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Volume 10, Issue 3 (August 2023)                   IJML 2023, 10(3): 187-195 | Back to browse issues page

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Taheri Sarvtin M, Kamali M. A Review of the Latest Findings of Candida Colonization and Candidiasis in Patients with Psoriasis and Its Management. IJML 2023; 10 (3) :187-195
URL: http://ijml.ssu.ac.ir/article-1-477-en.html
A Review of the Latest Findings of Candida Colonization and Candidiasis in Patients with Psoriasis and Its Management
Mehdi Taheri Sarvtin , Mohadeseh Kamali *
Department of Medical Mycology and Parasitology, Faculty of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran
Keywords: Candida, Colonization, Patient, Psoriasis
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Introduction
Psoriasis is a common inflammatory skin disease characterized by thick and erythema-raised plaques with silvery scales, affecting about 0.6-4.8% of the worldwide population [1, 2]. Psoriasis affects both males and females at about the same rate, but in males' onset is earlier than in females [3]. Clinical symptoms of psoriasis begin between the ages of 20 and 30 years, although children and adolescents may also be affected [4]. These symptoms are more common in elbows, knees, and scalp [3]. Psoriasis is the most common autoimmune disease, which, due to the long duration of the conflict, will cost a lot for the patient [5]. In addition, patients may experience problems such as depression, anxiety, malnutrition, sexual dysfunction, reduced quality of life, cardiovascular diseases, stroke, lymphoma, diabetes mellitus, and metabolic syndrome [2, 5]. High levels of triglycerides and cholesterol have also been reported in some people with psoriasis [6]. There is still no definitive treatment for this disease and only symptomatic treatment is used for affected people [5]. The pathogenesis of this disease is not completely understood, but an interaction between genetic and environmental factors has been recognized [3]. Among the environmental factors that have been considered in the pathogenesis of this disease, we can mention microbial factors and the formation of antibodies against them [5]. Candida species are one of the most important microbial agents playing a role in the creation or exacerbation of psoriasis which has been discussed in some articles [7-9]. Therefore, we decided to study the published articles on the role of Candida species in psoriasis and prepare a comprehensive report on the role of Candida species in the disease. In this study, we will provide the necessary suggestions in the field of diagnostic methods, improving the treatment of patients and preventing its recurrence.
Overview of Candida species and its history
Candida species is one of the most important fungal colonizers on the skin and mucosal surfaces of the human body such as the genitourinary tract, oral cavity, and gastrointestinal tract [10-14]. Many species of the Candida genus are commensal members of the human normal microflora; however, following some alterations in the host, some of these Candida species can also become opportunistic pathogens, by taking advantage of various predisposing factors, including locally or systematically impaired immune system, diabetes and use of steroids and broad-spectrum antibiotics [15, 16]. There are approximately 200 different species in the Candida genus, but only a few are harmful and can cause infections in humans [17]. C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, C. krusei, C. dubliniensis, C. famata, and especially C. albicans are species that can cause disease in humans [15, 18, 19]. Candida genus was first described by Wilkinson in 1849; subsequently, Hausmann showed in 1875 that it is responsible for vaginal and oral candidiasis. Christine Marie Burkhout was the one who described the species albicans in 1923 during her thesis at the University of Utrecht. The word Albican is derived from the Latin word Albicare, meaning white, and Candida is derived from the Latin word ‘Toga [17]. Over time, the genus Candida began to be classified and many other species were discovered. Currently, there are more than 200 species [20, 21].
Epidemiology of Candida species
Although the number of epidemiological studies on the Candida genus is still increasing worldwide, there is little information in some parts of the world, mainly due to the lack of accurate, specific, and sensitive diagnoses in routine clinical laboratories. The epidemiology of Candida species can be different depending on the geographic region, age, sex, underlying disease, and sampling location. In the Middle East and North Africa, An evident shift has been observed in the epidemiology of Candida species associated with invasive candidiasis in these countries from the predominant C. albicans toward the non-albicans species. Among them, while C. tropicalis prevails in Lebanon, Saudi Arabia, and UAE, C. parapsilosis is the most common species in Turkey, Kuwait, and Egypt [22]. In the Asia-Pacific region, C. albicans is the predominant Candida species causing invasive candidiasis/candidemia in Japan, Australia, Korea, Hong Kong, Singapore, Malaysia and Thailand whereas C. tropicalis is the most common Candida species in Pakistan and India [23]. In Iran, C. albicans, C. parapsilosis, C. glabrata and C. tropicalis are mentioned as causes of candidemia [24]. 
