Fluoroscopy-induced chronic radiation dermatitis (FICRD) can be a challenging diagnosis for the dermatopathologist, as often a history of radiation exposure is not provided. With the expanded use of minimally invasive procedures, there is increased fluoroscopic exposure and a high index of suspicion for FICRD is prudent. Recognition of characteristic clinical and histopathological features can be helpful in distinguishing chronic radiation dermatitis from entities in the histological differential diagnosis such as morphea and lichen sclerosus. We present a brief review of the literature as well as two additional cases of FICRD. Case 1 is a 44-year-old man with an atrophic lateral back patch for several years. Chart review revealed a history of cardiac radiofrequency ablation and congenital heart disease with correction. Case 2 is a 64-year-old woman with an ulcerated, atrophic left flank plaque, with a history of mesenteric artery angiography and stent placement. In our two cases, as well as the cases in the literature, a diagnosis of FICRD is associated with key features. In the evaluation of a sclerosing process, chronic radiation dermatitis should be suspected histologically by the findings of ulceration, prominent telangiectasias, atypical stellate fibroblasts, absence of a lymphocytic infiltrate/inflammation and/or presence of hyperkeratosis.

Vitiligo and alopecia areata are two cutaneous diseases believed to be primarily autoimmune in pathogenesis. While the coexistence of the two conditions in the same patient has been well-described, reports of the two disease processes occurring in the same location are rare. We report the case of a 10-year-old male with an unremarkable past medical history who presented with a single localized area of poliosis with depigmented underlying skin on the frontal scalp. The hair in the affected area was relatively decreased in density. A punch biopsy of the depigmented patch demonstrated features consistent with both vitiligo and alopecia areata. The decreased number of large hair follicles and a focal peribulbar lymphocytic infiltrate around an anagen follicle were suggestive of alopecia areata. A panel of melanocyte-specific stains revealed absent melanocytes in the epidermis, consistent with vitiligo. Loss of microphthalmia-associated transcription factor-positive root sheath cells was seen, suggestive of loss of melanocyte stem cells. The combination of clinical and histopathologic findings supports the theory of a common pathogenesis of alopecia areata and vitiligo.

Signet ring cell change is a benign process that can be mistaken for signet ring cell adenocarcinoma. Signet ring cell change remains confined within the basement membrane and lacks an infiltrative growth pattern. It typically lacks cellular atypia, nuclear hyperchromasia, prominent nucleoli, or mitotic activity. This study illustrates a case of signet ring cell change with mitotic activity in a background of Helicobacter pylori gastritis with a penetrating ulcer. The signet ring cell change shows normal E-cadherin expression, absence of p53 expression, and confinement within glands on reticulin staining. The intact gastric mucosa adjacent to the signet ring cells shows significant mitotic activity, which likely explains the mitoses within the signet ring cell change. Mitotic activity in signet ring cells should be interpreted in the context of adjacent mucosa and should not preclude the diagnosis of benign signet ring cell change. Reticulin staining of the involved glands is helpful for excluding the invasion of the lamina propria in signet ring cell change.