Why is it important to know about the implications of alcohol consumption and psoriasis--a mini-review.
Psoriasis is a chronic skin and joints inflammatory condition. The disturbance between keratinocytes and CD4+lymphocytes leads to epidermic manifestations due to the overproduction of cytokines and keratinocyte hyperproliferation and differentiation. Psoriasis is considered trigger for comorbidities, rather than being associated with them. Patients with psoriasis are more at risk to develop heart disease, metabolic syndrome, or adult-onset diabetes. (1-3) 1Psoriasis affects over 100 million people globally, with a prevalence ranging between 0.09% and 11.4%. (4)
Environmental and genetic risk factors contribute to the development of psoriasis skin and joints lesions and are related to their severity, the therapeutic response, and even contributing to maintaining remission. (5) The severity of psoriasis is directly related to patients' quality of life, who are exposed to recurrent negative feelings that predispose them to major depressive disorders and alcohol abuse. Patients diagnosed with psoriasis are found to experience alcohol misuse and to drink excessively, and some of them are addicted to alcohol. (6), (7)
Therapeutic options are varied, from local therapy, phototherapy, systemic oral therapy or biological therapy including monoclonal antibodies treatments. (8) Worsening psoriasis lesions by concomitant alcohol intake when biological treatment is administered is found responsible for the dysregulation of the immune response, consecutive to the overproduction of proinflammatory cytokines and interleukins. (9), (10) Due to the variable response to therapy, multiple types of research are underway to find new therapeutic solutions with as few adverse effects as oral vitamin D or metformin. (3), (11)
Alcohol consumption was associated with different diseases and complaints (hepatic, neurologic, gastric), including the susceptibility of infections and overresponse in systemic inflammation. In this mini-review, we aimed to discuss the issue of drinking alcohol in patients with psoriasis. From one point of view, whether alcohol is a trigger aggravating factor in psoriasis, and on the other hand, whether the condition itself causes the person to consume more alcohol and the risks to which he is exposed in this situation.
Alcohol and its possible mechanism role in the occurrence of psoriatic lesions.
Alcohol and acetaldehyde, its metabolite, affect the immune system by initiating and aggravating inflammation following the increase of tumor necrosis factor-alpha (TNF-[alpha]) and lymphocyte proliferation. (12) Acute alcohol consumption has an immunosuppressive effect, while chronic alcohol consumption stimulates the response of inflammatory cells. (8)
Drinking habits apparently exacerbate preexisting comorbidities. (10) Psoriasis appears to be the most autoimmune favorable condition to be activated for those who heavy habitual drinkers when compared to Crohn's disease, where drinking alcohol once a week seems to protect against the onset of the disease. (13) Another example would be multiple sclerosis, where alcohol consumption is not considered a trigger and potentially can have neuroprotective achievement. (14), (15) It has been suggested that alcohol is a probable trigger for psoriasis. Clinicians are aware that patients with the worsening activity of psoriasis lesions are at risk to consume alcohol excessively. (1618)
Studies have shown in psoriasis that alcohol intake increases the production of TNF[alpha], contributing to the inflammatory process by increasing pro-inflammatory cytokines' activity and decreasing compliance with treatment. (9), (19) Alcohol and its metabolites increase skin permeability and disorganize the skin barrier function. (2023) The lipid composition and sebum content of the dermal barrier can be disturbed by dietary factors, including alcohol intake, (24) because nutrients are essential factors for keratinocyte proliferation and differentiation. (25)
Another effect of alcohol consumption could be the impact on epidermal T helper cells response. On murine cells, significant changes in CD4+T cell methylation were reported in patients with psoriasis. (23), (26) Mast cells from connective tissues are considered to play a role in psoriasis pathogenesis; alcohol can affect mast cell counts and degranulation. (24) Ethanol and its metabolites affect innate and adaptive immunity and may influence directly and indirectly immune cell processes. (25)
The suspicion of alcohol abuse in patients with psoriasis is based on histopathological abnormalities results reported on liver biopsies, these being the most common in patients with psoriasis due to alcoholic cirrhosis. (10) Figure 1 summarizes the negative effect of alcohol on cellular proliferation, cellular differentiation and skin barrier.
