Muhammad Amer

Johns Hopkins University, Baltimore, Maryland, United States

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Publications (9)26.06 Total impact

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    ABSTRACT: Background Inverse association between lower level of 25-hydroxyvitamin D [25(OH)D] and higher prevalence of peripheral arterial disease (PAD) among individuals with cardiovascular diseases (CVD) is known. Less is known about the relationship between 25(OH)D and ankle-brachial blood pressure index (ABPI) in asymptomatic adults. We hypothesized a nonlinear relationship between 25(OH)D and ABPI in asymptomatic adults without PAD.Methods Data from the continuous NHANES (2001–2004) was used. Minimum of the two reported ABPI value was chosen for each individual (>18 years). Linear regression models with spline adjusted for demographic and traditional risk factors for CVD were used to examine nonlinear relationship between 25(OH)D and ABPI. Mean changes in ABPI per 10 ng/mL change in 25(OH)D were reported.ResultsMean (SD) age and 25(OH)D levels of 4979 participants (48% females) were 60.4 (13.22) years and 22.1 (8.68) ng/mL, respectively, while mean (SD) ABPI was 1.07 (0.15). We observed positive association between 25(OH)D and ABPI both in the univariable and multivariable regression models (all p < 0.05). In univariable regression with spline, a significant increase in ABPI (ß = 0.03, 95% CI: 0.02–0.04) was observed until 25(OH)D reached but not above 27 ng/mL. Similarly, in multivariable spline models, 25(OH)D was positively associated with ABPI (ß = 0.02, 95% CI: 0.01–0.03) only up to 27 ng/mL.Conclusions In asymptomatic adults without PAD, rising serum 25(OH)D concentration but not above 27 ng/mL was associated with statistically significant increase in ABPI. Clin Trans Sci 2014; Volume #: 1–5
    Clinical and Translational Science 07/2014; · 2.33 Impact Factor
  • Muhammad Amer, Rehan Qayyum
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    ABSTRACT: Context:Hyperhomocysteinemia is an independent risk factor for premature atherosclerosis and thromboembolism. 25-Hydroxyvitamin D [25(OH)D] may modulate the expression of genes involved in homocysteine metabolism.Objective:Little is known about the relationship between homocysteine and 25(OH)D. We hypothesized an inverse and nonlinear association between 25(OH)D and homocysteine.Design:We analyzed data from the continuous National Health and Nutrition Examination Survey 2001-2006 for asymptomatic adults (≥18 y).Setting:Linear regression models with spline adjusted for cardiovascular disease risk factors were used to explore nonlinearity.Main Outcomes Measure:Mean change (β-coefficients with 95% confidence intervals) in homocysteine was reported per 10 ng/mL change in 25(OH)D.Results:Mean (SD) age and homocysteine levels of 14ü630 participants were 47.2 (20) years and 8.8 (4.7) μ mol/L, respectively, whereas the median (interquartile range) of 25(OH)D was 21 (15-27) ng/mL. Without using spline, we observed an inverse relation between homocysteine and 25(OH)D both in simple [0.25 (-0.34 to -0.02) μ mol/L] and multivariable [0.13 (-0.18 to -0.01) μ mol/L] regression. With spline, in a univariate model, an increase in 25(OH)D was associated with a significant decrease in homocysteine [0.56 (-0.75 to -0.37) μ mol/L] until 25(OH)D reaches but not if above its median (21 ng/mL). Similarly, in multivariable spline models, the inverse relationship between homocysteine and 25(OH)D remain significant [0.49 (-0.67 to -0.31) μ mol/L] only below the population median of 25(OH)D.Conclusions:From a large community-based cohort of asymptomatic adults, we found an inverse relation between 25(OH)D and homocysteine among those with 25(OH)D concentration of 21 ng/mL or less. We did not observe any statistical decrease in homocysteine once 25(OH)D concentration rose above 21 ng/mL.
