CASE 1
A 17-year-old Middle Eastern female presented with 7-year history of progressive, diffuse keloids on the chest and back with concomitant poorly controlled acne vulgaris in a similar distribution. Previous keloid treatments included three years of bi-monthly intralesional corticosteroid therapy without improvement. However, once adequate control of her acne was obtained with topical clindamycin, benzoyl peroxide, tretinoin, and oral doxycycline, she continued to develop new keloid lesions. Symptomatology included significant “shooting” pains and pruritus that disrupted her schoolwork and social functioning. A family history of keloids was confirmed. She was evaluated by radiation oncology, but radiation was not recommended prior to exhausting other therapeutic options given her age and concern for long term increased risk of malignancies.
Physical examination revealed approximately 4% BSA involvement of large exophytic nodules coalescing into irregular brawny linear plaques with raised, erythematous and tender borders on the upper back and chest. Given the extent of disease, symptomatology, poor response to intralesional corticosteroids, and a prior report of clinical improvement to dupilumab,1 the patient and her family elected to proceed with dupilumab treatment after discussion of the off-label indication, adverse event profile, and current approved indications of dupilumab. The patient was started on 300 mg of intramuscular dupilumab every two weeks for 12 weeks. As a parallel treatment, a single keloid was chosen to receive subepidermal injection of 0.1 cc of dupilumab once at the start of therapy. After the 12-week course, the patient reported no reduction in any lesions, experienced enlargement of a few existing lesions, and developed new keloids. This was confirmed with photographic comparison using global and lesion specific clinical photography. The patient also denied improvement in the associated pruritus or pain of her keloids. A mutual decision was made to discontinue dupilumab after three months of therapy and initiate pulsed-dye-laser and CO2 laser augmented corticosteroid treatment.
Physical examination revealed approximately 4% BSA involvement of large exophytic nodules coalescing into irregular brawny linear plaques with raised, erythematous and tender borders on the upper back and chest. Given the extent of disease, symptomatology, poor response to intralesional corticosteroids, and a prior report of clinical improvement to dupilumab,1 the patient and her family elected to proceed with dupilumab treatment after discussion of the off-label indication, adverse event profile, and current approved indications of dupilumab. The patient was started on 300 mg of intramuscular dupilumab every two weeks for 12 weeks. As a parallel treatment, a single keloid was chosen to receive subepidermal injection of 0.1 cc of dupilumab once at the start of therapy. After the 12-week course, the patient reported no reduction in any lesions, experienced enlargement of a few existing lesions, and developed new keloids. This was confirmed with photographic comparison using global and lesion specific clinical photography. The patient also denied improvement in the associated pruritus or pain of her keloids. A mutual decision was made to discontinue dupilumab after three months of therapy and initiate pulsed-dye-laser and CO2 laser augmented corticosteroid treatment.
CASE 2
A 17-year-old black male presented to dermatology with a one-year history of rapidly progressive diffuse keloids on the mandible, upper back, and upper chest arising in the setting of poorly controlled folliculitis and pseudofolliculitis barbae of the jaw and trunk. Previous treatments included surgical excision of single lesion on the mandible followed by a post excision intralesional corticosteroid series without recurrence and a 2-month course of isotretinoin with continued progression of folliculitis and keloidal disease. The patient denied any associated pruritus, pain, or appreciable erythema. The patient reported a family history of keloids.
Physical examination revealed approximately 3% BSA involvement of large, hyperpigmented exophytic nodules coalescing into plaques on the mandible, upper chest, and upper back. Given the extent of involvement and after family discussion of off label treatment, the patient was started on dupilumab 300mg every two weeks for 12 weeks. As a parallel treatment, a single keloid was chosen to receive subepidermal injection of 0.1cc of dupilumab once at the start of therapy. After the 12-week course, the patient denied any reduction in size or elevation of his lesions, which was confirmed with photographic monitoring. His lesions remained asymptomatic. A mutual decision was made to discontinue dupilumab after 3 months of
Physical examination revealed approximately 3% BSA involvement of large, hyperpigmented exophytic nodules coalescing into plaques on the mandible, upper chest, and upper back. Given the extent of involvement and after family discussion of off label treatment, the patient was started on dupilumab 300mg every two weeks for 12 weeks. As a parallel treatment, a single keloid was chosen to receive subepidermal injection of 0.1cc of dupilumab once at the start of therapy. After the 12-week course, the patient denied any reduction in size or elevation of his lesions, which was confirmed with photographic monitoring. His lesions remained asymptomatic. A mutual decision was made to discontinue dupilumab after 3 months of
