Recent emergence of immune checkpoint inhibitors (ICIs) has revolutionized the treatment of cancers and produced prolonged response by boosting the immune system against tumor cells. The primary target antigens are cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4), a downregulator of T-cell activation, and programmed cell death-1 receptor (PD-1), a regulator of T-cell proliferation. This enhanced immune response can induce autoimmune adverse effects in many organs. Although skin toxicities are the most common, sarcoidal inflammation with exclusive cutaneous involvement is a rare occurrence with only 6 cases reported to date. We report 2 cases with unusual features. One patient is a female who was treated for metastatic renal cell carcinoma with combination of ipilimumab (anti-CTLA-4) and nivolumab (anti-PD-1). She developed deep nodules showing sarcoidal dermatitis and panniculitis on histopathologic exam. The second patient is a male with melanoma of eyelid conjunctiva who was treated prophylactically with ipilimumab. He presented with papules/plaques confined to black tattoos, where the biopsy revealed sarcoidal dermatitis. By a comprehensive literature review, we intend to raise awareness about this potential skin side effect in the growing number of patients receiving targeted immunotherapies. It is crucial to have a high index of suspicion and perform timely biopsies to implement appropriate management strategies.

Neutrophilic dermatosis of the dorsal hands is an underrecognized entity, which is a distributional variant of Sweet's syndrome. It is often clinically misdiagnosed as an infectious process in overwhelming majority of the cases and the treatment is therefore delayed. Also, its association with underlying systemic and neoplastic disorders makes the need for an accurate diagnosis more crucial. We present a 45-year-old Caucasian woman who was initially diagnosed as having a hand infection with unsuccessful courses of antibiotic therapy. A later biopsy revealed a diffuse dermal infiltrate of neutrophils with leukocytoclasis, vasculopathic changes, and marked papillary dermal edema. Patient responded rapidly to oral prednisone treatment. By sharing a new case and comprehensive review of available published literature, we intend to raise awareness of this underreported entity and emphasize the role of timely biopsy of the lesions that will not only lead to an accurate diagnosis, but also avoid unnecessary antibiotic treatments, potentially aggressive management strategies such as surgical debridement or amputation, and referrals to wound care centers. More importantly, it will prompt a search to exclude any possible association, particularly hematopoietic malignancies.

Introduction:We examined the association between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) and hypothesized that diabetes is associated with an increased pathological burden in clinically and pathologically diagnosed AD. Methods: All data were obtained from the Uniform Data Set (UDS) v3, the Neuropathology Data Set, and the Researcher's Data Dictionary-Genetic Data from the National Alzheimer's Coordinating Center. The dataset (37 cases with diabetes and 1158 cases without) relies on autopsy-confirmed data in clinically diagnosed AD patients who were assessed for diabetes type in form A5 or D2 during at least one visit. Differences in scores were explored using a general linear model. Effect sizes were calculated using sample means and standard deviations (Cohen's d). Results: The presence of diabetes was associated with a lower Thal phase of amyloid plaques (A score; 4.6 ± 0.79 vs. 4.3 ± 0.85, P < .05) and lower Braak stage for neurofibrillary degeneration (B score; 5.58 ± 0.72 vs. 5.16 ± 0.96, P < 0.05) but not for density of neocortical neuritic plaques (CERAD score-C score). The National Institute on Aging-Alzheimer's Association Alzheimer's disease neuropathologic change (ABC score) was not different between AD+DM and AD-DM. Discussion: This pilot study found a significantly lower Thal phase of amyloid plaques and Braak stage for neurofibrillary degeneration in AD-confirmed individuals with diabetes compared to those without. Thus type 2 DM is not associated with increased AD pathology in clinically and pathologically confirmed cases of AD.