The impact of alcohol consumption and psoriasis evolution
More drinking persons are found among patients with psoriasis, and overdrinking is a common practice in these patients. (27) There seems to be a link between the type of alcohol and the amount consumed (Figure 2) from the perspective of exacerbation or onset of psoriasis. (28), (29) It was found that drinking alcohol increased susceptibility to bacterial infections affecting the surinfection of psoriatic pustules. (12)
Casano et al. have reported that the association of psoriasis to alcohol leads to severe inflammatory lesions on the face and flexion areas with minimal scaling; also, hyperkeratotic lesions at the acral level are frequently described. (10)
A relatively small number of observational studies have followed the context of alcohol consumption with the severity of psoriasis. A positive correlation between quantity, type and frequency of alcohol consumption and aggravation of psoriasis has been observed. (28,30) Mahajan et al. showed that alcohol regular consumption was associated with a pattern of alcohol drinking named alcohol use disorder (AUD). Daily alcohol intake was reported in about 33% of patients with chronic psoriasis. Severe psoriasis PASI (psoriasis area and severity index) scores and BSA (body surface area) are found in alcohol consumers compared to persons who do not drink alcohol. Cessation of alcohol consumption may improve psoriasis severity. This can be due to the therapeutic compliance of patients, as alcohol intake and addiction is related as a significant cause of lack of treatment compliance. (31)
Comorbidities associated with psoriasis are exacerbated, leading to an increase in the mortality rate of these patients (Figure 2). The premature mortality rate can increase by 60% in patients with associated psoriasis and alcohol dependence, alcoholic liver disease, fibrosis and cirrhosis, cardiovascular disease, psychosis. (17,32)
Approximately 10 to 17 % of patients experience a deleterious effect of psoriasis on their lives, and have suicidal feelings and suicidal attempts. (33) People with severe psoriasis associate anxiety or depression symptoms or depressive disorders that alter their quality of life; excessive alcohol consumption and no compliance with treatment lead to an inadequate therapeutic response, including overexpression of severe mental disease. (33)
Psoriasis therapy, depending on the severity, starts from topical treatment and reaches biological treatment. The predisposition to infections is increased by the association between biological therapy that induces immune cells and alcohol. (9)
An appropriate solution to the approach to alcohol consumption in patients with psoriasis would be the neuro-endocrine approach. Addictive behaviour treatment can focus both on unbalanced neural circuits and alcohol metabolism. (34)
Psychiatrists have focused on carefully balancing by treatment programs the neural circuits of reward, alcohol dependence and abstinence, and obtaining patient satisfaction. The metabolic pathway involved in alcohol metabolization may be largely considered. (35) Medications available in the treatment of alcohol dependence include dopamine receptors and serotonin antagonists (such as olanzapine), selective serotonin reuptake inhibitors (such as sertraline), 5-HT3R antagonist and naltrexone.
There is a relationship between dopamine and the physiology of psoriasis. In the reversed psoriasis, the lesions remitted after levodopa for Parkinson's disease, probably due to increased cyclic AMP. (36)
Future studies on psoriasis therapies in the case of alcohol drinkers could target both the patient's problems and neurotransmitter distribution and modulation involved in this continuum of inflammatory processes.
Excessive alcohol intake contributes to the pathophysiology of psoriasis. Medical history about the individual's type of consumption and quantity can be useful for treating psoriasis disease. Patients tend not to recognize alcohol consumption in front of the doctor or support the consumption of smaller amounts then the real ones, these in a context where doctors must be fine observers of non-typical and subtle signs and symptoms related to alcohol abuse.
The multidisciplinary team, including the family doctor and the patient's family/relatives has an essential role in monitoring alcohol consumption to prevent relapses and good treatment compliance.
Authors' contributions statement: GCB, IVG, ON and AMAS: conceptualization, methodology, study design, software; GCB, IVG, AMAS and ON: writing original draft preparation; AMAS and AS writing reviewing and editing; AAS and MN: supervision. All authors read and approved the final version of the manuscript.
Conflicts of interest: Both authors - none to declare.
Funding: None to declare.
(1.) Lai YC, Yew YW. Psoriasis as an independent risk factor for cardiovascular disease: an epidemiologic analysis using a national database. J Cutan Med Surg. 2016;20:327-33. https://doi.org/10.1177/1203475415602842
(2.) Li W, Han J, Hu FB, Curhan GC, Qureshi AA. Psoriasis and risk of type 2 diabetes among women and men in the United States: a population-based cohort study. J Invest Dermatol. 2012;132:291-8. https://doi.org/10.1038/jid.2011.319
(3.) Stanescu AMA, Simionescu AA, Florea M, Diaconu CC. Is metformin a possible beneficial treatment for psoriasis? A scoping review. J Pers Med. 2021;11:251. https://doi.org/10.3390/jpm11040251
(4.) World Health Organization. 2016. Global report on psoriasis. Accessed on: 14 March 2021. Available at: http://www.who.int.
