H epatitis C viral infection is a common cause of chronic liver disease, with a worldwide prevalence of 3%. About 140 million people worldwide and 4 million in the United States are infected with HCV. An estimated 65% to 80% of the individuals infected with HCV develop persistent infection. As many as 20% to 50% of these individuals develop cirrhosis and 5% develop hepatocellular carcinoma. 1,2 The rate of disease progression varies widely, and unknown factors other than alcohol use, obesity, and age may influence the longterm clinical outcome of the disease. In recent years many efforts have been made to identify receptors involved in viral entry into host cells. Two molecules are proposed to function as HCV receptors, namely, the low-density lipoprotein receptor (LDLR) and CD81. [3][4][5] Experiments in vitro showed competitive inhibition of binding between HCV and LDLR by purified LDL. 3 If similar inhibition occurs in vivo, the serum concentration of beta-lipoproteins may influence HCV proliferation because cell infection is required for replication of the virus. 6 Serum HCVAg levels negatively correlated with serum beta-lipoproteins, supporting the concept that LDLR is the HCV receptor and that beta-lipoproteins competitively inhibit infection of hepatocytes with HCV. 6 Additional in vivo evidence has been reported by in situ hybridization studies on keratinocytes obtained from vasculitic lesions of patients with type II cryoglobulinemia. 3 These keratinocytes with upregulation of LDL receptors were found to have the positive HCV RNA strand compared to keratinocytes obtained from normal skin of the same person with low levels of LDL receptors. In those with chronic HCV infection, polymorphisms of the LDLR can influence the severity of fibrosis (single-nucleotide polymorphism [SNP] in exon 8), clearance of virus (SNP in exon 10), Abbreviations: LDLR, low-density lipoprotein receptor; VLDL, very-low-density lipoprotein; HDL, high-density lipoprotein; EVR, early viral response; ETR, endof-treatment response.

INTRODUCTION: Asthma and chronic obstructive pulmonary disease (COPD) are ongoing concerns to the health system. Poor inhaler technique results in less than optimal delivery of medicine to the lungs and consequent inadequate symptom control. AIM: This study aimed to assess inhaler technique amongst people with asthma and/or COPD. The secondary aims were to investigate who provided education on inhaler technique and whether age, gender or ethnicity was associated with poor inhaler technique. METHODS: People with asthma or COPD who presented to a community pharmacy with a prescription for a respiratory inhaler were invited to participate in the study. Participants completed a brief questionnaire and had their inhaler technique assessed against a standard checklist. RESULTS: There were 103 participants from 26 pharmacies, 86 with asthma and 17 with COPD. Just over half (52.5%) of the assessments indicated good inhaler technique, with 68% of people using the Turbuhaler having good technique compared to 53% for the pressurised metered dose inhaler (pMDI) with spacer and 47% for the pMDI alone. The majority of people (76%) received their initial inhaler technique instruction from their doctor. Over half of participants did not recall having their inhaler technique rechecked. DISCUSSION: After prescribing appropriate therapy, correct inhaler technique is a cornerstone of achieving adequate therapy. Rechecking inhaler technique is a gap in care that needs to be addressed from an interdisciplinary perspective. KEYWORDS: Asthma; chronic obstructive pulmonary disease; dry powder inhalers; metered dose inhalers; spacer inhalers

No abstract

No abstract