Candida colonization in patients with psoriasis
Candida colonization in patients with psoriasis has been investigated by several studies. Various studies have shown more oral Candida colonization in patients with psoriasis compared to healthy people [25-28]. In these studies, the prevalence of oral Candida species isolation in patients with psoriasis has been reported to range widely between 23% and 78% [26-28]. So far, research has focused mainly on oral Candida colonization, while data on skin and intestinal colonization is limited. In conducted studies, psoriasis patients and controls did not differ significantly in the rate of Candida spp. Isolated from the skin [9, 26]. In the study of Elsner et al., the candida isolated from the stool of patients with psoriasis was significantly more than that of control subjects [29]. No significant relationship between age, sex, duration of disease, and colonization rate in patients has been reported in the mentioned articles [26, 29]. Reports on the relationship between the severity of the disease and the Candida colonization rate are different [26, 29, 30]. In Elsner et al. and Leibovici et al. studies, there was no significant relationship between the severity of the disease and the amount of Candida colonization [26, 29], but in Picciani et al.'s study, a significant association between the clinical severity of psoriasis and Candida colonization was seen [30].
Possible role of Candida species in psoriasis
Although Candida species are involved in the initiation or exacerbation of psoriasis, the exact mechanism is not known [5]. In this article, we will refer to some of the mentioned mechanisms. Candida spp. antigens, especially C. albicans surface proteins, have superantigen-like effects that lead to the activation of T lymphocytes independent of antigen presentation and excessive release of pro-inflammatory cytokines and exacerbation of psoriasis [9, 31]. Some studies have focused on the identification of somatic protein profiles of various Candida species isolated from psoriatic patients. In these studies, 12 somatic proteins have been identified in C. albicans (11 to 93.3 kDa), 12 somatic proteins in C. parapsilosis (11 to 109.6 kDa), 12 somatic proteins in C. guilliermondii (11 to 74.1 kDa), 12 somatic proteins in C. lipolytica (11 to >180 kDa), 7 somatic proteins in C. tropicalis (11 to 74.1 kDa) and 45 somatic proteins in C. famata (18 to > 180 kDa) [2, 32]. In these studies, it has not been determined which of these proteins can play a role in triggering or aggravating psoriasis; therefore, additional studies are required in this matter. Candida species can also aggravate psoriasis through toxin production [5]. Overgrowth of Candida in the intestine and other parts of the body causes a large amount of toxins to enter the blood. In a normal state, Candida toxin is neutralized by the liver, but when this toxin is high, the liver is not able to neutralize it. As a result, the toxin is deposited in the skin and causes the aggravation of lesions in psoriasis [6].
Candidiasis in patients with psoriasis
In addition to the colonization and exacerbation of psoriatic lesions, Candida species can cause a disease called candidiasis in different parts of the body of patients with psoriasis [33]. Infection in patients may be due to the nature of the disease or due to treatment [5]. The advent of some specific immunomodulating treatments for psoriasis has highlighted the association of psoriasis with various infections [34]. Interlukine(IL)-17 plays an important role in preventing candidiasis [9]. Some IL-17 inhibiting drugs such as Ixekizumab and Secukinumab used in the treatment of psoriasis, can increase candidiasis in patients with psoriasis [9, 35]. Disturbance in the production of anti-Candida antibodies has also been reported, which may be effective in increasing candidiasis [25]. Candida species can cause the following diseases in psoriasis patients:  
Oral Candidiasis
Four types of oral candidiasis may be seen in people with psoriasis, which include: thrush, denture stomatitis, chronic hyperplastic, and perleche [33]. Patients with oral candidiasis can be asymptomatic or may present various clinical features such as sore throat, difficulty swallowing, and halitosis [33, 36]. This form of the disease can usually be diagnosed through physical examination and clinical history [33, 37]. Traditionally, microscopic examination using potassium hydroxide and lesion swab culture on selective media can also help in diagnosis [33, 38]. The diagnosis and treatment of all forms of candidiasis are listed in Table No. 1
Cutaneous candidiasis
Cutaneous candidiasis is a superficial infection of the skin and tends to occur in warm and moist areas of the skin including groin, abdominal skin folds, inframammary skin, and interdigital spaces [39, 40]. The mortality rate of cutaneous candidiasis is relatively low; however, if infections remain untreated for a long time, they may cause systemic candidiasis, with a mortality rate of approximately 25–50% [39]. Cutaneous candidiasis can be diagnosed based on the clinical appearance of the skin, the presence of pseudohyphae in wet potassium hydroxide mounts, and positive fungal culture from scraping of the affected areas [33, 40] (Table 1).
