Objectives: To investigate opioid prescribing patterns among patients with fibromyalgia (FM) in terms of age, gender, race, type of opioids, and to examine changes in opioid prescription over the past 8 years compared to the US Food and Drug Administration (FDA)-approved FM medications.Design: Retrospective review of data using the Healthcare Enterprise Repository for Ontological Narration database. The collected data were analyzed descriptively and a chi-square test for trend was used to analyze a possible linear relationship between the proportions of opioid and non-opioid users along the time.Participants: Patients with a diagnosis of FM who had received opioid prescriptions from January 1, 2010 to December 31, 2017, and FM patients who had received prescriptions of FDA-approved FM medications in the same period. Main outcome measure: Trends in opioid and non-opioid prescriptions in patients with FM.Results: The opioid medications were prescribed more frequently in 2010 (40 percent) and 2011 (42 percent), but the percentages have decreased since 2012 and reached the lowest numbers in 2016 (27 percent). The chi-square test for trend shows that from 2010 to 2017 the prescriptions of opioids had a statistically significant (p 0.0001) decrease.Conclusion: This study suggests that the frequency of prescribed opioids in FM patients has decreased since 2012. This decline could be attributed to (1) FDA monitoring programs, (2) national efforts to increase awareness of the addictive and harmful effects of opioids, and (3) the growing research on the efficacy of non-opioid therapies to treat chronic pain conditions including FM.

Alguns dos fatores de risco podem estar associados a características do sistema musculoesquelético [2]. Especificamente, ao alinhamento do complexo tornozelo-pé, a capacidade dos abdutores e rotadores laterais do quadril de produzir torque, assim como a rigidez passiva de rotadores laterais do quadril.Testes clínicos podem informar sobre essas características. Contudo, antes de serem utilizados, é preciso verificar suas propriedades clinimétricas. Assim, o objetivo da primeira fase deste estudo foi investigar as propriedades clinimétricas dos testes clínicos que serão utilizados para verificar as características do sistema musculoesquelético. A verificação dessas propriedades permitirá o uso seguro dos dados a serem coletados na segunda fase deste estudo. Materiais e métodosRealizou-se uma investigação metodológica, em que cinco voluntários foram avaliados em duas visitas, por um mesmo avaliador. Todos os voluntários assinaram o termo de consentimento. Este estudo foi aprovado pelo Comitê de Ética em Pesquisa do Centro Universitário de Belo Horizonte (parecer nº 2.109.523).Critérios de elegibilidade -Voluntários com idade entre 18 e 60 anos e sem queixa musculoesquelética que

Cardiac Na/K-ATPase (NKA) inhibition by cardiotonic steroids (CTS) modulates intracellular Na+ and Ca2+, leading to increased force of contraction. In contrast, hypertrophy of cardiomyocytes (CM) is triggered by CTS through stimulation of reactive oxygen species (ROS) and fetal gene re-expression independently of changes in intracellular Na+ or Ca2+. Based on recent evidence that NKAα1 serves an isoform-specific function in the regulation of oxidative metabolism and ROS generation, we used a genetic approach in the mouse and in human cardiac cells (AC16) to test the hypothesis that NKAα1 is required for cardiac hypertrophy. Cardio α1-/- mice, a conditional KO of NKAα1 in the heart, were viable without overt abnormality of cardiac structure or function. NKAα1 was undetectable in heart lysates or isolated CM of adult cardio α1-/- mice. Despite a compensatory upregulation of NKAα2, Na/K-ATPase activity in crude heart homogenates and NKA currents in CM were reduced by about 60%. Decreased ROS (assessed by total protein carbonylation) and reduced fatty acid oxidation (FAO) and oxidative phosphorylation pathways (revealed by RNA-seq analysis) were noted at baseline. RT-qPCR revealed downregulated genes involved with FAO and the electron transport chain (such as, Acadl and Ndufa9, about 20% decrease, n=6) in cardio α1-/- hearts. The activity of the electron transport chain complex I was decreased in cardio α1-/- hearts (0.3354 vs 0.2732 mOD/min/mg of protein, p<0.05). When 3-month-old male mice were challenged with angiotensin II (1.5 mg.kg-1.day-1 for 1 week, n=6-15), cardio α1-/- mice did not develop cardiac hypertrophy, as assessed by heart weight to tibia length ratio, but displayed exacerbated cardiac fibrosis, revealed by Trichrome staining, consistent with the postulated role of CM NKAα1 isoform-specific function in cardiac hypertrophy in vivo. In vitro, CRISPR-Cas9-mediated KO of NKAα1 in AC16 cells led to a drastic downregulation of NKAα1 compared to WT AC16 cells. In contrast to WT AC16 cells, NKAα1 KO cells did not respond to the α-adrenergic agonist phenylephrine (50 μM for 24h) with the expected increase in cell area (2243 vs 3520 μm2 for WT, p<0.05; 2454 vs 2563 μm2 for KO, p>0.05). These data suggest that NKAα1 isoform-specific function is required for cardiac hypertrophy. Mechanistically, our data support an isoform-specific regulatory function of NKAα1 in normal FAO, electron transport chain activity, and ROS generation, which are critical for CM hypertrophy. Supported by NIH Grant R15 HL145666 and American Heart Association Grant 22POST917776 (Marco T. Pessoa) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.