Dermatologic Consequences of Substandard, Spurious, Falsely Labeled, Falsified, and Counterfeit Medications.

This article explores dermatologic consequences of substandard, spurious, falsely labeled, falsified, and counterfeit (SSFFC) pharmaceutical products. Many of these SSFFC products are neither safe nor effective, and are more likely to cause adverse events than the proper preparations. These products also affect the health of populations by generating drug-resistant pathogens and failing to control the spread of disease. This article reviews classification systems for fraudulent medications, provides a general overview of medical and public health problems associated with substandard medications, provides examples of dermatologic consequences of each category, and presents recommended steps to take when clinicians encounter suspected SSFFC products.

Comparison of a Smartphone Otoscope and Conventional Otoscope in the Diagnosis and Management of Acute Otitis Media.

Acute otitis media (AOM) is a leading cause of health encounters and antimicrobial prescriptions in children worldwide. We assessed (1) the rates of antimicrobial prescribing by pediatric emergency department clinicians using a smartphone otoscope device as compared with a conventional otoscope and (2) clinician acceptability of the smartphone device. We conducted a randomized control study in children's hospital emergency departments over 6 months. More than 1500 encounters were analyzed. The odds of prescribing antibiotics after being given a diagnosis of AOM by clinicians assigned to the smartphone group was 11% higher than the conventional group (18.8% vs 18.0%, odds ratio = 1.106, P = .600). Eight (73%) of the 11 physicians in the smartphone group preferred the smartphone device over the conventional otoscope. Use of a smartphone otoscope for detection of AOM in a pediatric emergency department setting did not lead to an increased likelihood of AOM diagnosis.

A positive regulatory role for suppressor of cytokine signaling 1 in IFN-gamma-induced MHC class II expression in fibroblasts.

Suppressor of cytokine signaling 1 (SOCS1) is rapidly induced following stimulation by several cytokines. SOCS1 negatively regulates cytokine receptor signal transduction by inhibiting Janus family tyrosine kinases. Lack of such feedback regulation underlies the premature death of SOCS1(-/-) mice due to unbridled IFN-gamma signaling. We used mouse embryo fibroblasts derived from SOCS1(-/-) mice to investigate the role of SOCS1 in IFN-gamma signaling pathways. SOCS1(-/-) fibroblasts were exquisitely sensitive to the IFN-gamma-mediated growth arrest and showed sustained STAT1 phosphorylation. However, SOCS1(-/-) fibroblasts were inefficient in MHC class II surface expression following IFN-gamma stimulation, despite a marked induction of the MHC class II transactivator and MHC class II gene expression. Retroviral transduction of wild-type SOCS1 relieved the growth-inhibitory effects of IFN-gamma in SOCS1(-/-) fibroblasts by inhibiting STAT1 activation. SOCS1R105K, carrying a mutation within the phosphotyrosine-binding pocket of the Src homology 2 domain, did not inhibit STAT1 phosphorylation, yet considerably inhibited IFN-gamma-mediated growth arrest. Strikingly, expression of SOCS1R105K restored the IFN-gamma-induced MHC class II expression in SOCS1(-/-) cells, indicating that expression of SOCS1 facilitates MHC class II expression in fibroblasts. Our results show that SOCS1, in addition to its negative regulatory role of inhibiting Janus kinases, has an unanticipated positive regulatory function in retarding the degradation of IFN-gamma-induced MHC class II proteins in fibroblasts.