Vulvovaginal candidiasis (VVC)
Vulvovaginal candidiasis is a global issue and is the second most common cause of vaginitis in women after bacterial vaginosis [41]. It is estimated that 75% of women experience at least one VVC infection during their lives and 40%–45% will have two or more episodes [42]. Concomitant fungal infections can worsen psoriasis; therefore, VVC needs to be identified and treated quickly in these patients [33]. Vulvovaginal candidiasis can be diagnosed based on clinical symptoms and physical examination   (Table 1). Diagnosis is confirmed by direct microscopic examination and culture. Most cases of this disease are uncomplicated and easily treated. A longer and different treatment is needed in complicated cases such as recurrent disease, infection due to a non-albicans candida species, and severe disease [43].
Candidal balanitis
Candidal balanitis is defined as inflammation of the glans penis in the presence of Candida species and typically affects sexually active adult males [44, 45]. The disease often occurs in uncircumcised men patients with diabetes and patients with primary inflammatory dermatoses, such as psoriasis [46]. Candidal balanitis can be diagnosed based on the clinical appearance and direct microscopic examination and culture may be helpful in some cases [33, 47] (Table 1). The sensitivity of the microscopic examination can vary depending on the sampling method, and the "adhesive tape" method is more accurate than swabbing [47].
Table 1. Guideline for the diagnosis and treatment of candidiasis
Disease Symptoms Treatment
Oral candidiasis Thrush Thick, white plaques on the tongue, buccal and gingival mucosa that are easily scratched Clotrimazole troches, nystatin suspension, oral fluconazole, Itraconazole solution, posaconazole suspension
Denture stomatitis Inflammation and erythema of the oral mucosal areas covered by the denture
Chronic hyperplastic White patch on the gums and inside the cheeks that cannot be scratched easily
Perleche Erythema or fissuring at the corners of the mouth
Cutaneous candidiasis Thin, bright-red plaques that can be erosive, dry, scaly, oozing, or macerated. Pustules and collarette scales may also appear. Itching or burning may be present as well. Clotrimazole  cream, oral fluconazole
Vulvovaginal candidiasis Pruritus, hyperemia, vaginal discomfort and leucorrhea, burning, soreness, cheese-like or watery vaginal discharge, dyspareunia, and vaginal and vulvar erythema Clotrimazole  cream, Butoconazole  cream
Candidal balanitis Redness, soreness, or swelling of the penis
White, shiny patches at the top of the penis. Burning sensation during urination or sex		 Clotrimazole cream, Miconazole cream

Table 2. Some  biological drugs for the treatment of psoriasis in adults
Drug Biological composition Therapeutic
target		 Candidiasis risk
Adalimumab Monoclonal IgG1 antibody TNF Increase
Infliximab Monoclonal IgG1 antibody TNF Increase
Etanercept Recombinant TNF-α receptor TNF Increase
Certolizumab pegol IgG1antibody Fab' fragment TNF Increase
Secukinumab Monoclonal IgG1 antibody IL-17A Increase
Ixekizumab Monoclonal IgG4 antibody IL-17A Increase
Brodalumab Monoclonal IgG2 antibody IL-17A receptor Increase
Ustekinumab Monoclonal IgG1 antibody IL-12/IL-23p40 little increase
Guselkumab Monoclonal IgG1 antibody IL-23p19 low
Tildrakizumab Monoclonal IgG1 antibody IL-23p19 Infrequent
Risankizumab Monoclonal IgG1 antibody IL-23p19 No
TNF= Tumor necrosis factor; IL= Interlukine
Discussion
