Comment20194.3

Comment: A squamous cell carcinoma of the lower lip with a discoid lupus erythematosus   by Boubacar Ahy Diatta, Salimatou Diallo, Matar Ndiaye, Silly Touré, Gisèle Wotto Gaye, Mame Thierno Dieng

 

author: Abbass El-Outa, DDS, DES Clin. Man., E-mail: abbass@abbass.org

American University of Beirut Medical Center, Beirut, Lebanon; Private Practice of Oral Medicine and Restorative Dentistry, Beirut, Lebanon

Submission: 29.09.2019; Acceptance: 30.09.2019


Chronic discoid lupus erythematosus (DLE) presents a known pre-disposing dermatosis for the development of skin squamous cell carcinoma (SCC) [1,2]. Indeed, SCC developing from lesions or scars of DLE have been reported ever since 1886 [3]. However, only few cases exist in the literature describing oral squamous cell carcinoma in patients with DLE. The majority of these cases report sun-exposed, labial squamous cell carcinoma – especially lower lip, with male predilection and peak in the 5th decade of life [4]. These tumours are usually moderately- or well-differentiated, as in this case report.
Prognosis of SCC arising in DLE seems to be poorer than SCC arising in normal mucosa/skin [5,6]. Therefore, strict long-term follow-up should be scheduled. Patients should be monitored for changes in lip mucosa, and actinic changes should be managed immediately.
In an overview of published cases of SCC arising in areas affected by DLE in India by Fernandes et al., the mean age was around 50 years, with a long period of latency between DLE onset and SCC development (9.59 ± 5.6 years) [7]. Aside from well-established risk factors for oral squamous cell carcinoma – smoking, alcohol and HPV, predisposing factors for lip scc include accumulated ultraviolet exposure from sunlight, chronic immunosuppressive treatment, and chronic injuries, burns and scars. 
In this case, authors reported the presence of a hypopigmented lesion on the patient’s leg. Special care of sun-exposed, hypopigmented areas should be taken; in one study, Sherman et al. reported that hypo/de-pigmented plaques in patients with DLE only developed SCC if those plaques were on sun-exposed areas [8]. Given the fact that lips are more prone to actinic damage than skin due to the absence of melanin as protective layer and continuous sun-exposure, actinic cheilitis of lips presents a serious precancerous condition that necessitates immediate management. Therefore, patients should always be instructed to use sun screens on lips.
Concerning staging, the described tumor seems to be of stage II (T2N0M0). Authors did not mention depth of infiltration of the neoplasm; a limiting factor in predicting the progression of oral SCC is the depth. 
The authors argue that the SCC in this report developed on a discoid lupus erythematosus lesion (as mentioned in Figure 1 caption). However, there is no evidence to definitely suggest or refute such claim, especially histologically. According to other studies, several etiological factors have been suggested in the development of SCC in patients with DLE; aside from arising from the inflammatory and injured lesions of DLE, immunosuppressive therapy seems to be an important pre-disposing factor [9]. In this case report, the patient may have developed the labial SCC not only from a pre-existing DLE lesion, but also due to chronic immunosuppressive therapy or even de novo development due to actinic changes.
To conclude, the discussed paper presents an interesting and rare case of lip squamous cell carcinoma in a patient with chronic discoid lupus erythematosus. The reported case seems to be in accordance with other cases in the literature concerning male predominance, age, and degree of differentiation of the tumor. Such reports are essential for future research designs to unveil the underlying pathogenesis of such combination.

REFERENCES

1.  Kramer IR, Lucas RB, Pindborg JJ, Sobin LH. Definition of leukoplakia and related lesions: an aid to studies on oral precancer. Oral Surg Oral Med Oral Pathol. 1978;46:518–39. 
2. Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36:575–80. 
3. Cassarino DS, Derienzo DP, Barr RJ. Cutaneous squamous cell carcinoma: a comprehensive clinicopathologic classification. Part one. J Cutan Pathol. 2006;33:191–206. 
4. Arvanitidou IE, Nikitakis NG, Georgaki M, Papadogeorgakis N, Tzioufas A, Sklavounou A. Multiple primary squamous cell carcinomas of the lower lip and tongue arising in discoid lupus erythematosus: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125:e22–30. 
5. Liu W, Shen ZY, Wang LJ, Hu YH, Shen XM, Zhou ZT, et al. Malignant potential of oral and labial chronic discoid lupus erythematosus: A clinicopathological study of 87 cases. Histopathology. 2011;59:292–8. 
6. Reibel J. Prognosis of oral pre-malignant lesions: significance of clinical, histopathological, and molecular biological characteristics. Crit Rev Oral Biol Med. 2003;14:47–62. 
7. Fernandes MS, Girisha BS, Viswanathan N, Sripathi H, Noronha TM. Discoid lupus erythematosus with squamous cell carcinoma: A case report and review of the literature in Indian patients. Lupus. 2015;24:1562–6. 
8. Sherman RN, Lee CW, Flynn KJ. Cutaneous squamous cell carcinoma in black patients with chronic discoid lupus erythematosus. Int J Dermatol. 1993;32:677–9. 
9. Egiziano G, Bernatsky S, Shah AA. Cancer and autoimmunity: Harnessing longitudinal cohorts to probe the link. Best Pract Res Clin Rheumatol. 2016;30:53–62. 


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