Correspondence
The contribution of drugs to lichen sclerosus doi: 10.1111/ced.12264 Clayton et al.1 published a study of oral and vulval lichen planus (LP) and its association with the use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and nonsteroidal anti-inflammatory drugs (NSAIDs). We have extended this study to vulval lichen sclerosus (LS). LS is another interface dermatosis with a prominent lymphocytic infiltrate, which can show clinical and immunological overlap with LP.2,3 There is increasing evidence that LS involves autoimmune mechanisms.3,4 We conducted a retrospective study in patients with vulval LS. The study was approved by the Central Oxford Research Ethics Committee, and all participants gave informed consent (COREC numbers CO3.081 and CO2.290). The patient group consisted of 200 adult women of northern European origin who attended the Churchill Hospital, Oxford, with vulval LS, between October 2004 and April 2006. They had a mean age of 63.04 years (range 26 – 85). The vulval LS had been diagnosed clinically and confirmed histologically in 140 patients. In the remaining 60, biopsy was either contraindicated or refused. The control population consisted of 974 unselected women had a mean age of 67 years (range 34 – 99) recruited from the community through general practices. Compared with normal controls, patients with vulval LS were more likely to be on NSAIDs, but less likely to be on ACE Inhibitors and beta-blockers. There were differences with regard to usage of beta-blockers (4% vs. 10%, P < 0.01) and ACE inhibitors (3% vs. 12%, P = 0.001) (Table 1).
Table 1 Comparison of drug usage in patients with vulval lichen sclerosus and controls, and correlations with clinical data.
Subjects, n Drugs, n (%) NSAIDs Βeta-blockers ACE inhibitors
Vulval LS
Controls
P*
200
974
-
10 (5) 8 (4) 5 (3)
36 (4) 97 (10) 120 (12)
0.51 < 0.01 < 0.001
ACE, angiotensin-converting enzyme; LS, lichen sclerosus; NSAID, nonsteroidal anti-inflammatory drug. *The McNemar test was used for statistical analysis.
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Clinical and Experimental Dermatology (2014) 39, pp216–234
LS is characterized by an inflammatory infiltrate of T cells into the dermis and epidermis, while the mechanism of action of ACE inhibitors includes a decrease in inflammatory cell infiltrate. In this study, we found an inverse association between vulval LS and ACE inhibitors. We therefore believe that ACE inhibitors may diminish the LS inflammatory process, and protect patients from developing the disease. We also found an inverse association between patients with vulval LS and beta-blockers. The possible mechanism of action of beta-blockers relies on blocking cyclic AMP levels, resulting in upregulation of keratinocyte proliferation, and reduced differentiation and increased motility of lymphocytes, which may influence the clinical expression of patients with LS patients. There was no difference between patients and controls in the number taking NSAIDs (5% vs. 4%, P = 0.51). In conclusion, this report represents the first study on drug usage in patients with vulval LS. We found an inverse relationship between the presence of vulval LS and use of beta-blockers and ACE inhibitors. Larger studies are warranted to elucidate the relationship between the disease process and medication use. M. Baldo, I. Ali, and F. Wojnarowska Department of Dermatology, Oxford Radcliffe NHS Trust and University of Oxford, Churchill Hospital, Oxford, UK E-mail: [email protected] Conflict of interest: none declared Accepted for publication 4 September 2013
References 1 Clayton R, Chaudhry S, Ali I et al. Mucosal (oral and vulval) lichen planus in women: are angiotensinconverting enzyme inhibitors protective, and beta-blockers and non-steroidal anti-inflammatory drugs associated with the condition? Clin Exp Dermatol 2010; 35: 384–7. 2 Cooper SM, Ali I, Baldo M, Wojnarowska F. The association of lichen sclerosus and erosive lichen planus of the vulva with autoimmune disease: a case-control study. Arch Dermatol 2008; 144: 1432–5. 3 Baldo M, Bailey A, Bhogal B et al. T cells reactive with the NC16A domain of BP180 are present in vulval lichen sclerosus and lichen planus. J Eur Acad Dermatol Venereol 2010; 24: 186–90. 4 Meyrick Thomas RH, Ridley CM, McGibbon DH, Black MM. Lichen sclerosus et atrophicus and autoimmunity – a study of 350 women. Br J Dermatol 1988; 118: 41–6.
