Clinical and investigative medicine. Medecine clinique et experimentale (Clin Investig Med )

Publisher: Canadian Medical Association; Canadian Society for Clinical Investigation, Canadian Medical Association


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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: The aim of this study was to evaluate the effects of pomegranate (PMG) extract and carvacrol (CARV) on methotrexate (MTX)-induced oxidative stress and bone marrow toxicity. Methods: Wistar albino rats (32 rats) were divided into four groups (n=8): Group 1 was control; Group 2 was given a single intraperitoneal injection of methotrexate (20 mg/kg); Group 3 was treated with carvacrol (73 mg/kg i.p.) one day before MTX (20 mg/kg i.p.) injection; and, Group 4 received a single dose of MTX (20 mg/kg i.p) while PMG was administered orally for seven days at 225 mg/kg. After animals were euthanized, blood samples were taken to evaluate hematological parameters and oxidative stress. In addition, the femur was cropped and bone marrow was extracted for examination. Results: White blood cell count, hemoglobin, hematocrit and platelet count were found to be decreased in the MTX group, but these changes were prevented in the groups that received CARV and PMG. Furthermore, decreased bone marrow cellularity was found in the groups treated with MTX, whereas the PMG and CARV groups had cellularity similar to controls. Strikingly, oxidative stress increased in the MTX group, but was ultimately decreased in the rats that received the antioxidants PMG and CARV. Conclusion: Carvacrol and PMG were found to be protective against methotrexate-induced oxidative bone marrow damage. Use of these antioxidants, in combination with chemotherapeutics, may help to reduce some adverse effects of methotrexate.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E93.
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    ABSTRACT: Purpose: The multifunctional RNA-binding protein, CUGBP1, regulates splicing, stability and translation of mRNAs. Previous studies have shown that CUGBP1 is expressed at high levels in the liver, although its role in hepatocellular carcinoma is unknown. Our aim was to determine if CUGBP1 could regulate hepatocellular carcinoma growth. Methods: Expression levels of CUGBP1 were analyzed in 70 hepatic carcinoma and 20 normal hepatic tissue samples by immunohistochemistry (IHC). Using lentivirus-mediated short hairpin RNA (shRNA), CUGBP1 expression in human hepatocellular carcinoma HepG2 cells was knocked-down. The effect of CUGBP1 on hepatic cancer cell growth was investigated. Results: CUGBP1 was expressed in 85.7% hepatocellular carcinoma specimens compared with 50% in normal liver specimens. CUGBP1 silencing remarkably decreased the proliferation of HepG2 cells, as determined by MTT assay. Flow cytometry analysis showed that knock-down of CUGBP1 led to G0/G1 phase cell cycle arrest, accompanied by sub-G1 accumulation. Moreover, depletion of CUGBP1 resulted in downregulation of cyclin B1 and upregulation of cyclin D1. Conclusion: These results suggest that CUGBP1 is essential for the growth of hepatocellular carcinoma cells. Knockdown of CUGBP1 might be a potential therapeutic approach for human hepatocellular carcinoma.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E10.
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    ABSTRACT: Purpose: Abnormal gastrointestinal permeability (GIP) has been implicated in a number of diseases, including chronic intestinal inflammatory disorders such as Crohn's as well as non-intestinal immunologic diseases such as diabetes and multiple sclerosis. Although evidence in the literature demonstrates mucosal abnormalities of the digestive barrier in asthma, previous studies have assessed only colonic permeability, while ignoring the mucosal-associated lymphoid tissue (MALT) rich areas of the small intestine. Alterations in GIP may lead to increased entry of allergenic proteins from the gut lumen into the systemic circulation, thus priming and activating the adaptive immune system and leading to inappropriate allergen sensitization and/or deregulated extra-intestinal inflammation. This study examines GIP in adults with moderate to severe asthma. Methods: Patients ingested a mixed-sugar solution and urine was collected. GIP was assayed using high-performance liquid chromatography. Demographics, atopy (assessed by allergen skin testing) and sputum cell counts were also assessed. Results: Fourteen patients with moderate to severe asthma were studied, half of whom were found to have abnormal GIP. Abnormal GIP did not correlate with sputum cell counts and there was no apparent association between atopy and intestinal permeability. Conclusion: This study demonstrated our ability to identify abnormal GIP in the MALT-rich, immunogenic small intestine of patients with asthma. The absence of a correlation between airway inflammation and increased GIP suggests that these two parameters are not causally linked, but rather define distinct entities that could separately or sequentially be involved with the development and propagation of asthma over time.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E53.
