamed H, Al-Ali A, Kherallah B. Are all wound products created equally? The re-emergence of natural honey. J Diabetic Foot Complications. 2015;7(2):26–41. 16. Mohamed HA. Management of stage III and IV pressure injuries in a paraplegic patient: the role of natural honey. Wounds Int J. 2016;7(4):33–36. 17. Mohamed H, Al Lenjawi B. Triangle of wound assessment made easy: revisited. Dermatol Open J. 2016;1(3):51–55.  18. Victor FC, Gottlieb AB. TNF-alpha and apoptosis: implications for the pathogenesis and treatment of psoriasis. J Drugs Dermatol. 2002;1(3):264–275. 19. Fingleton J, Sheahan D, Corin A, Weatherall M, Beasley R. A randomised controlled trial of topical Kanuka honey for the treatment of psoriasis. JRSM Open. 2014;5(3):2042533313518913.  20. Jaganathan SK, Mandal M. Involvement of non-protein thiols, mitochondrial dysfunction, reactive oxygen species and p53 in honey-induced apoptosis. Invest New Drugs. 2010;28(5):624–633. 21. Mahajan R, Handa S. Pathophysiology of psoriasis. Indian J Dermatol Venereol Leprol. 2013;79(7):1–9. 22. Morhenn VB, Nahm WJ, Mansbridge JN. Psoriatic keratinocytes are resistant to tumor necrosis factor alpha’s induction of mRNA for the NMDA-R2C subunit. Exp Dermatol. 2013;22(11):750–751. 23. Siegfried EC, Jaworski JC, Kaiser JD, Hebert AA. Systematic review of published trials: long-term safety of topical corticosteroids and topical calcineurin inhibitors in pediatric patients with atopic dermatitis. BMC Pediatr. 2016;16:75.  24. Roeder A, Schaller M, Schäfer-Korting M, Korting HC. Safety and efficacy of fluticasone propionate in the topical treatment of skin diseases. Skin Pharmacol Physiol. 2005;18(1):3–11.  25. Schneiter P, Tappy L. Kinetics of dexamethasone-induced alterations of glucose metabolism in healthy humans. Am J Physiol. 1998;275(5 Pt 1):e806–e813.  26. Kirkup ME, Birchall NM, Weinberg EG, Helm K, Kennedy CT. Acute and maintenance treatment of atopic dermatitis in children – two comparative studies with fluticasone propionate (0.05%) cream. J Dermatolog Treat. 2003;14(3):141-148. 27. Hanifin J, Gupta AK, Rajagopalan R. Intermittent dosing of fluticasone propionate cream for reducing the risk of relapse in atopic dermatitis patients. Br J Dermatol. 2002;147(3):528-537. 28. Furue M, Terao H, Rikihisa W, et al. Clinical dose and adverse effects of topical steroids in daily management of atopic dermatitis. Br J Dermatol. 2003;148(1):128-133. 29. Kassim M, Achoui M, Mansor M, Yusoff KM. The inhibitory effects of Gelam honey and its extracts on nitric oxide and prostaglandin E(2) in inflammatory tissues [published online ahead of print August 11, 2010]. Fitoterapia. 2010;81(8):1196–1201. 30. van den Berg A, van den Worm E, van Ufford HC, Halkes SB, Hoekstra MJ, Beukelman CJ. An in vitro examination of the antioxidant and anti-inflammatory properties of buckwheat honey. J Wound Care. 2008;17(4):172–174, 176–178. 31. Ghazali WS, Romli AC, Mohamed M. Effects of honey supplementation on inflammatory markers among chronic smokers: a randomized controlled trial. BMC Complement Altern Med. 2017;17(1):175  

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