Psoriasis is a chronic inflammatory disease with long-term treatment [48]. Some of these drugs can increase the risk of Candida infection in these patients [49]. Several biological therapies are available that target various inflammatory cytokines; these include tumor necrosis factor (TNF) antagonists, IL-17 inhibitors, IL-12/23p40 inhibitors, and IL-23p19 inhibitors. An increase in the risk of Candida infection has been seen in the treatment with IL-17 inhibitors [48]. As an important factor in innate and adaptive immunity, IL-17 plays a fundamental role in the defense against yeast and other microorganisms at mucosal and cutaneous interfaces, so its inhibition can increase candidiasis [48, 50]. It is mentioned that the use of IL-23p19 inhibitors has a lesser role in increasing the risk of candidiasis in psoriatic patients [48]. Candida infections in patients with psoriasis often occur in areas that are not easily visible and are often asymptomatic; so, dermatologists should always inquire about oral or genital discomfort to identify candidiasis [33]. There is no requirement to screen patients for Candida infections before initiating therapy with biologic drugs [51]. Candida infection is suspected in patients with psoriasis, it is best to confirm the diagnosis by culture or molecular diagnosis to rule out non-albicans species of Candida, as some of them are intrinsically resistant to azoles [50]. Isolation of Candida alone does not necessarily indicate disease and must be accompanied by clinical signs and symptoms [33]. The majority of Candida infections in patients with psoriasis are localized and mild to moderate in severity; therefore, these infections cannot be a reason to discontinue treatment by biological drugs [50]. In these patients, candidiasis can be definitively treated with antifungal drugs [33]. The initial choice of treatment usually depends on the severity of the disease and whether the patient is pregnant [51]. In uncomplicated mild cases, topical antifungal treatment is preferable to systemic treatment. In cases of moderate to severe infection or if the disease is resistant to topical treatment, systemic antifungal therapy may be necessary [50]. Current guidelines state that systemic azoles (itraconazole, fluconazole, posaconazole, and isavuconazole) should be avoided in pregnant women, especially those in the first trimester, because of the possibility of birth defects associated with these drugs [52]. C. albicans is the most common species and empiric therapy should aim to target this species [51]. If candidiasis persists despite antifungal therapy, (re) confirmation of Candida infection, species determination, and susceptibility testing is recommended [50]. Relapse is not uncommon and subsequent treatment recommendations remain unchanged, although a longer course is sometimes used [51].
Conclusion
Increased Candida colonization and candidiasis have been confirmed in patients with psoriasis due to the nature of the disease and the use of some biological drugs. It is necessary to check patients for candidiasis during the treatment. Diagnosis of candidiasis is based on clinical and laboratory symptoms. Anti-IL-23p19 agents appear to have an acceptable safety profile in adults with moderate to severe psoriasis. An increase in candida colonization and candidiasis can aggravate psoriasis. More studies are needed to investigate the exact mechanism of this phenomenon. In candidiasis, topical therapy is generally effective and safe. Azoles are mostly used to treat Candida infections.
Conflict of Interest
The authors declare that there is no conflict of interest.
Acknowledgment
I would like to thank all the medical staff of Jiroft University of Medical Sciences who helped me in conducting this research.


References

[1]. Puig L, Costanzo A, Muñoz‐Elías EJ, Jazra M, Wegner S, Paul CF, et al. The biological basis of disease recurrence in psoriasis: a historical perspective and current models. Br J Dermatol. 2022; 186(5): 773-781.
[2]. Taheri Sarvtin M, Hedayati MT, Abastabar M, Shokohi T. Debaryomyces hansenii colonization and its protein profile in psoriasis. Iranian Journal of Dermatology 2014; 17(4): 134-37.