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    ABSTRACT: Purpose: Sedentary behavior has been proposed as an independent cardio-metabolic risk factor even in adults who are physically active through recreational activity. Because little is known about the metabolic effects of sedentariness in seniors, the relationship between sedentary behavior and cardio-metabolic risk was examined in physically active older adults. Methods: Fifty-four community dwelling men and women > 65 years of age (mean 71.5 years) were enrolled in this cross-sectional observational study. Subjects were in good health and free of known diabetes. Activity levels (sedentary, light, moderate to vigorous activity time per day) were recorded with accelerometers worn continuously for 7 days. Cardio-metabolic risk factors measured consisted of the American Heart Association diagnostic criteria for metabolic syndrome (waist circumference, triglycerides, high-density lipoprotein, systolic blood pressure and fasting glucose) as well as low-density lipoprotein (LDL). The relationships between activity measures and cardio-metabolic risk factors were examined. Significant variables were then entered into a stepwise multivariate regression model. Results: All but one subject achieved exercise levels recommended by the American College of Sports Medicine. The average proportion of time spent at a sedentary activity level each day was 72.7%. From the regression analysis, the only significant association found between cardio-metabolic risk outcomes and activity predictors was between LDL and sedentary time, with LDL detrimentally associated with average sedentary time per day (Standardized Beta Correlation Coefficient 0.302, p < 0.05). Conclusion: Sedentary behavior is associated with an adverse metabolic effect on LDL in seniors, even those who meet guideline recommendations for an active "fit" adult.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E108.
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    ABSTRACT: Purpose: Tetramethylpyrazine (TMP) is an effective Chinese plant-derived medicine for colitis in the clinic, but the underlying molecular mechanisms of its use remain poorly understood. The purpose of this study was to investigate the mechanisms involved in its therapeutic action. Methods: A colitis mouse model was induced by oxazolone enema. TMP was administered at 80 mg/kg/day and sulphasalazine (SASP) was used as positive control and administered at 100 mg/kg/day for the treatment of colitis. On the fourth day after enema, mice were sacrificed. The inflammatory response was assessed by the disease activity index and histology. Colon mucosa was isolated and biochemically analyzed. In addition, in vitro studies were performed to evaluate the activity of TMP in Caco-2 cells. Results: Our results showed that TMP improved the colonic inflammatory status as evidenced by histological findings, as well as SASP. These effects were associated with a decrease in nucleus translocation of NF-κB. Paired with this inhibitive activity, there was a decrease in downstream signaling, such as C-MYC, iNOS and COX-2. In vitro assays revealed that TMP inhibited NF-κB translocation and its downstream production of inflammatory factors, such as TNF-α, IL-6 and IL-8, and that ROS production that was induced by LPS in Caco-2 cells. Conclusion: TMP improved the colitis induced by oxazoline, and its activity was associated with inhibition of NF-κB translocation, and subsequent inhibition of pro-inflammatory factor production and oxidative stress.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E1.
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    ABSTRACT: Purpose: There is evidence of a social disparity pertaining to the epidemiology and burden of illness of diabetes. The purpose of this study was to assess the association between household income strata and therapeutic goal achievement rates for LDL-cholesterol (LDL-C) (< 2.5 mmol/L) in Canadian diabetic patients. Methods: Data (household income, cardiovascular risk factors, drug profile, clinical and laboratory variables) were obtained from a previous cross-sectional study of diabetic patients who filled a prescription for a lipid-lowering drug in selected pharmacies across Canada. Telephone interviews were conducted. Physicians, identified by the participating patients, were requested to complete a short questionnaire for clinical data. Achievement of LDL-C goals according to the Canadian diabetes guidelines were assessed and incorporated into regression models corresponding to household income strata. Results: Seven household income strata were defined in the cohort (from less than 20,000 CDN$, up to 70,000 CDN$ by increments of 10,000 CDN$). LDL-C goals were attained in 34% of patients in the total cohort. There were no significant differences amongst household income strata for LDL-C goal achievement (p = 0.80). There were no significant differences in patient characteristics (age, sex, BMI) and cardiovascular risks according to the household income strata in this cohort, except age more than 65 in the lower income strata. Conclusion: This study demonstrates that household income was not a factor to achieve therapeutic goals for LDL-C for patients with diabetes in this dataset, although goal attainment was less than ideal overall. Future studies should address limitations of this work including small sample size, recruitment bias and lack of data on third party insurance coverage.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E47.
