A 76-year-old female patient was referred from her specialty center because of a large ulceration of 2.5 cm in diameter, affecting the left lateral border of the tongue.
It is indicated that ulceration began abruptly for a month and a half, rapidly increasing in size.
1.
The patient reported various clinical history of hypertension (treatment with torasemide and captopryl), dyslipaemia (treatment with statins), depression, chronic constipation, osteoporosis (treatment for several years with tramadol, alendronate).
After clinical inspection of the lingual ulcerative lesion and when a possible lingual neoplasia was suspected, an incisional biopsy of the ulcerative border was performed.
The biopsy was diagnosed with lingual ulcer with absence of viral inclusions, fungal structures or signs of malignancy, which explained the existence of the ulceration.
After performing the biopsy, which ruled out neoplasic growth, the possible existence of a chronic traumatic cause that justified the lingual ulcer lesion was evaluated.
In this sense an extraction of tooth 36 was performed, which presented a large destructive carious lesion, not susceptible to conservative treatment.
It was also indicated to suspend treatment with alendronic acid, citing the patient for successive controls.
One month later, the persistence of the ulcer with an increase in its diameter was confirmed, and a second biopsy of the ulcerous anterior border was performed again.
The morphological and immunohistochemical study showed a penetrating lingual ulcerative lesion that reached the lingual muscular plane.
There was an intense neoangiogenesis, with immune ukemic front vessels with atypical CD10 nuclei, a polymorphous inflammatory infiltrate with frequent presence of eosinophils, as well as mononucleated elements, often with histiocytic phenotype.
There were also elements of a macrophage/epicytic nature (CD68 +) and a population of fusiform cells of myofibroblastic aspect, with reactivity to F-XIIIa.
The cell proliferation index (Ki67 +) was high in the bed of the ulcerative lesion, being observed nuclear staining in 20% of CD30 + mononucleated cells.
With all these data the diagnosis of lingual eosinophilic ulcer with atypical mononucleated elements CD30 + was emitted, consistent with TUGSE, recommending prolonged evolutionary control of the patient.
1.
After performing monthly controls of the patient, at the 5th month of evolution after the 2nd biopsy, a notable reduction in the size of the lesion was observed, with a gradual disappearance of the gastrointestinal tract, which gradually reduced its diameter until almost complete
The patient continues to attend quarterly clinical controls scheduled in the long term, until completing a 24-month follow-up.
