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AbstractBackgroundRecipients of solid organ transplants are prone to various complications that are seldom encountered in immunocompetent individuals. Post‐transplant lymphoproliferative disorder (PTLD) is the best known and commonest Epstein‐Barr Virus (EBV)‐associated malignancy post solid organ transplant. EBV‐associated smooth muscle tumors (EBV‐SMT) including leiomyomas and leiomyosarcomas are rare and much less studied than PTLD. We recently encountered two cases of EBV‐SMT post lung transplantation and here we summarize their clinical features and course together with a literature review.MethodClinical data and treatment details of two patients who developed EBV‐SMT were reviewed and retrieved up to December 31, 2017. English literature was searched through the PubMed database from 1965 to 2017 for studies of the association between lung transplant and EBV‐SMT.ResultsThe incidence of PTLD is higher among lung transplant recipients compared to kidney transplant recipients, an observation that has been attributed to stronger immune suppression in the lung patients. EBV‐SMT showed a higher incidence among kidney recipients than among lung recipients, suggesting that the degree of immunosuppression may be a less important factor in the development of EBV‐SMT. EBV‐SMT has most often been seen among lung transplant recipients with EBV mismatch.ConclusionsBecause EBV‐SMT is a rare tumor, its incidence, risk factors, and optimal management have not been well‐defined and further study is needed.

Introduction: African American women are 5 times less likely than white women to meet at least 5 or more ideal cardiovascular health metrics as defined by the American Heart Association Life’s Simple 7 (LS7) components (smoking, diet, physical activity, BMI, blood pressure, total cholesterol, and glucose). There are few studies probing the influence of sociocultural factors, such as body image dissatisfaction (BID), on these disparities. A better understanding of the impact of BID on cardiovascular health could assist in the design of more effective behavior change interventions for African American women. Hypothesis: We hypothesized that BID would have a negative association with cardiovascular health in overweight and obese African American women. Methods: We enrolled 32 women (mean age 49 years [SD 12.9]), from 5 predominantly African American churches participating in a larger community-based participatory study (FAITH! App Pilot Study) of a mobile health lifestyle intervention among African American women and men. We conducted a cross-sectional analysis of baseline data to evaluate the association between BID and both cardiovascular health and select psychosocial factors (e.g. motivation for healthy eating, diet self-regulation). A LS7 composite score was calculated as a measure of overall cardiovascular health (range 0-14). The Pulvers scale, consisting of images of women across the BMI spectrum, was used to measure perceived current and goal body size (rating of figures, 1-9; underweight to very obese). A BID score was calculated as the difference between perceived current and desired body image (range -8-8; BID < 0 [desire to be heavier], BID > 0 [desire to be thinner], BID = 0 [no dissatisfaction]). The BID score range for our cohort was 0-4. Thus, we categorized BID as no/low BID (BID score 0-1) or high BID (BID score 2-4). Results: Twenty-two percent (7/32) of women were overweight (BMI 25-29.9) and 78% (25/32) were obese (BMI (≥ 30). Forty-four percent (14/32) had no/low BID and 56% (18/32) had high BID. Those with high BID were more likely to be obese as compared to no/low BID (94% (17/18) versus 57% (8/14), p=0.03). Although not statistically significant, the mean LS7 composite score was 1 point higher among those with no/low BID, versus high BID (8.83 versus 7.76, p=0.25). Compared to women with high BID, those with no/low BID were more likely to have greater: intrinsic motivation (P=0.01) and integrated regulation for healthy eating (P=0.007), and self-regulation to reduce fat and caloric intake (P=0.01). Conclusion: Ultimately, although small, our study suggests that African-American women with obesity are more likely to have high BID. High BID was associated with lower motivation and self-regulation, which predict cardiovascular health. BID and other psychosocial factors for behavior change are potential targets for culturally-tailored lifestyle interventions in this group.

Summary Objective Seizures develop in 80% of patients with anti– N ‐methyl‐ d ‐aspartate receptor (NMDAR) encephalitis, and these represent a major cause of morbidity and mortality. Anti‐NMDAR antibodies have been linked to memory loss in encephalitis; however, their role in seizures has not been established. We determined whether anti‐NMDAR antibodies from autoimmune encephalitis patients are pathogenic for seizures. Methods We performed continuous intracerebroventricular infusion of cerebrospinal fluid (CSF) or purified immunoglobulin (IgG) from the CSF of patients with anti‐NMDAR encephalitis or polyclonal rabbit anti‐NMDAR IgG, in male C57BL/6 mice. Seizure status during a 2‐week treatment was assessed with video‐electroencephalography. We assessed memory, anxiety‐related behavior, and motor function at the end of treatment and assessed the extent of neuronal damage and gliosis in the CA1 region of hippocampus. We also performed whole‐cell patch recordings from the CA1 pyramidal neurons in hippocampal slices of mice with seizures. Results Prolonged exposure to rabbit anti‐NMDAR IgG, patient CSF, or human IgG purified from the CSF of patients with encephalitis induced seizures in 33 of 36 mice. The median number of seizures recorded in 2 weeks was 13, 39, and 35 per mouse in these groups, respectively. We observed only 18 brief nonconvulsive seizures in 11 of 29 control mice (median seizure count of 0) infused with vehicle (n = 4), normal CSF obtained from patients with noninflammatory central nervous system (CNS) conditions (n = 12), polyclonal rabbit IgG (n = 7), albumin (n = 3), and normal human IgG (n = 3). We did not observe memory deficits, anxiety‐related behavior, or motor impairment measured at 2 weeks in animals treated with CSF from affected patients or rabbit IgG. Furthermore, there was no evidence of hippocampal cell loss or astrocyte proliferation in the same mice. Significance Our findings indicate that autoantibodies can induce seizures in anti‐NMDAR encephalitis and offer a model for testing novel therapies for refractory autoimmune seizures.

Purpose of review To describe a recently characterized autoimmune, inflammatory central nervous system (CNS) disorder known as autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy. Recent findings Affected patients present with symptoms of one or more of meningitis (headache and neck ache), encephalitis (delirium, tremor, seizures, or psychiatric symptoms), and myelitis (sensory symptoms and weakness). Optic disc papillitis (blurred vision) is common. CNS inflammation is evident in characteristic T1 postgadolinium enhancement of GFAP-enriched CNS regions, and lymphocytic cerebrospinal fluid (CSF) white cell count elevation. CSF is more reliable than serum for GFAP-immunoglobulin G (IgG) testing. Ovarian teratoma commonly coexists, particularly among patients with accompanying N-methyl-D-aspartate receptor or aquaporin-4 autoimmunity. Parainfectious autoimmunity is suspected in some other patients, though the culprit organism is rarely verified. Pathophysiologic relevance of T cells is underscored by neuropathology and cases of dysregulated T-cell function (HIV or checkpoint inhibitor cancer therapy). Corticosteroid-responsiveness is a hallmark of the disease. Relapses occur in approximately 20% of patients, necessitating transition to a steroid-sparing drug. Reported outcomes vary, though in the authors’ experience, early and sustained intervention usually portends recovery. Summary Autoimmune GFAP astrocytopathy is a treatable autoimmune CNS disease diagnosable by GFAP-IgG testing in CSF. This disease presents opportunities to explore novel mechanisms of CNS autoimmunity and inflammation.