[3]. Alesci A, Lauriano ER, Fumia A, Irrera N, Mastrantonio E, Vaccaro M, et al. Relationship between immune cells, depression, stress, and psoriasis: Could the use of natural products be helpful? Molecules 2022; 27(6): 1953.
[4]. Armstrong AW. Psoriasis. JAMA Dermatol. 2017; 153(9): 956.
[5]. Taheri Sarvtin M, Hedayati MT, Ayatollahi Mosavi SA, Afsarian MH. An overview on the role of microbial agents in psoriasis. Mazand Univ Med Sci. 2012; 23(98): 364-85.
[6]. Taheri Sarvtin M, Hedayati MT, Shokohi T, Hajheydari Z. Serum lipids and lipoproteins in patients with psoriasis. Arch Iran Med. 2014; 17(5): 343-46.
[7]. Lesan S, Toosi R, Aliakbarzadeh R, Daneshpazhooh M, Mahmoudi L, Tavakolpour S, et al.  Oral Candida colonization and plaque type psoriasis: Is there any relationship? J Investig Clin Dent. 2018; 9(3): 12335.
[8]. Ventura A, Mazzeo M, Gaziano R, Galluzzo M, Bianchi L, Campione E. New insight into the pathogenesis of nail psoriasis and overview of treatment strategies. Drug Des Devel Ther. 2017; 11: 2527-535.
[9]. Pietrzak A, Grywalska E, Socha M, Roliński J, Franciszkiewicz-Pietrzak K, Rudnicka L, et al. Prevalence and possible role of Candida species in patients with psoriasis: A systematic review and meta-analysis. Mediators Inflamm. 2018; 2018: 9602362.
[10]. Javad G, Taheri Sarvtin M, Hedayati M T, Hajheydari Z, Yazdani J, Shokohi T. Evaluation of Candida colonization and specific humoral responses against Candida albicans in patients with atopic dermatitis. Biomed Res Int. 2015; 2015: 849206.
[11]. Taheri Sarvtin M, Zand Parsa AF, Kordbacheh P, Hashemi SJ, Mahmoudi M, Daie R, et al. A comparison of candida colonization in the oral cavity of removeable denture wearers and individuals with natural teeth: A short report. JRUMS 12(12): 1025-1032.‏
[12]. Taheri Sarvtin M, Zand Parsa AF, Kordbacheh P, Hashemi SJ, Mahmoudi M, Daie R et al. The comparison of oral candida flora in smokers and non-smokers.‏ AMUJ 2010; 13(1): 78-82.
[13]. Kamali M, Taheri Sarvtin M, Parsanasab H. Prevalence of candida infection in patients with type 2 diabetes mellitus in Sari, North of Iran. Biomed Pharmacol J. 2016; 9(2): 731-34.‏
 [14]. Mehni S, Tork Zahrani S, Taheri Sarvtin M, Mojab F, Mirzaei M, Vazirnasab H. Therapeutic effects of bunium perscicum boiss (Black Zira) on candida albicans vaginitis. Biom Pharmacol J. 2015; 8(2): 1103-109.‏
[15]. Taheri Sarvtin M, Kamali M, Yazdani J. A review on the risk factors, presentations and treatment of candidemia. JJUMS 2016; 2(2): 55-60.‏
[16]. Ghazi S, Rafei R, Osman M, El Safadi D, Mallat H, Papon N, et al. The epidemiology of Candida species in the Middle East and North Africa. JMM. 2019; 29(3): 245-52.‏
[17]. Qadir MI, Asif H. An overview to candidiasis-a Candida infection. Int J Adv Res MicroBiol Immunol. 2020; 2(1): 31-33.‏
[18]. Kumar S, Kumar A, Roudbary M, Mohammadi R, Černáková L, Rodrigues CF. Overview on the infections related to rare candida species. Pathogens 2022; 11(9): 963.‏
[19]. Kamali M, Sarvtin MT. Insights into candida albicans: a new perspective on pathogenic factors and regulatory mechanisms. IJML 2023; 10 (2): 91-106.
 [20]. Kabir MA, Hussain MA, Ahmad Z. Candida albicans: A model organism for studying fungal pathogens. ISRN Microbiology 2012; 1(1): 1-16.
