Exacerbation of psoriasis by the hypolipidemic agent, gemfibrozil

Fisher, D. A.

doi:10.1001/archderm.124.6.854

Cited by 13 publications

(7 citation statements)

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“…For example, elevated levels of cholesterol have been detected in psoriatic patients (Benton et al, 1963), and lipid-lowering drugs can induce exacerbation of psoriasis (Fisher et al, 1988), suggesting an involvement of cholesterol in this disease. Psoriatic epidermis exhibits altered expression of differentiation marker genes: a K14-specific antibody only stains a small subset of basal keratinocytes (Parent et al, 1994), psoriatic skin exhibits diminished K10 expression (van Erp et al, 1989), basal and several rows of suprabasal cells are devoid of K10 (Bernerd et al, 1992) and involucrin is precociously expressed and present in all but basal epidermal layers (Watanabe et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Cholesterol Depletion Upregulates Involucrin Expression in Epidermal Keratinocytes Through Activation of p38

Jans

Atanasova

Jadot

et al. 2004

Journal of Investigative Dermatology

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Cholesterol has been recently suggested to regulate the early steps of keratinocyte differentiation through lipid rafts. In many cell types, depletion of cholesterol activates signaling proteins like epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), or extracellular signal-regulated kinase (ERK) known to affect cell differentiation. In this study, we explored the effects of cholesterol depletion on the phenotype of cultured keratinocytes, using a treatment with methyl-beta-cyclodextrin (MbetaCD) to extract cholesterol and a treatment with lovastatin to inhibit cholesterol neosynthesis. Analysis of the expression of differentiation marker genes in early differentiating confluent cultures reveals that cholesterol depletion induces downregulation of keratin 14 (K14) and keratin 10 (K10) and upregulation of involucrin. MbetaCD treatment induces phosphorylation of EGFR, HER2, and ERK, but not HER3. Inhibition of EGFR with PD153035 impairs the MbetaCD-induced phosphorylation of EGFR, HER2, and ERK, but does not impair the alteration of K14, K10, or involucrin gene expression, indicating that other signaling proteins regulate this phenomenon. p38 has been suggested to regulate the expression of involucrin during keratinocyte differentiation. We found that MbetaCD treatment induces a prolonged phosphorylation of p38 in general and p38alpha in particular. An inhibition of p38 with PD169316 impairs the upregulation of involucrin mRNAs by a treatment with MbetaCD, but not by a p38delta-activating TPA treatment, which might suggest that cholesterol depletion alters involucrin gene expression through activation of p38alpha/beta.

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Section: Discussionmentioning

confidence: 99%

Cholesterol Depletion Upregulates Involucrin Expression in Epidermal Keratinocytes Through Activation of p38

Jans

Atanasova

Jadot

et al. 2004

Journal of Investigative Dermatology

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“…One small pilot study evaluated the efficacy of simvastatin in treating plaque psoriasis and found a significant reduction in PASI scores of 47.34% 120. Fibrates, another class of lipid-lowering drugs, may exacerbate psoriasis 121,122…”

Section: Cardiovascular Disease and Risk Factorsmentioning

confidence: 99%

Psoriasis and comorbidities: links and risks

Ni¹,

Chiu²

2014

CCID

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Psoriasis is a chronic inflammatory skin disease affecting approximately 2% of the population worldwide. In the past decade, many studies have drawn attention to comorbid conditions in psoriasis. This literature review examines the epidemiological evidence, pathophysiological commonalities, and therapeutic implications for different comorbidities of psoriasis. Cardiovascular disease, obesity, diabetes, hypertension, dyslipidemia, metabolic syndrome, nonalcoholic fatty liver disease, cancer, anxiety and depression, and inflammatory bowel disease have been found at a higher prevalence in psoriasis patients compared to the general population. Because of the wide range of comorbid conditions associated with psoriasis, comprehensive screening and treatment must be implemented to most effectively manage psoriasis patients.

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“…In the literature, it was reported that antidiabetic drugs could also trigger psoriasis [37–40]. In our study, the number of patients on antidiabetic agents was 35 (12%), and other drugs, which our patients used and were known as triggers, were terbinafine [41–43] and antimalarial drugs [1–8].…”

Section: Discussionmentioning

confidence: 61%

Triggering drug use in patients with psoriasis: an investigative report from Turkey

Öğretmen

Aşkin

Hız

et al. 2014

pdia

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IntroductionThe patients clinically diagnosed with psoriasis were investigated for drug use that may trigger psoriasis.AimTo minimize the triggering drug use and help the medical treatment of psoriasis patients.Material and methodsThe study involved 289 psoriatic patients who attended our clinic in 2010–2012 and were asked to bring their drug lists of the last year, which they obtained from the pharmacy's record system. They were advised not to use the drugs that may trigger psoriasis. Data analyses were performed using SPSS program version 19.0.ResultsA total of 289 patients were included in the study. Two hundred and twenty-one patients were using non-steroidal anti-inflammatory drugs; 133 patients were using anti-reflux drugs; 35 patients were using antidiabetic drugs; 31 patients were using calcium-channel blockers and 24 patients were using β-blockers. In our study group, there was no significantly difference between median PASI scores of the patients using a triggering drug and those of who are not using a triggering drug. However, there was a positive low correlation between PASI rates and numbers of drugs used (r = 0.180, p = 0.013).ConclusionsMany other factors may trigger psoriasis, therefore the effect of stopping or minimizing the drug use on disease remission is not known. Because of the high triggering drug use rate, it is important to enlighten psoriasis patients about triggering drugs.

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Exacerbation of psoriasis by the hypolipidemic agent, gemfibrozil

Cited by 13 publications

References 0 publications

Cholesterol Depletion Upregulates Involucrin Expression in Epidermal Keratinocytes Through Activation of p38

Cholesterol Depletion Upregulates Involucrin Expression in Epidermal Keratinocytes Through Activation of p38

Psoriasis and comorbidities: links and risks

Triggering drug use in patients with psoriasis: an investigative report from Turkey

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