E-Consults in Dermatology: A Retrospective Analysis.

Dermatology electronic consultations (e-consults) placed by primary care providers (PCPs) can increase access to specialty care while reducing wait times and providing accurate clinical outcomes. These e-consults also may reduce barriers for underserved patients who historically have limited access to dermatologic care. Our retrospective chart review examines patient outcomes from a dermatology e-consult program at a tertiary care medical center. E-consults effectively increased access to dermatology care while shortening wait times and reducing health care expenditures.

New onset inflammatory bowel disease in patient treated with secukinumab: Case report and review of literature.

Psoriasis is a chronic autoimmune skin disorder that can vary in severity and extent of disease. While localized disease can be managed with topical medications, widespread disease often requires systemic therapy including biologics. This medication class targets different components of the immune system and thus modulates disease activity. The biologic secukinumab is a human monoclonal antibody against interleukin-17A used for the treatment of psoriasis and psoriatic arthritis; cases of inflammatory bowel disease (IBD) have been observed in clinical trials to be associated with this medication. This review aims to provide evidence for the relationships between secukinumab treatment and the development of IBD. We have examined review articles and original research papers, published between 2010 and 2020, using the following keywords: psoriasis, psoriatic arthritis, secukinumab, IBD, Crohn's disease, ulcerative colitis, interleukin-17, IL-17, IL-17 inhibitor. Case reports have noted an association between secukinumab use and IBD and have called for IBD pre-screening in patients who will be prescribed this medication. Clinical trials concluded that secukinumab was associated with IBD, while retrospective studies have had mixed results, with most studies showing no statistical significance between secukinumab and IBD but having seen patients with history of IBD or family histories experience new-onset IBD or flare-ups. Given the utilization of secukinumab as a therapy for psoriasis and psoriatic arthritis, appropriate screening and risk stratification could help limit morbidity and mortality that can be associated with secukinumab-induced IBD.

Long-acting phosphodiesterase-5 inhibitor, tadalafil, induces sustained cardioprotection against lethal ischemic injury.

The ability of pharmacological preconditioning mimetics to confer long-lasting and sustained cardioprotection may be a logical criterion to develop a drug that can be used clinically for cardioprotection. We propose here that the use of long-acting phosphodiesterase-5 inhibitor, tadalafil, may confer sustained cardioprotection against ischemia. Tadalafil (5 mg/kg) was administered orally to male C57B/6J mice (n = 6 in each treatment subgroup at each time point studied). Hearts were isolated and subjected to 40 min of ischemia and 30 min of reperfusion on Langendorff's apparatus at 1, 12, 24, 36, 48, 60, 72, and 108 h after tadalafil administration. In 1- to 48-h subgroups, tadalafil was given once at 0 h only. In 60- and 72-h subgroups, tadalafil was given twice at 0 and 36 h. Similarly, in the 108-h subgroup, tadalafil was administered at 0, 36, and 72 h. In the same subgroups, wortmannin (15 microg/kg ip), an inhibitor of phosphatidylinositol 3-kinase or 5-hydroxydecanoic acid (5 mg/kg ip), an inhibitor of mitochondrial ATP-sensitive K(+) channels, was given together with tadalafil, and the hearts were subjected to ischemia-reperfusion at 36 h to determine whether the effect of tadalafil on ischemia-reperfusion injury was abolished. As a result, tadalafil treatment reduced left ventricular end-diastolic pressure and increased left ventricular developed pressure as well as reduced lactate dehydrogenase release. This protection remained till 36-40 h, and thereafter it vanished. The readministration of tadalafil at 36 and 72 h restored the protection till 108 h. Tadalafil treatment accelerated Akt phosphorylation in cardiac tissue and decreased myocyte apoptosis. The administration of wortmannin abolished the beneficial effects of tadalafil on hemodynamic parameters and myocyte apoptosis, together with significantly reduced Akt phosphorylation. 5-Hydroxydecanoic acid also abolished the antiapoptotic effect of tadalafil. It is concluded that tadalafil treatment induces the long-term protection of ischemic myocardium via phosphatidylinositol 3-kinase/Akt signaling pathway.