[21]. Spampinato C, Leonardi D. Candida infections, causes, targets, and resistance mechanisms: traditional and alternative antifungal agents. Biomed Res Int. 2013; 2013: 204237.
[22]. Ghazi S, Rafei R, Osman M, El Safadi D, Mallat H, Papon N, et al. The epidemiology of Candida species in the Middle East and North Africa. J Mycol Med. 2019; 29(3): 245-52.
[23]. Wang H, Xu YC, Hsueh PR. Epidemiology of candidemia and antifungal susceptibility in invasive Candida species in the Asia-Pacific region. Future Microbiol. 2016; 11(11): 1461-477.‏
[24]. Vaezi A, Fakhim H, Khodavaisy S, Alizadeh A, Nazeri M, Soleimani A, et al. Epidemiological and mycological characteristics of candidemia in Iran: A systematic review and meta-analysis. J Mycol Med. 2017; 27(2):146-52.
[25]. Taheri Sarvtin M, Shokohi T, Hajheydari Z, Yazdani J, Hedayati MT. Evaluation of candidal colonization and specific humoral responses against Candida albicans in patients with psoriasis.  Int J Dermatol. 2014; 53(12): 555-60.
[26]. Leibovici V, Alkalay R, Hershko K, Ingber A, Westerman M, Leviatan‐Strauss N, et al. Prevalence of Candida on the tongue and intertriginous areas of psoriatic and atopic dermatitis patients. Mycoses 2008; 51(1): 63-6.‏
[27]. Bedair AA, Darwazeh AM, Al-Aboosi MM. Oral Candida colonization and candidiasis in patients with psoriasis. Oral Surg Oral Med Oral Pathol Oral Radiol. 2012; 114(5): 610-15.
[28]. Waldman A, Gilhar A, Duek L, Berdicevsky I. Incidence of Candida in psoriasis: A study on the fungal flora of psoriatic patients. Mycoses. 2001;44 (3-4): 77-81.
[29]. Elsner K, Holstein J, Hilke FJ, Blumenstock G, Walker B, Schmidt S, et al. Prevalence of Candida species in Psoriasis. Mycoses 2021; 65(2): 247-54.‏
[30]. Picciani BLS, Michalski-Santos B, Carneiro S, Sampaio AL, Avelleira JCR, Azulay DR, et al. Oral candidiasis in patients with psoriasis: correlation of oral examination and cytopathological evaluation with psoriasis disease severity and treatment. JAAD 2013; 68(6): 986-91.‏
[31]. Devore-Carter D, Kar S, Vellucci V, Bhattacherjee V, Domanski P,  Hostetter MK. Superantigen-like effects of a Candida albicans polypeptide. J Infect Dis. 2008; 197(7): 981-89.
[32]. Kamali M, Taheri Sarvtin MT. Study on somatic protein profile of six various yeasts isolated from patients with psoriasis. Adv biores. 2017; 8(1): 178-81.‏
[33]. Armstrong AW, Bukhalo M, Blauvelt A. A clinician’s guide to the diagnosis and treatment of candidiasis in patients with psoriasis. Am J Clin Dermatol. 2016; 17(4): 329-36.
[34]. Rademaker M, Agnew K, Anagnostou N, Andrews M, Armour K, Baker C, et al. Psoriasis and infection. A clinical practice narrative. Australas J Dermatol. 2019; 60(2): 91-98.
[35]. Crowley JJ, Warren RB, Cather JC. Safety of selective IL‐23p19 inhibitors for the treatment of psoriasis. J Eur Acad Dermatol Venereol. 2019; 33(9): 1676-684.
[36]. Nenoff P, Kru¨ger C, Schaller J, Ginter-Hanselmayer G, Schulte- Beerbu¨hl R, Tietz HJ. Mycology—an update part 2: dermatomycoses: clinical picture and diagnostics. J Dtsch Dermatol Ges. 2014; 12(9): 749-77.
[37]. Picciani BL, Michalski-Santos B, Carneiro S, Sampaio AL, Avelleira JC, Azulay DR, et al. Oral candidiasis in patients with psoriasis: correlation of oral examination and cytopathological evaluation with psoriasis disease severity and treatment. J Am Acad Dermatol. 2013; 68(6): 986-91.
