{'fraction_non_alphanumeric': 0.03192407247627265, 'fraction_numerical': 0.009203336209375898, 'mean_word_length': 5.476722532588455, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
A case of a gibberellin-regulated protein-positive patient allergic to various fruits

EJD, vol. 31, n◦ 1, January-February 2021 A 76-year-old man with a one-month history of painful swelling in the left lower leg was admitted to our department. He had received treatment for CML with 20 mg/day dasatinib for the previous three years. He had a history of cerebral infarction and Stanford type A aortic dissection. Examination revealed that the lower portion of his left leg exhibited dark red erythema, oedema, and was warm to touch (figure 1A). He was febrile, and his body temperature was 37.5◦C. Laboratory tests revealed a normal white blood cell count, but the level of C-reactive protein was elevated (4.82; normal range <0.30 mg/dL). Bacterial cellulitis was initially suspected based on this presentation. Treatment with bed rest, leg elevation, and antibiotics (intravenous ampicillin/sulbactam) was initiated, however, the skin lesions gradually spread peripherally. Further examination with computed tomography angiography and ultrasound revealed no evidence of deep venous thrombosis or venous stasis. Histopathological examination revealed numerous inflammatory cells in the subcutaneous fat lobules and septa (figure 1B), which comprised lymphocytes, eosinophils, and histiocytes (figure 1C). Tissue cultures for bacteria, acid-fast bacilli, and fungi were all negative. From these findings, it was suspected that the patient had drug-induced panniculitis, and subsequently, treatment with dasatinib was discontinued. The skin lesions gradually disappeared after one week following the discontinuation of dasatinib treatment (figure 1D). The discontinuation of dasatinib therapy did not exacerbate the patient’s CML, and the skin lesions did not recur thereafter. Dasatinib-induced panniculitis has been reported in only two patients to date, however, the clinicopathological features differed from those of the case presented herein [3]. TKI-associated panniculitis is a rare adverse event characterized by multiple erythematous nodules on the arms and legs [4, 5]. In contrast, this case presented with diffuse dark red erythema and oedema on the leg mimicking cellulitis. Although TKIs exert their antitumour effects through inhibition of the aberrant kinase activity of the BCR-ABL1 fusion protein, produced by the Philadelphia chromosome translocation, the exact pathomechanism associated with drug-induced panniculitis is unclear. Panniculitis has been reported to occur several months or even up to one year after initial treatment with TKIs [4]. Our case highlights that disease can present even after years of treatment. TKI-induced panniculitis is histopathologically characterized by acute inflammatory infiltrates, primarily comprising neutrophils within the lobules [3, 4]. In this case, however, lymphocytic and eosinophilic infiltrates also extended into the septa, which may reflect long-term or severe panniculitis. TKIinduced panniculitis has previously been reported to rapidly improve following withdrawal of the causative drug, as in our case. The reintroduction of TKI treatment may be possible in combination with systemic corticosteroids [4]. Although drug-induced panniculitis is rare, dermatologists should be aware that it is a potential adverse event during dasatinib treatment. Additional evidence is necessary, which will aid in our understanding of the pathomechanism and clinicopathological features of TKI-associated panniculitis.