(5.) Zhao M, Lu Q. The aberrant epigenetic modifications in the pathogenesis of psoriasis. J Investig Dermatol Symp Proc. 2018;19:S81-2. https://doi.org/10.1016/j.jisp.2018.09.007
(6.) Svanstrom C, Lonne-Rahm SB, Nordlind K. Psoriasis and alcohol. Psoriasis (Auckl). 2019;9:75-9. https://doi.org/10.2147/PTT.S164104
(7.) Zink A, Herrmann M, Fischer T, et al. Addiction: an underestimated problem in psoriasis health care. J Eur Acad Dermatol Venereol. 2017;31:1308-15. https://doi.org/10.1111/jdv.14204
(8.) Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with biologics. J Am Acad Dermatol. 2019;80:1029-72. https://doi.org/10.1016/j.jaad.2018.11.057
(9.) Farkas A, Kemeny L. Alcohol, liver, systemic inflammation and skin: a focus on patients with psoriasis. Skin Pharmacol Physiol. 2013;26:119-26. https://doi.org/10.1159/000348865
(10.) Cassano N, Vestita M, Apruzzi D, Vena GA. Alcohol, psoriasis, liver disease, and anti-psoriasis drugs. Int J Dermatol. 2011;50:1323-31. https://doi.org/10.1111/j.1365-4632.2011.05100.x
(11.) Stanescu AMA, Simionescu AA, Diaconu CC. Oral vitamin d therapy in patients with psoriasis. Nutrients. 2021;13:163. https://doi.org/10.3390/nu13010163
(12.) Farkas A, Kemeny L Psoriasis and alcohol: is cutaneous ethanol one of the missing links? Br J Dermatol. 2010;162:711-6. https://doi.org/10.1111/j.1365-2133.2009.09595.x
(13.) Han DY, Fraser AG, Dryland P, Ferguson LR. Environmental factors in the development of chronic inflammation: a case-control study on risk factors for Crohn's disease within New Zealand. Mutat Res. 2010;690:116-22. https://doi.org/10.1016/j.mrfmmm.2009.09.002
(14.) Quesnel S, Feinstein A. Multiple sclerosis and alcohol: a study of problem drinking. Mult Scler. 2004;10:197-201. https://doi.org/10.1191/1352458504ms992oa
(15.) Goodin DS. Survey of multiple sclerosis in Northern California. Mult Scler. 1999;5:78-88.
(16.) McAleer MA, Mason DL, Cunningham S, et al. Alcohol misuse in patients with psoriasis: identification and relationship to disease severity and psychological distress. Br J Dermatol. 2011;164:1256-61.
(17.) Tobin AM, Higgins EM, Norris S, Kirby B. Prevalence of psoriasis in patients with alcoholic liver disease. Clin Exp Dermatol. 2009;34:698-701.
(18.) Kirby B, Richards HL, Mason DL, Fortune DG, Main CJ, Griffiths CE. Alcohol consumption and psychological distress in patients with psoriasis. Br J Dermatol. 2008;158:138-40.
(19.) Zhu KJ, Zhu CY, Fan YM. Alcohol consumption and psoriatic risk: a meta-analysis of case-control studies. J Dermatol. 2012;39:770-3.
(20.) Farkas A, Kemeny L, Szell M, Dobozy A, Bata-Csorgo Z. Ethanol and acetone stimulate the proliferation of HaCaT keratinocytes: the possible role of alcohol in exacerbating psoriasis. Arch Dermatol Res. 2003;295:56-62.
(21.) Park H, Kim K. Association of alcohol consumption with lipid profile in hypertensive men. Alcohol Alcohol. 2012;47:282-7. https://doi.org/10.1093/alcalc/ags019
(22.) 22. Lim S, Shin J, Cho Y, Kim KP. Dietary patterns associated with sebum content, skin hydration and pH, and their sex-dependent differences in healthy Korean adults. Nutrients. 2019;11:619.
(23.) Park GT, Han J, Park SG, Kim S, Kim TY. DNA methylation analysis of CD4+ T cells in patients with psoriasis. Arch Dermatol Res. 2014;306:259-68.
(24.) Harvima IT, Nilsson G, Suttle MM, Naukkarinen A. Is there a role for mast cells in psoriasis? Arch Dermatol Res. 2008;300:461-78.
