Superior ophthalmic vein thrombosis: A rare complication of Graves’ orbitopathy

Superior ophthalmic vein thrombosis is a rare, life- and sight-threatening complication of both infectious and inflammatory orbital disease as well as hypercoagulable state. Only one case of superior ophthalmic vein thrombosis due to thyroid eye disease has been reported in the literature. This article describes the diagnosis and management of a case of superior ophthalmic vein thrombosis due to Graves’ orbitopathy. Early diagnosis is critical to facilitate timely therapeutic intervention. Superior ophthalmic vein thrombosis should be considered in the differential diagnosis of acute on chronic proptosis in the setting of Graves’ orbitopathy, and may represent and under-recognized and under-diagnosed clinical entity.     

Hepatitis B and C virus infections transmitted through organ transplantation investigated by CDC,United States, 2014‐2017

We evaluated clinical outcomes among organ recipients with donor‐derived hepatitis B virus (HBV) or hepatitis C virus (HCV) infections investigated by CDC from 2014 to 2017 in the United States. We characterized new HBV infections in organ recipients if donors tested negative for total anti‐HBc, HBsAg and HBV DNA, and new recipient HCV infections if donors tested negative for anti‐HCV and HCV RNA. Donor risk behaviors were abstracted from next‐of‐kin interviews and medical records. During 2014‐2017, seven new recipient HBV infections associated with seven donors were identified; six (86%) recipients survived. At last follow‐up, all survivors had functioning grafts and five (83%) had started antiviral therapy. Twenty new recipient HCV infections associated with nine donors were identified; 19 (95%) recipients survived. At last follow‐up, 18 (95%) survivors had functioning grafts and 14 (74%) had started antiviral treatment. Combining donor next‐of kin interviews and medical records, 11/16 (69%) donors had evidence of injection drug use and all met Public Health Service increased risk donor (IRD) criteria. IRD designation led to early diagnosis of recipient infection, and prompt implementation of therapy, likely reducing the risk of graft failure, liver disease, and death.     

Control of Borrelia burgdorferi-specific CD4+-T-cell effector function by interleukin-12- and T-cell receptor-induced p38 mitogen-activated protein kinase activity

Infection with Borrelia burgdorferi, the causative agent of Lyme disease, results in a Th1 response and proinflammatory cytokine production. Mice deficient for MKK3, an upstream activator of p38 mitogen-activated protein (MAP) kinase, develop a lower Th1 response and exhibit an impaired ability to produce proinflammatory cytokines upon infection with the spirochete. We investigated the contribution of p38 MAP kinase activity in gamma interferon (IFN-gamma) production in CD4+ T cells in response to specific antigen through T-cell receptor (TCR)- and interleukin-12 (IL-12)-mediated signals. The specific inhibition of p38 MAP kinase in T cells and the administration of a pharmacological inhibitor of the kinase during the course of infection with the spirochete resulted in reduced levels of IFN-gamma in the sera of infected mice. Our results also demonstrate that although p38 MAP kinase activity is not required for the differentiation of B. burgdorferi-specific CD4+ T cells, the production of IFN-gamma by Th1 effector cells is regulated by the kinase. Both TCR engagement and IL-12 induced the production of the Th1 cytokine through the activation of the p38 MAP kinase pathway. Thus, the inhibition of this pathway in vitro resulted in decreased levels of IFN-gamma during restimulation of B. burgdorferi-specific T cells in response to anti-CD3 and IL-12 stimulation. These results clarify the specific contribution of the p38 MAP kinase in the overall immune response to the spirochete and its role in the effector function of B. burgdorferi-specific T cells.     

Preliminary evidence for an emerging nonmetropolitan mortality penalty in the United States

We discovered an emerging non-metropolitan mortality penalty by contrasting 37 years of age-adjusted mortality rates for metropolitan versus nonmetropolitan US counties. During the 1980s, annual metropolitan-nonmetropolitan differences averaged 6.2 excess deaths per 100,000 nonmetropolitan population, or approximately 3600 excess deaths; however, by 2000 to 2004, the difference had increased more than 10 times to average 71.7 excess deaths, or approximately 35,000 excess deaths. We recommend that research be undertaken to evaluate and utilize our preliminary findings of an emerging US nonmetropolitan mortality penalty.