ª 2014 British Association of Dermatologists
The contribution of drugs to lichen sclerosus doi: 10.1111/ced.12264 Clayton et al.1 published a study of oral and vulval lichen planus (LP) and its association with the use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and nonsteroidal anti-inflammatory drugs (NSAIDs). We have extended this study to vulval lichen sclerosus (LS). LS is another interface dermatosis with a prominent lymphocytic infiltrate, which can show clinical and immunological overlap with LP.2,3 There is increasing evidence that LS involves autoimmune mechanisms.3,4 We conducted a retrospective study in patients with vulval LS. The study was approved by the Central Oxford Research Ethics Committee, and all participants gave informed consent (COREC numbers CO3.081 and CO2.290). The patient group consisted of 200 adult women of northern European origin who attended the Churchill Hospital, Oxford, with vulval LS, between October 2004 and April 2006. They had a mean age of 63.04 years (range 26 – 85). The vulval LS had been diagnosed clinically and confirmed histologically in 140 patients. In the remaining 60, biopsy was either contraindicated or refused. The control population consisted of 974 unselected women had a mean age of 67 years (range 34 – 99) recruited from the community through general practices. Compared with normal controls, patients with vulval LS were more likely to be on NSAIDs, but less likely to be on ACE Inhibitors and beta-blockers. There were differences with regard to usage of beta-blockers (4% vs. 10%, P < 0.01) and ACE inhibitors (3% vs. 12%, P = 0.001) (Table 1).
Table 1 Comparison of drug usage in patients with vulval lichen sclerosus and controls, and correlations with clinical data.
Subjects, n Drugs, n (%) NSAIDs Βeta-blockers ACE inhibitors
Vulval LS
Controls
P*
200
974
-
10 (5) 8 (4) 5 (3)
36 (4) 97 (10) 120 (12)
0.51 < 0.01 < 0.001
ACE, angiotensin-converting enzyme; LS, lichen sclerosus; NSAID, nonsteroidal anti-inflammatory drug. *The McNemar test was used for statistical analysis.
234
Clinical and Experimental Dermatology (2014) 39, pp216–234
LS is characterized by an inflammatory infiltrate of T cells into the dermis and epidermis, while the mechanism of action of ACE inhibitors includes a decrease in inflammatory cell infiltrate. In this study, we found an inverse association between vulval LS and ACE inhibitors. We therefore believe that ACE inhibitors may diminish the LS inflammatory process, and protect patients from developing the disease. We also found an inverse association between patients with vulval LS and beta-blockers. The possible mechanism of action of beta-blockers relies on blocking cyclic AMP levels, resulting in upregulation of keratinocyte proliferation, and reduced differentiation and increased motility of lymphocytes, which may influence the clinical expression of patients with LS patients. There was no difference between patients and controls in the number taking NSAIDs (5% vs. 4%, P = 0.51). In conclusion, this report represents the first study on drug usage in patients with vulval LS. We found an inverse relationship between the presence of vulval LS and use of beta-blockers and ACE inhibitors. Larger studies are warranted to elucidate the relationship between the disease process and medication use. M. Baldo, I. Ali, and F. Wojnarowska Department of Dermatology, Oxford Radcliffe NHS Trust and University of Oxford, Churchill Hospital, Oxford, UK E-mail: [email protected] Conflict of interest: none declared Accepted for publication 4 September 2013
References 1 Clayton R, Chaudhry S, Ali I et al. Mucosal (oral and vulval) lichen planus in women: are angiotensinconverting enzyme inhibitors protective, and beta-blockers and non-steroidal anti-inflammatory drugs associated with the condition? Clin Exp Dermatol 2010; 35: 384–7. 2 Cooper SM, Ali I, Baldo M, Wojnarowska F. The association of lichen sclerosus and erosive lichen planus of the vulva with autoimmune disease: a case-control study. Arch Dermatol 2008; 144: 1432–5. 3 Baldo M, Bailey A, Bhogal B et al. T cells reactive with the NC16A domain of BP180 are present in vulval lichen sclerosus and lichen planus. J Eur Acad Dermatol Venereol 2010; 24: 186–90. 4 Meyrick Thomas RH, Ridley CM, McGibbon DH, Black MM. Lichen sclerosus et atrophicus and autoimmunity – a study of 350 women. Br J Dermatol 1988; 118: 41–6.
ª 2014 British Association of Dermatologists