[38]. Cuenca-Estrella M, Verweij PE, Arendrup MC, Arikan-Akdagli S, Bille J, Donnelly JP, et al. ESCMID* guideline for the diagnosis and management of Candida diseases 2012: diagnostic procedures. Clin Microbiol Infect. 2012; 18(S7): 9-18.
[39]. Bilal H, Hou B, Shafiq M, Chen X, Shahid MA, Zeng Y. Antifungal susceptibility pattern of Candida isolated from cutaneous candidiasis patients in eastern Guangdong region: A retrospective study of the past 10 years. Front Microbiol. 2022; 13: 981181.‏
[40]. Farhan RK, Ahmed T, Mohammad S. Epidemiology of cutaneous candidiasis among patients attending Tikrit Teaching Hospital. Med J Tikrit Univ. 2017; 22(1): 212-19.
[41]. Phillips NA, Rocktashel M, Merjanian L. Ibrexafungerp for the treatment of vulvovaginal candidiasis: design, development and place in therapy. Drug Des Devel Ther. 2023; 17(3): 363-67.
[42]. Lima WG, Araújo MGF, Brito JCM, Castilho RO, Cardoso VN, Fernandes SOA. Antifungal effect of hydroethanolic extract of Fridericia chica (Bonpl.) LG Lohmann leaves and its therapeutic use in a vulvovaginal candidosis model. J Mycol Med. 2022; 32(3): 101255.
[43]. Pappas PG, Kauffman CA, Andes D, Benjamin DK Jr, Calandra TF, Edwards JE Jr, et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis. 2009; 48(5): 503-35.
[44]. Khan A, Moni SS, Ali M, Mohan S, Jan H, Rasool S, et al. Antifungal activity of plant secondary metabolites on Candida albicans: An updated review. Curr Mol Pharmacol. 2023; 16(1): 15-42.‏
[45]. Mehta H, Devana SK, Gupta S, De D,  Mahajan R. Candidiasis presenting as pseudocircinate balanitis in a preschooler. Pediatr Dermatol. 2022; 39(5): 830-31.‏‏
[46]. Edwards S, Bunker C, Ziller F, van der Meijden WI. 2013 European guideline for the management of balanoposthitis. Int J STD AIDS. 2014; 25(9): 615-26.
[47]. Alamalmi MAQ, Blada MBR.  Balanitis: due to bad hygiene inYemeni Men’s. JCCRCS. 2021; 5(4): 1-10. ‏
[48]. Crowley JJ, Warren RB, Cather JC. Safety of selective IL‐23p19 inhibitors for the treatment of psoriasis. JEADV. 2019; 33(9): 1676-684.‏ ‏ ‏‏
[49]. Rodríguez-Cerdeira C, González-Cespón JL, Martínez-Herrera E, Carnero-Gregorio M, López-Barcenas A, Sergeev A, et al. Candida infections in patients with psoriasis and psoriatic arthritis treated with interleukin-17 inhibitors and their practical management. Ital J Dermatol Venerol. 2021; 156(5): 545-57.
[50]. Saunte DM, Mrowietz U, Puig L, Zachariae C. Candida infections in patients with psoriasis and psoriatic arthritis treated with interleukin‐17 inhibitors and their practical management. Br J Dermatol. 2017; 177(1): 47-62.‏
[51]. Yeung J, Bunce PE, Lynde CW, Turchin I, Vender RB. Review and practical guidance on managing fungal infections in patients with psoriasis receiving anti-IL-17 therapies. J Cutan Med Surg. 2022; 26(S 1): 3-23.
[52]. Pappas PG, Kauffman CA, Andes DR, Clancy CJ, Marr KA, Ostrosky-Zeichner L, et al. Clinical practice guideline for the management of candidiasis: 2016 update by the Infectious Diseases Society of America. Clin Infect Dis. 2016; 62(4): 1-50.
Type of Study: Research | Subject: Mycology
Received: 2023/04/5 | Accepted: 2023/07/23 | Published: 2023/10/2
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