Osteomyelitis of the Cervical Spine Presenting as Acute ST-Segment Elevation.

Acute ST-segment elevation (STE) on electrocardiogram (EKG) is very frequently associated with myocardial infarction, which requires prompt diagnosis and treatment. However, there are multiple other causes of acute STE, both cardiac and noncardiac. Here we describe a unique case of acute inferior and lateral STE caused by osteomyelitis and abscess of the lower cervical vertebrae.

Benzodiazepine Overuse in Elders: Defining the Problem and Potential Solutions.

Objective To determine the prevalence of benzodiazepine use in adults aged 65 and older at two West Virginia academic medical centers as phase one of a benzodiazepine deprescribing strategy.  Design Cross-sectional Setting Two academic hospitals in West Virginia with 107,504 hospitalized adults age 65 and older from the years 2010 to 2018 with information on admission medication use.  Measurements Use of benzodiazepines based on presence on the admission medication list. Demographics, select co-morbidities, and laboratory tests were also recorded.  Results The prevalence of benzodiazepine use was 13.5% and use remained relatively constant with increasing age over 65, even in those over age 89.  Conclusion Efforts aimed at assessing the true need for benzodiazepine use and deprescribing need to be employed, particularly with advancing age.

Dementia Care: Confronting Myths in Clinical Management.

Every day, patients with dementia, their families, and their physicians face the enormous challenges of this pervasive life-changing condition. Seeking help, often grasping at straws, victims, and their care providers are confronted with misinformation and myths when they search the internet or other sources. When Persons with Dementia (PWD) and their caregivers believe and/or act on false information, proper treatment may be delayed, and ultimately damage can be done. In this paper, we review commonly misunderstood issues encountered in caring for PWD. Our goal is to equip Primary Care Practitioners (PCPs) with accurate information to share with patients and families, to improve the outcomes of PWD to the greatest extent possible. While there are innumerable myths about dementia and its causes and treatments, we are going to focus on the most common false claims or misunderstandings which we hear in our Internal Medicine practice at Marshall Health. We offer suggestions for busy practitioners approaching some of the more common issues with patients and families in a clinic setting.

Recognizing Guttate Psoriasis and Initiating Appropriate Treatment.

Guttate psoriasis is a less common form of psoriasis. It manifests with numerous small, teardrop shaped, scaly plaques on the trunk and extremities. The etiology includes both environmental and genetic factors. It commonly arises 3-4 weeks following a beta hemolytic streptococcal infection. In some cases, it may be misdiagnosed as an allergy to the antibiotics being used to treat the streptococcal infection. The treatment of guttate psoriasis can vary by severity, but the mainstay treatment includes photo therapy and topical steroids. This case report presents the etiology, clinical findings and current treatment options of guttate psoriasis. It also discusses importance of differentiating guttate psoriasis from an antibiotic allergy. The confusion between the two can often delay and make treatment more difficult.

Fructose Mediated Non-Alcoholic Fatty Liver Is Attenuated by HO-1-SIRT1 Module in Murine Hepatocytes and Mice Fed a High Fructose Diet.

BACKGROUND: Oxidative stress underlies the etiopathogenesis of nonalcoholic fatty liver disease (NAFLD), obesity and cardiovascular disease (CVD). Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. Sirtuin1 (SIRT1) belongs to the family of NAD-dependent de-acyetylases and is modulated by cellular redox. HYPOTHESIS: We hypothesize that fructose-induced obesity creates an inflammatory and oxidative environment conducive to the development of NAFLD and metabolic syndrome. The aim of this study is to determine whether HO-1 acts through SIRT1 to form a functional module within hepatocytes to attenuate steatohepatitis, hepatic fibrosis and cardiovascular dysfunction. METHODS AND RESULTS: We examined the effect of fructose, on hepatocyte lipid accumulation and fibrosis in murine hepatocytes and in mice fed a high fructose diet in the presence and absence of CoPP, an inducer of HO-1, and SnMP, an inhibitor of HO activity. Fructose increased oxidative stress markers and decreased HO-1 and SIRT1 levels in hepatocytes (p<0.05). Further fructose supplementation increased FAS, PPARα, pAMPK and triglycerides levels; CoPP negated this increase. Concurrent treatment with CoPP and SIRT1 siRNA in hepatocytes increased FAS, PPARα, pAMPK and triglycerides levels suggesting that HO-1 is upstream of SIRT1 and suppression of SIRT1 attenuates the beneficial effects of HO-1. A high fructose diet increased insulin resistance, blood pressure, markers of oxidative stress and lipogenesis along with fibrotic markers in mice (p<0.05). Increased levels of HO-1 increased SIRT1 levels and ameliorated fructose-mediated lipid accumulation and fibrosis in liver along with decreasing vascular dysfunction (p<0.05 vs. fructose). These beneficial effects of CoPP were reversed by SnMP. CONCLUSION: Taken together, our study demonstrates, for the first time, that HO-1 induction attenuates fructose-induced hepatic lipid deposition, prevents the development of hepatic fibrosis and abates NAFLD-associated vascular dysfunction; effects that are mediated by activation of SIRT1 gene expression.

Increased HO-1 levels ameliorate fatty liver development through a reduction of heme and recruitment of FGF21.

OBJECTIVE: Obese leptin deficient (ob/ob) mice are a model of adiposity that displays increased levels of fat, glucose, and liver lipids. Our hypothesis is that HO-1 overexpression ameliorates fatty liver development. METHODS: Obese mice were administered cobalt protoporphyrin (CoPP) and stannic mesoporphyrin (SnMP) for 6 weeks. Heme, HO-1, HO activity, PGC1α, FGF21, glycogen content, and lipogenesis were assessed. RESULTS: CoPP administration increased hepatic HO-1 protein levels and HO activity, decreased hepatic heme, body weight gain, glucose levels, and resulted in decreased steatosis. Increased levels of HO-1 produced a decrease in lipid droplet size, Fatty acid synthase (FAS) levels involving recruitment of FGF21, PPARα, and Glut 1. These beneficial effects were reversed by inhibition of HO activity. CONCLUSION: Increased levels of HO-1 and HO activity reduced the levels of obesity by reducing hepatic heme and lipid accumulation. These changes were manifested by decreases in cellular heme, increases in FGF21, glycogen content, and fatty liver. The beneficial effect of HO-1 induction results from an increase in PPARα and FGF21 levels and a decrease in PGC1α, levels they were reversed by SnMP. Low levels of HO-1 and HO activity are responsible for fatty liver.