Topical anesthesia is routinely employed to facilitate diagnostic and therapeutic procedures that involve the oropharynx. Although this practice is usually safe, there is always the potential that methemoglobinemia might be induced by the topical anesthetic agent. The clinician should consider this possible complication when the patient experiences signs or symptoms of oxygen desaturation in the absence of another explanation. Because methemoglobinemia can be life-threatening, early recognition and treatment are extremely important.

Glucose binds irreversibly to a variety of structures, including hemoglobin and proteins, by non-enzymatic glycosylation. Glycosylated Hemoglobin A1c (HbA1c) measures the blood glucose control over the lifespan of the RBCs. The importance of routinely assessing HbA1c in diabetic patients is well established. Both individual and institutional performance in the diabetes arena may be judged by the number of patients reaching target HbA1c values. In some patients, however, the HbA1c does not accurately portray glycemic control and may delay treatment for poorly-controlled diabetes. We report on a patient in whom the HbA1c values were falsely low as a result of hemolytic anemia associated with Myelodysplastic syndrome. The patient had consistent elevation of glucose values. Fructosamine measurement was able to confirm poorly-controlled diabetes and assist in improving diabetes control. Fructosamine is unaffected by disorders of red blood cells, which have a profound potential influence on HbA1c. Fructosamine also has the advantage of accurately reflecting shorter-term changes in glycemia that correspond to the half-life of albumin. In diabetic patients with HbA1c values below the lower limit of normal, a routine Fructosamine level should be performed. We recommend a Fructosamine level should be considered in all patients with red blood cell disorders or with discrepancies between glucose measurements and HbAlc values. Fructosamine, an inexpensive assay, is currently underused in the clinical practice. A guideline for using Fructosamine levels is included and some of the pitfalls in relying solely on the HbAlc are discussed.

Reports have shown that a negative T cell costimulatory pathway mediated by PD-1 (programmed death-1) and PDL-1 (programmed death ligand-1) is associated with T cell exhaustion and persistent viral infection. Persistent hepatitis C virus (HCV) infection in humans is also characterized by impaired T lymphocyte function, but the role of the PD-1 and PDL-1 pathway in HCV infection is unknown. Here we report that T cells isolated from chronically HCV-infected patients express significantly higher levels of PD-1 when compared with healthy donors. In addition, PD-1 and PDL-1 expression is upregulated on healthy donor T cells exposed to HCV core, a nucleocapsid protein that is immunosuppressive; upregulation of PD-1 is mediated through interaction of HCV core with the complement receptor, gC1qR. Importantly, T cell functions that are dysregulated by HCV core, including T cell activation, proliferation, and apoptosis, can be restored by blocking PD-1 and PDL-1 engagement. Our results indicate that HCV core can upregulate a key negative T cell signaling pathway associated with viral persistence and highly expressed on the T cells of persistently infected individuals. This upregulation of the PD-1 and PDL-1 pathway in humans represents a novel and perhaps common mechanism by which a virus usurps host machinery to facilitate persistence.

OBJECTIVE - This study was undertaken to quantify the expression of muscle GLUT in type 2 diabetes and to determine if treatment with an insulin-enhancing thiazolidenedione drug, pioglitazone, would alter its expression. RESEARCH DESIGN AND METHODS - Twelve patients with type 2 diabetes were randomly assigned to treatment with either pioglitazone or placebo in a double-blinded 8-week protocol. Protein and mRNA for GLUT4 and GLUT5 were quantified in muscle homogenates from biopsies of vastus lateralis before and after treatment. The five additional GLUT family isoforms expressed in muscle had mRNA quantified in these samples. RESULTS - Baseline and posttreatment repeat measurements of GLUT4 protein were not different from control measurements. Compared with normal subjects, GLUT5 protein increased 2.5-fold, and GLUT5 mRNA was 82% higher in the pretreatment samples from the diabetic subjects. Concentrations of mRNA for the six other GLUTs (GLUT1, GLUT3, GLUT4, GLUT8, GLUT11, and GLUT12) were not different from control subjects before or after treatment. The proportion of type I (red) fibers (46%) in diabetic muscle was not affected by pioglitazone treatment. Pioglitazone treatment decreased muscle GLUT5 mRNA and protein by 52 and 40%, respectively, whereas placebo did not alter GLUT5 expression. Both red and white fibers had higher GLUT5 expression in the baseline diabetic muscle samples, and a pioglitazone-related decrease in GLUT5 protein also occurred in both. CONCLUSIONS - GLUT5 was dramatically increased in diabetic muscle, and pioglitazone treatment reversed this overexpression. The role of this fructose transporter expression in the insulin-enhancing effect of pioglitazone in muscle is unclear.

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Intestinal nematodes affect more than a billion people worldwide. They are commonly found in regions with poor fecal sanitation, such as developing countries. Although most of the nematode infections are non-fatal diseases, they contribute to significant morbidities such as loss of work capacity and malnutrition. We are presenting an 80-year-old male who was diagnosed with Ascaris Lumbricoides after a return from recent travel to Greece, with some clinical endoscopic images.

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