154 research outputs found

    Risks of myeloid malignancies in patients with autoimmune conditions

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    Autoimmune conditions are associated with an elevated risk of lymphoproliferative malignancies, but few studies have investigated the risk of myeloid malignancies. From the US Surveillance Epidemiology and End Results (SEER)-Medicare database, 13 486 myeloid malignancy patients (aged 67+ years) and 160 086 population-based controls were selected. Logistic regression models adjusted for gender, age, race, calendar year and number of physician claims were used to estimate odds ratios (ORs) for myeloid malignancies in relation to autoimmune conditions. Multiple comparisons were controlled for using the Bonferroni correction (P<0.0005). Autoimmune conditions, overall, were associated with an increased risk of acute myeloid leukaemia (AML) (OR 1.29) and myelodysplastic syndrome (MDS, OR 1.50). Specifically, AML was associated with rheumatoid arthritis (OR 1.28), systemic lupus erythematosus (OR 1.92), polymyalgia rheumatica (OR 1.73), autoimmune haemolytic anaemia (OR 3.74), systemic vasculitis (OR 6.23), ulcerative colitis (OR 1.72) and pernicious anaemia (OR 1.57). Myelodysplastic syndrome was associated with rheumatoid arthritis (OR1.52) and pernicious anaemia (OR 2.38). Overall, autoimmune conditions were not associated with chronic myeloid leukaemia (OR 1.09) or chronic myeloproliferative disorders (OR 1.15). Medications used to treat autoimmune conditions, shared genetic predisposition and/or direct infiltration of bone marrow by autoimmune conditions, could explain these excess risks of myeloid malignancies

    Automated office blood pressure measurements in primary care are misleading in more than one third of treated hypertensives: The VALENTINE-Greece Home Blood Pressure Monitoring study

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    Abstract Background This study assessed the diagnostic reliability of automated office blood pressure (OBP) measurements in treated hypertensive patients in primary care by evaluating the prevalence of white coat hypertension (WCH) and masked uncontrolled hypertension (MUCH) phenomena. Methods Primary care physicians, nationwide in Greece, assessed consecutive hypertensive patients on stable treatment using OBP (1 visit, triplicate measurements) and home blood pressure (HBP) measurements (7 days, duplicate morning and evening measurements). All measurements were performed using validated automated devices with bluetooth capacity (Omron M7 Intelli-IT). Uncontrolled OBP was defined as ≥140/90 mmHg, and uncontrolled HBP was defined as ≥135/85 mmHg. Results A total of 790 patients recruited by 135 doctors were analyzed (age: 64.5 ± 14.4 years, diabetics: 21.4%, smokers: 20.6%, and average number of antihypertensive drugs: 1.6 ± 0.8). OBP (137.5 ± 9.4/84.3 ± 7.7 mmHg, systolic/diastolic) was higher than HBP (130.6 ± 11.2/79.9 ± 8 mmHg; difference 6.9 ± 11.6/4.4 ± 7.6 mmHg, p Conclusions In primary care, automated OBP measurements are misleading in approximately 40% of treated hypertensive patients. HBP monitoring is mandatory to avoid overtreatment of subjects with WCH phenomenon and prevent undertreatment and subsequent excess cardiovascular disease in MUCH

    Deciphering the Association Between Psoriasis and Obesity: Current Evidence and Treatment Considerations

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    PURPOSE OF REVIEW: Obesity and psoriasis represent chronic inflammatory states that are interconnected in a vicious cycle, sharing also a degree of synergy. In this review, we aim to decipher the various lines of evidence supporting the bidirectional association between psoriasis and obesity highlighting their pathophysiologic connections as well as we attempt to strategize a therapeutic holistic approach for obese psoriatic patients. RECENT FINDINGS: Recent meta-analyses have shown that (1) genetically higher BMI increased the odds of psoriasis occurrence; (2) obesity is associated with higher incidence and prevalence of psoriasis as well as psoriasis severity; (3) obesity is associated with lower efficacy to anti-TNF agents and may predict biologic treatment discontinuation; and (4) weight loss through diet and physical exercise may improve pre-existing psoriasis and prevent from de novo psoriasis. Methotrexate, acitretin, and cyclosporine could worsen hypertension, liver steatosis, and dyslipidemia. Since infliximab and ustekinumab are weight adjusted, they may be ideal drugs to treat obese psoriatic patients. IL-17 inhibitors are very effective independently from body weight; however, they tend to present better clearance rates in normal weight patients. There is a paucity on weight data regarding the efficacious IL-23 inhibitors. Apremilast may induce weight loss as an adverse effect presenting also some beneficial metabolic actions. Finally, simvastatin and some antidiabetic drugs could decrease psoriasis severity. More mechanistic, observational studies and well-conducted RCTs are necessary to decipher the enigmatic link between psoriasis and obesity, and to provide evidence-based specific guidelines for the screening and management of obese psoriatic patients

    Is There an Obesity Paradox in Critical Illness? Epidemiologic and Metabolic Considerations

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    PURPOSE OF REVIEW: Obesity represents a global epidemic with serious implications in public health due to its increasing prevalence and its known association with a high morbidity and mortality burden. However, a growing number of data support a survival benefit of obesity in critical illness. This review summarizes current evidence regarding the obesity paradox in critical illness, discusses methodological issues and metabolic implications, and presents potential pathophysiologic mechanisms. RECENT FINDINGS: Data from meta-analyses and recent studies corroborate the obesity-related survival benefit in critically ill patients as well as in selected populations such as patients with sepsis and acute respiratory distress syndrome, but not trauma. However, this finding warrants a cautious interpretation due to certain methodological limitations of these studies, such as the retrospective design, possible selection bias, the use of BMI as an obesity index, and inadequate adjustment for confounding variables. Main pathophysiologic mechanisms related to obesity that could explain this phenomenon include higher energy reserves, inflammatory preconditioning, anti-inflammatory immune profile, endotoxin neutralization, adrenal steroid synthesis, renin-angiotensin system activation, cardioprotective metabolic effects, and prevention of muscle wasting. The survival benefit of obesity in critical illness is supported from large meta-analyses and recent studies. Due to important methodological limitations, more prospective studies are needed to further elucidate this finding, while future research should focus on the pathophysiologic role of adipose tissue in critical illness
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