    The Journal of Clinical Endocrinology and Metabolism 11/2013; · 6.31 Impact Factor
  • Muhammad Amer, Rehan Qayyum
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    ABSTRACT: BACKGROUND: Observational studies have suggested a strong relationship between 25(OH)D and all-cause and cardiovascular disease mortality. A few studies also have described a nonlinear trend for this relationship in population subgroups, but less is known about this relationship in healthy adults. We examined the presence of a nonlinear relationship between 25(OH)D and all-cause and cardiovascular disease mortality among healthy adults. METHODS: We examined 10,170 participants (≥18 years of age) using National Health and Nutrition Examination Survey data (2001-2004) combined with National Death Index for vital status information through December 2006. Cox proportional hazard models with spline (single knot at population median of 25[OH]D) were fit to estimate hazard ratios (HRs) for all-cause and cardiovascular disease mortality for each 10-unit increase in serum 25(OH)D. Models were adjusted for demographic and conventional cardiovascular disease risk factors. RESULTS: Mean age of study participants was 46.6 (20.5) years, while median (interquartile range) 25(OH)D was 21 (15-27) ng/mL. After a median follow-up of 3.8 years (range 2.8-4.9), 509 all-cause and 184 cardiovascular diseases-related deaths were observed. In univariate analysis, 25(OH)D decreased hazards of all-cause (HR 0.59; 95% confidence interval [CI], 0.45-0.77) and cardiovascular disease (HR 0.56; 95% CI, 0.38-0.82) mortality below but not above its population median. In adjusted models, 25(OH)D retained the inverse association for all-cause (HR 0.54; 95% CI, 0.35-0.84) and cardiovascular disease (HR 0.50; 95% CI, 0.26-0.98) mortality below but not above its population median. CONCLUSIONS: We found an inverse association between 25(OH)D and all-cause and cardiovascular disease mortality in healthy adults with serum 25(OH)D levels of ≤21 ng/mL. Clinical trials for the primary prevention of cardiovascular disease with 25(OH)D supplementation may target healthy adults with serum 25(OH)D levels of ≤21 ng/mL to validate these findings.
    The American journal of medicine 04/2013; · 5.30 Impact Factor
  • Muhammad Amer, Rehan Qayyum
    The American journal of cardiology 07/2012; 110(1):165. · 3.58 Impact Factor
  • Muhammad Amer, Rehan Qayyum
    The American journal of cardiology 07/2012; 110(1):163. · 3.58 Impact Factor
  • Muhammad Amer, Rehan Qayyum
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    ABSTRACT: The inverse relation between vitamin D supplementation and inflammatory biomarkers among asymptomatic adults is not settled. We hypothesized that the inverse relation is present only at lower levels and disappears at higher serum levels of vitamin D. We examined the relation between 25-hydroxyvitamin D [25(OH)D] and C-reactive protein (CRP) using the continuous National Health and Nutrition Examination Survey data from 2001 to 2006. Linear spline [single knot at median serum levels of 25(OH)D] regression models were used. The median serum 25(OH)D and CRP level was 21 ng/ml (interquartile range 15 to 27) and 0.21 mg/dl (interquartile range 0.08 to 0.5), respectively. On univariate linear regression analysis, CRP decreased [geometric mean CRP change 0.285 mg/dl for each 10-ng/ml change in 25(OH)D, 95% confidence interval [CI] -0.33 to -0.23] as 25(OH)D increased ≤21 ng/ml. However, an increase in 25(OH)D to >21 ng/ml was not associated with any significant decrease [geometric mean CRP change 0.05 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI -0.11 to 0.005) in CRP. The inverse relation between 25(OH)D below its median and CRP remained significant [geometric mean CRP change 0.11 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.16 to -0.04] on multivariate linear regression analysis. Additionally, we observed a positive relation between 25(OH)D above its median and CRP [geometric mean CRP change 0.06 mg/dl for each 10-ng/ml change in 25(OH)D, 95% CI 0.02 to 0.11) after adjusting for traditional cardiovascular risk factors. In conclusion, from this cohort of asymptomatic adults, independent of traditional cardiovascular risk factors, we observed a statistically significant inverse relation between 25(OH)D at levels <21 ng/ml and CRP. We found that 25(OH)D at a level ≥21 ng/ml is associated with an increase in serum CRP. It is possible that the role of vitamin D supplementation to reduce inflammation is beneficial only among those with a lower serum 25(OH)D.
