Cross-sectional characteristics of pediatric-onset discoid lupus erythematosus: Results of a multicenter, retrospective cohort study.

BACKGROUND: The incidence of systemic lupus in children with discoid lupus is unknown. OBJECTIVE: This study assessed the baseline characteristics of patients with pediatric discoid lupus erythematosus (pDLE). METHODS: Medical records at 17 sites were reviewed for pediatric dermatology and rheumatology patients with discoid lupus erythematosus. The inclusion criteria were clinical and/or histopathologic diagnosis of discoid lupus erythematosus with an age at onset of <18 years. Baseline data were collected at the first documented visit. Outcomes included diagnosis of systemic lupus erythematosus (SLE) at the baseline visit using the 1997 American College of Rheumatology (primary) and the 2012 Systemic Lupus International Collaborating Clinics (secondary) criteria. RESULTS: Of the >1500 charts reviewed, 438 patients met the inclusion criteria. The cohort was predominantly female (72%) and racially/ethnically diverse. A diagnosis of SLE at the baseline visit (pDLE + SLE) was rendered in 162 (37%) patients using the American College of Rheumatology and in 181 (41%) patients using the Systemic Lupus International Collaborating Clinics criteria. Patients with pDLE + SLE were older at the time of rash onset (median, 12.9 vs 8.9 years; P < .001), with shorter time from discoid lupus erythematosus onset to diagnosis, compared with patients with pDLE-only (median, 2 vs 7 months; P < .001). Patients with pDLE + SLE were more likely to be female (P = .004), with generalized discoid lupus erythematosus and clinically aggressive disease, including end-organ involvement, positive serologies, and higher- titer levels of antinuclear antibodies (P < .001). LIMITATIONS: Retrospective study. CONCLUSION: A diagnosis of discoid lupus erythematosus in adolescence should prompt thorough screening for SLE.

Inverse association for diagnosis of Alzheimer's disease subsequent to both melanoma and non-melanoma skin cancers in a large, urban, single-centre, Midwestern US patient population.

BACKGROUND: Although literature demonstrates a decreased risk of Alzheimer's disease (AD) in individuals with various cancers, including squamous cell cancers (SCC) and basal cell cancers (BCC) comprising non-melanoma skin cancers (NMSC), there is a paucity of literature to substantiate an association between malignant melanoma (MM) and AD. OBJECTIVE: The aim of this study was to determine whether an association exists between MM and AD as well as for NMSC and AD. METHODS: A large urban, Midwestern, US, single-centre, medical record (EMR) data repository was searched between January 2001 and December 2015, to identify all patients at age ≥60 and <89 years with a clinic follow-up of at least 1 year and no diagnosis for AD, MM or NMSC at the time of the study entry. Data collected included age, gender, race and duration of follow-up. MM and NMSC were detected by ICD-9 codes and ICD-10 codes. Incident diagnosis of AD was also detected by ICD-9 and ICD-10 codes. Logistic regression analysis was utilized to obtain crude and adjusted odds ratios (ORs). RESULTS: Data for a total of 82 925 patients with known race and gender and were detected. After adjusting for confounding factors (race, gender, age, cerebrovascular disease, peripheral vascular disease and diabetes), there was a significant decreased risk of subsequent AD in patients with MM (OR: 0.39; 95% CI: 0.16-0.96; P = 0.042) as well as in patients with BCC (OR: 0.18; 95% CI: 0.08-0.45; P < 0.0001) and for patients with SCC (OR: 0.08; 95% CI: 0.01-0.56; P = 0.013). CONCLUSION: These findings add to the growing body of evidence for a decreased risk of AD in patients with various cancers and highlight the need for ongoing research to elucidate both neurologic and biologic mechanisms that may underlie this apparent inverse association.

Testosterone and social isolation influence adult neurogenesis in the dentate gyrus of male rats.

Testosterone has been previously shown to enhance adult neurogenesis within the dentate gyrus of adult male rats, whereas social isolation has been shown to cause a decrease in adult neurogenesis under some conditions. The current study tested the combined effects of testosterone and social isolation upon adult neurogenesis using two experiments involving adult male rats. For both experiments, half of the subjects were pair-housed and half were housed individually for the duration of the experiments (34 days). For experiment 1, the subjects were divided into four groups (n=8/group): (1) sham/pair-housed, (2) sham/isolated, (3) castrate/pair-housed, and (4) castrate/isolated. Rats in the castrate groups were bilaterally castrated, and rats in the sham groups were sham castrated. For experiment 2, all rats were castrated, and the effects of testosterone were tested using daily injections of testosterone propionate (0.500 mg/rat for 15 days) or the oil vehicle. Subjects were divided into four groups (n=8/group): (1) oil/pair-housed, (2) oil/isolated, (3) testosterone/pair-housed, and (4) testosterone/isolated. All rats were injected with 5-bromo-2'-deoxyuridine (BrdU, 200 mg/kg body mass), and immunohistochemistry was used to determine levels of neurogenesis following a 16-day cell survival period. For experiment 1, castrated subjects had significantly fewer BrdU-labeled cells along the granule cell layer and subgranular zone (GCL+SGZ) of the dentate gyrus than did intact subjects, and this effect was mainly due to low levels of neurogenesis in the castrate/isolated group. For experiment 2, social isolation caused a significant decrease in neurogenesis within the GCL+SGZ relative to the pair-housed groups. Testosterone injections did not buffer against this effect but instead tended to cause a decrease in neurogenesis. Thus, social isolation reduced hippocampal neurogenesis, but the effects of testosterone were inconsistent. This suggests that normal circulating levels of testosterone may buffer against the neurogenesis-impairing effects of isolation, whereas high doses of testosterone do not.