Painful diamond-shaped tongue lesion in elderly man - Clinical Advisor

Painful diamond-shaped tongue lesion in elderly man

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A 62-year-old white man with a past medical history of latent tuberculosis, vitiligo, and psoriasis presents for follow-up for treatment of psoriasis. The patient’s psoriasis has proven refractory to numerous treatments over the years, so he began treatment with secukinumab, a monoclonal antibody against interleukin-17A. After 2 months of therapy, the patient reports new-onset tongue pain. Physical examination demonstrates an erythematous, edematous, diamond-shaped plaque on the posterior dorsum of the patient’s tongue. 

Median rhomboid glossitis (MRG), also known as central papillary atrophy and posterior midline atrophic candidiasis, refers to well-demarcated regions of depapillation on the dorsal tongue, typically occurring midline, anterior to the foramen cecum. Although generally asymptomatic, patients with MRG may...

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Median rhomboid glossitis (MRG), also known as central papillary atrophy and posterior midline atrophic candidiasis, refers to well-demarcated regions of depapillation on the dorsal tongue, typically occurring midline, anterior to the foramen cecum. Although generally asymptomatic, patients with MRG may present with pain or pruritus. MRG may also involve a similar erythematous lesion, known as a “kissing lesion,” on the overlying palate, where it comes in contact with the tongue.1 The condition was once believed to be caused by failure of the lateral processes to properly fuse over the tuberculum impar of the tongue during embryogenesis, resulting in a region prone to Candida infection. However, authors today more commonly ascribe the lesions to Candida albicans infection alone.2,3 

MRG occurs in an estimated 0.01% to 1.0% of the adult population; the condition affects three times more men than women.3,4 Incidence is increased in patients with diabetes and those who are immunosuppressed, as well as patients on broad-spectrum antibiotics.1,3 Association of MRG with other risk factors for oral candidiasis, including smoking and use of dentures, has been disputed.1,5 

The diagnosis of MRG is typically made based upon clinical appearance of lesions.2 Presence of a Candida species may be confirmed by scraping or culture, however Candida is present as part of the normal oral flora in up to 50% of people.2,4 Biopsy may be useful in cases of ambiguous morphology. Histopathology of MRG demonstrates inflammation with overlying atrophic to hypertrophic squamous epithelium, as well as loss of fungiform and filiform papillae. Candidal hyphae are frequently visible in hematoxylin and eosin stained sections, but they are typically better visualized with a fungal stain.2 

Asymptomatic cases of MRG may be merely observed, with no treatment required.6 In addition to MRG, the differential diagnosis for lesions of the tongue includes such conditions as geographic tongue, lichen planus, lingua plicata, squamous cell carcinoma, and secondary syphilis (Table).1,4,7,8 

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Topical antifungal agents, such as nystatin suspensions or clotrimazole troches, may be used for the treatment of symptomatic lesions.4 Persistent symptomatic lesions or those that are otherwise suspicious should be biopsied to exclude possible diagnosis of carcinoma.6 Presentation of MRG with “kissing lesions” on the overlying palate may indicate an underlying immunodeficiency and human immunodeficiency virus testing may be considered in such patients.4 

Use of secukinumab, a drug approved by the US Food and Drug Administration in January 2015 for the treatment of moderate to severe plaque psoriasis, has been associated with increased frequency of Candida infections, including those of the skin, oropharynx, and esophagus.9 Secukinumab is a human monoclonal antibody that binds to and neutralizes interleukin (IL)-17A. IL-17A is a cytokine produced by Th17 cells that promotes a neutrophil-dominant inflammatory response that is protective against numerous bacterial and fungal pathogens, including Candida albicans.10 The fact that increased activity of Th17 cells and elevated levels of IL-17A have also in recent years been linked to numerous chronic inflammatory conditions, including psoriasis, asthma, multiple sclerosis, and rheumatoid arthritis, has made it a promising target for therapies.9 

The use of secukinumab is the most likely cause of development of MRG in this patient, based upon timing of lesion occurrence, the known association between the drug and Candida infection, and the lack of other known risk factors for this patient. The patient was treated with 10-mg clotrimazole troches three times daily with complete resolution after 2 to 3 weeks. 

Helena Jenkinson, BS, is a medical student and Sarah Pinney, MD, is a dermatology professor at the McGovern Medical School of the University of Texas at Houston.

References

  1. Goregen M, Miloglu O, Buyukkurt MC, Caglayan F, Aktas AE. Median rhomboid glossitis: a clinical and microbiological study. Eur J Dent. 2011;5:367-372.
  2. Nelson BL, Thompson L. Median rhomboid glossitis. Ear Nose Throat J. 2007;86:600-601. 
  3. Joseph BK, Savage NW. Tongue pathology. Clin Dermatol. 2000;18:613-618.
  4. Reamy BV, Derby R, Bunt CW. Common tongue conditions in primary care. Am Fam Physician. 2010;81:627-634.
  5. Arendorf TM, Walker DM. Tobacco smoking and denture wearing as local aetiological factors in median rhomboid glossitis. Int J Oral Surg. 1984;13:411-415.
  6. Mueller DT, Callanan VP. Congenital malformations of the oral cavity. Otolaryngol Clin North Am. 2007;40:141-160.
  7. Assimakopoulos D, Patrikakos G, Fotika C, Elisaf M. Benign migratory glossitis or geographic tongue: an enigmatic oral lesion. Am J Med. 2002;113:751-755.
  8. Bruce AJ, Rogers RS 3rd. Oral manifestations of sexually transmitted diseases. Clin Dermatol. 2004;22:520-527.
  9. Mease PJ, McInnes IB, Kirkham B, et al; FUTURE 1 Study Group. Secukinumab inhibition of interleukin-17A in patients with psoriatic arthritis. N Engl J Med. 2015;373:1329-1339.
  10. Miossec P, Korn T, Kuchroo VK. Interleukin-17 and type 17 helper T cells. N Engl J Med. 2009;361:888-898.
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