    The American journal of cardiology 01/2012; 109(2):226-30. · 3.58 Impact Factor
  • Muhammad Amer, Jurga Adomaityte, Rehan Qayyum
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    ABSTRACT: Administering intermittent boluses of furosemide to patients with acute decompensated heart failure (ADHF) often leads to unfavorable hemodynamic changes. Continuous infusion may induce similar or greater diuresis without adverse hemodynamic consequences. We conducted a systemic review and meta-analysis of randomized clinical trials that compared the effects of continuous infusion and intermittent bolus of furosemide in patients hospitalized with ADHF. We searched PubMed, EMBASE, and The Cochrane Central Register of Controlled Trials databases from their inception until March 2011. Two investigators independently abstracted data on study characteristics, quality, and selected outcomes. Differences between investigators were resolved by mutual consensus. Comparisons were reported as the weighted mean difference (WMDs). Ten trials involving a total of 564 patients were included. When administered as a continuous infusion, furosemide resulted in greater diuresis (WMD, -240.54 mL/24 hours/100 mg furosemide; 95% confidence interval [CI], -462.42 to -18.66) and reduction in total body weight (WMD, -0.78 kg; 95% CI, -1.54 to -0.03), than when administered in intermittent boluses. Urinary sodium excretion (WMD, -20.26 mmol/24 hours; 95% CI, -60.48 to 19.96) and duration of hospital stay (WMD, 0.99 days; 95% CI, -2.08 to 4.06) were not different between the 2 groups. This meta-analysis showed statistical support for administering furosemide as a continuous infusion for greater diuresis and reduction in total body weight in patients hospitalized with ADHF. With the exception of greater diuresis, available data are homogenous for the reported outcomes but lack information on clinical endpoints. Larger studies are needed to provide robust recommendations for clinical practice.
    Journal of Hospital Medicine 11/2011; 7(3):270-5. · 1.40 Impact Factor
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    ABSTRACT: Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit production of prostaglandins by acting on cyclooxygenase (COX) isoenzymes 1 and 2. Nonselective NSAIDs inhibit both COX 1 and 2 isoenzymes (eg, ibuprofen and naproxen). Selective NSAIDs act on COX-1 (eg, aspirin) or COX-2 (eg, celecoxib) isoenzymes, respectively. Prostaglandins are produced in platelets and gastric mucosal cells through constitutively expressed COX-1 isoenzyme. They are involved in the regulation of hemostasis, functional integrity of the gastrointestinal and renal tracts, platelet function, and macrophage differentiation. Inhibition of COX-1 isoenzymes impedes platelet aggregation, impairs maintenance of protective gastric mucosal barrier, and affects renal function. Prostaglandin production in inflamed tissue results from de novo induction of COX-2 expression by inflammatory cytokines and other noxious stimuli. Thus, COX-2 isoenzyme inhibition either selectively or nonselectively helps in reducing inflammation in the setting of musculoskeletal disorders. Safety and efficacy of NSAIDs are related to their relative actions on COX-1 or COX-2 inhibition. Given the multisystem (gastrointestinal, hematopoietic, and renal) adverse effect profile of COX-1 inhibition, formulation of NSAIDs with relative COX-2 selectivity became a highly desirable target during the 90's. However, studies in the first half of this decade revealed adverse effects of COX-2 inhibition on the cardiovascular system, including increased risks of myocardial infarction, exacerbation of stable congestive heart failure, and worsening high blood pressure. Randomized trials and meta-analyses confirmed these findings, which led to withdrawal of some of the COX-2 inhibitors from the market by the federal Food and Drug Administration a few years ago. Here, we review the effects of COX-2 isoenzyme inhibitors on the cardiovascular system to provide a safe strategy for prescribing these agents in patients with existing cardiovascular disease. We did not find adequate long-term randomized controlled trials appropriately powered to evaluate cardiovascular outcomes. Potentially, all NSAIDs possess a fair risk of adverse effects on gastrointestinal, cardiovascular, and renal systems. Until more evidence for safety via randomized trials is available, we recommend caution in prescribing COX-1 and 2 inhibitors for musculoskeletal disorders in patients with existing gastrointestinal or cardiovascular conditions.
