{'fraction_non_alphanumeric': 0.014414414414414415, 'fraction_numerical': 0.0024024024024024023, 'mean_word_length': 5.358778625954199, 'pattern_counts': {'":': 0, '<': 0, '<?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}}
Keloid formation on the great toe after chronic paronychia secondary to ingrown nail

Keloid is a clinically intractable fibro‐proliferative disease that spreads beyond the original scar or lesion. Although several theories have attempted to explain the mechanism of keloid formation, the phenomenon still remains obscure. Our present study examines a rare case of keloid formation that occurred on the great toe after a repeated paronychia secondary to an ingrown nail. The 22‐year‐old female patient had a large keloid with chronic paronychia and a history of ingrown nails on her left great toe on both the lateral nail folds. We excised the keloids and made new lateral nail grooves without extracting the nail. The open wounds were conservatively managed with the help of moisturized dressings until the wounds were completely epithelialised. Adjuvant therapies with oral medication, intermittent intralesional injection and toe care were performed during the follow‐up period. Histopathological analysis of the specimen revealed the presence of irregular, thick, glassy and dense collagen of keloid and inflammation of paronychia. During the 14‐month follow‐up period, adjuvant combination therapies successfully inhibited recurrence of keloid as well as paronychia and the normal appearance of the great toe was maintained. This study addresses a case of keloid formation on the great toe due to repeated recurrence of ingrown nails and consequent chronic paronychia. It is implied that if an ingrown nail is not controlled, it will result in the production of chronic inflammation and tension stress, which might trigger the formation of a secondary keloid.