(25.) Szentkereszty-Kovacs Z, Gaspar K, Szegedi A, Kemeny L, Kovacs D, Torocsik D. Alcohol in psoriasis - from bench to bedside. Int J Mol Sci 2021;22:4987.
(26.) Parlet CP, Waldschmidt TJ, Schlueter AJ. Chronic ethanol feeding induces subset loss and hyporesponsiveness in skin T cells. Alcohol Clin Exp Res. 2014;38:1356-64. https://doi.org/10.1111/acer.12358
(27.) Brenaut E, Horreau C, Pouplard C, et al. Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol. 2013;27 Suppl 3:30-5. https://doi.org/10.1111/jdv.12164
(28.) Poikolainen K, Reunala T, Karvonen J, Lauharanta J, Karkkainen P. Alcohol intake: a risk factor for psoriasis in young and middle aged men? BMJ. 1990;300:780-3. https://doi.org/10.1136/bmj.300.6727.780
(29.) Qureshi AA, Dominguez PL, Choi HK, Han J, Curhan G. Alcohol intake and risk of incident psoriasis in US women: a prospective study. Arch Dermatol. 2010;146:1364-9.
(30.) Gerdes S, Zahl VA, Weichenthal M, Mrowietz U. Smoking and alcohol intake in severely affected patients with psoriasis in Germany. Dermatology. 2010;220:38-43. https://doi.org/10.1159/000265557
(31.) Mahajan VK, Dhattarwal N, Chauhan PS, et al. The association of alcohol use disorder and chronic plaque psoriasis: results of a pilot study. Indian Dermatol Online J. 2020;12:128-33. http://doi:10.4103/idoj.IDOJ_226_20
(32.) Parisi R, Webb RT, Carr MJ, et al. Alcohol-related mortality in patients with psoriasis: a population-based cohort study. JAMA Dermatol. 2017;153:1256-62.
(33.) Liang SE, Cohen JM, Ho RS. Psoriasis and suicidality: a review of the literature. Dermatol Ther. 2019;32:e12771. https://doi.org/10.1111/dth.12771
(34.) Volkow ND, Wang GJ, Tomasi D, Baler RD. Unbalanced neuronal circuits in addiction. Curr Opin Neurobiol. 2013;23:639-48.
(35.) Ferraguti G, Pascale E, Lucarelli M. Alcohol addiction: a molecular biology perspective. Curr Med Chem. 2015;22:670-84.
(36.) AbouKhedr NA, Eid AA. Clinical efficacy of bromocriptine and the influence of serum prolactin levels on disease severity in patients with chronic plaque-type psoriasis. Alexandria J Med. 2013;49:385-9. https://doi.org/10.1016/j.ajme.2013.04.001
Gabriel Cristian Bejan (1), Ioana Veronica Grajdeanu (2,*), Oana Nicolescu (3), Anca Angela Simionescu (4), Maria Nitescu (5), Ana Maria Alexandra Stanescu (6)
Received: 16 May 2021; revised: 28 May 2021; accepted: 30 May 2021.
(1) MD, PhD, Department of Family Medicine, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Blv, 050474, Bucharest, Romania; (2)MD, PhD, Department of Family Medicine, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Blv, 050474, Bucharest, Romania; (3) MD, PhD, Department of Family Medicine, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Blv, 050474, Bucharest, Romania; (4)Department of Obstetrics and Gynecology, Carol Davila University of Medicine and Pharmacy, Filantropia Clinical Hospital, 11-13 Ion Mihalache Blv, district 1, 011132, Bucharest, Romania; (5) MD, PhD, Department of Nutrition, Carol Davila University of Medicine and Pharmacy, National Institute for Infectious Diseases "Prof.Dr. Matei Bal'", 1 Dr. Calistrat Grozovici Street, 021105, Bucharest, Romania; (6)MD, PhD, Department of Family Medicine, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Blv, 050474, Bucharest, Romania.
(*) Corresponding author: Ioana Veronica Grajdeanu, email@example.com
Article downloaded from www.jccp.ro
Published May 2021
ISSN 2457 - 7200
ISSN - L = 2457 - 7200
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|Author:||Bejan, Gabriel Cristian; Grajdeanu, Ioana Veronica; Nicolescu, Oana; Simionescu, Anca Angela; Nitesc|
|Publication:||Journal of Contemporary Clinical Practice|
|Date:||May 1, 2021|
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