    Cardiology in review 01/2010; 18(4):204-12.
  • Muhammad Amer
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    ABSTRACT: Cite this Article: Amer M. The Saga of Vitamin D: Does It Have a Role Beyond Musculoskeletal System and Calcium Homeostasis? J Pak Med Stud. 2012; 2(3): 84-85. Lower serum levels of vitamin D are strongly linked with an increased risk of all-cause and cardiovascular (CV) mortality [1, 2]. Several biological mechanisms have been proposed to elucidate etiological links underlying these associations. In some studies, supplementation with vitamin D has been found to be useful in reducing the risk of colon, rectum, and breast cancers [3, 4]. A number of epidemiological studies that examined associations between vitamin D deficiency and all-cause and CV mortality have limited external validity due to studied population subgroups [2, 5]. There is a possibility that the selected subgroups did not reflect true status of vitamin D and its impact on the prevention of all-cause or CV mortality in otherwise asymptomatic population. In addition, large number of the observational studies has used quartile based analytic approach to estimate associations between vitamin D status and mortality which could obscure findings at extremes of vitamin D from respective cohorts [6]. Moreover, the cutoff boundaries for selected quartiles were not uniform; for example, the mean serum vitamin D levels in the lowest quartiles ranged from 5.6 to 17.8 ng/mL [1, 2, 5, 7]. The relationship betweenvitamin D deficiency and systemic inflammation (as measured by circulating inflammatory biomarkers such as C-reactive protein, homocysteine and interleukins) in healthy individuals is also not yet settled. It appears that the anti-inflammatory properties of vitamin D may not be noticeable unless offered to individuals with severely low serum vitamin D levels. Moreover, vitamin D may play a detrimental role by increasing inflammation once it rises beyond a certain level [8]. Tarcin et al reported marked improvement in endothelial dysfunction, markers of oxidative stress and insulin sensitivity index among individuals [mean vitamin D levels of < 10.01 ng/mL (base line)] whose vitamin D levels improved to 30.04 ng/mL (after vitamin D supplementation for three months) [9]. Literature also suggests that the relationship between serum 25 (OH) D and mortality is non-linear such that there is an increased risk of death both at higher as well as lower circulating levels of vitamin D [1, 10, 11]. While data from the observational studies is overwhelming, randomized controlled trials are needed to establish causality between vitamin D status and mortality especially among individuals with no pre-existing CV disease or high CV risks. Based on the lack of established benefits of vitamin D supplementation, the Endocrine Society's Clinical Practice Guidelines did not recommend screening individuals who are not at risk of vitamin D deficiency or prescribing vitamin D for non-calcemic benefits [12]. With ongoing skepticism on its role in primary and secondary prevention, it seems that the long-drawn-out practice of vitamin D supplementation will soon lose its significance. However, healthcare providers are strongly encouraged to identify target patient population that could benefit from vitamin D supplementation for its non-calcemic and non-musculoskeletal effects on body. Until, randomized controlled trials do not completely rule out (or rule in) a substantial role of vitamin D supplementation in limiting CV disease progression, lowering certain cancer incidence, and decreasing all-cause mortality, the saga of a potential role of vitamin D beyond musculoskeletal and calcium homeostasis will continue.

Publication Stats

68 Citations
26.06 Total Impact Points


  • 2010–2014
    • Johns Hopkins University
      • Department of Medicine
      Baltimore, Maryland, United States
  • 2012
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States
  • 2011
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States