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    ABSTRACT: Purpose: Esophageal varices are a dangerous complication of liver cirrhosis. The development of cost effective, noninvasive means for prediction of large esophageal varices could reduce the use of upper gastrointestinal endoscopy in variceal screening and also provide an alternative way to confirm the results of conventional endoscopic diagnosis. Previously proposed predictive models are neither sensitive nor specific. Methods: A retrospective study based on a group of 104 liver cirrhosis patients was performed. Multiple statistical approaches were used to evaluate the association of large esophageal varices with 20 individual and six compound clinical laboratory variables. A new predictive model was developed. Results: Univariate analysis suggested that eight out of 26 variables were significantly associated with large esophageal varices. Further stepwise logistic regression eventually identified three variables (hemoglobin level, portal vein diameter and the ratio of platelet count/spleen diameter) that contributed significantly to the final regression model. Receiver operating characteristic (ROC) curve analysis showed that this new regression model achieved 77.8% and 72% of diagnostic sensitivity and specificity, respectively, for the prediction of large esophageal varices. In our study group, its diagnostic accuracy (AUROC=0.814) was found to be significantly higher than six predictive models previously published. Conclusions: No single variable offers self-sufficient predictive function for large esophageal varices. A comprehensive model using multiple variables significantly improves the predictive accuracy in screening the most at risk patients with potential variceal hemorrhage.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E38.
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    ABSTRACT: Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E58.
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    ABSTRACT: Purpose: Diastolic heart failure is characterized by the presence of heart failure symptoms despite preserved systolic function. Cytokines released during allergic reactions may impair diastolic heart function, either through their direct toxic effects or by inducing coronary artery spasm. The purpose of this study was to examine the effects of acute allergic reactions on diastolic heart function. Methods: Fifty patients, randomly selected from those who were admitted to the emergency room between May 2010 and December 2010 with the complaints of rash and itching, and who were subsequently diagnosed with allergic reactions based on the clinical and laboratory findings, were included in the study as the allergy group. Thirty healthy volunteers, in whom the diagnosis of allergy was ruled out based on the clinical and laboratory data, were use as the control group. Diastolic heart functions were evaluated in patients presenting with allergic reaction as well as in control subjects. Results: There was no significant difference between the two groups in terms of basal systolic functions, diameters of the cavities and wall thicknesses, and biochemical parameters. Color M mode flow progression velocities, E ratios, E/A ratios and mitral lateral annulus tissue Doppler velocities measured by echocardiography at Day 0 and Day 5 were significantly altered in the allergy group (p < 0.05). Conclusion: Impairment in diastolic functions was observed following acute allergic reactions. Acute allergic reactions could be a cause of mortality and morbidity if they lead to the development of diastolic heart failure.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E70.
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    ABSTRACT: Purpose: Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model. Methods: Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined. Results: Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2. Conclusion: Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E26.
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    ABSTRACT: Purpose: The purpose of this study was to investigate the effect of carvacrol (CAR) on methotrexate (MTX)-induced renal damage in rats. Methods: Twenty-four male rats were equally divided into three groups: group I, control treatment; group II, MTX-treated; and group III, MTX+CAR-treated. A single dose of CAR (73 mg/kg) was administered intraperitoneally to group III on the first day of the experiment and a single dose of MTX (20 mg/kg) was administered intraperitoneally to groups II and III on the second day of the experiment. Blood samples and kidney tissue were obtained from each animal on day 8 for the measurement of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI). Light microscopy was used for histopathological examination of kidney specimens. Results: MDA, TOS and OSI levels were significantly greater in the group receiving MTX alone relative to the control animals, while the TAS level was significantly reduced in the MTX group compared with the control group. The administration of CAR was associated with significantly decreased MDA, TOS, and OSI levels and increased TAS levels relative to the rats treated with MTX alone. Animals treated with CAR exhibited decreased tubular degeneration and architectural impairment relative to animals treated with MTX alone; however, the difference in histological scores did not meet the threshold of statistical significance. Conclusions: MTX treatment results in oxidative damage to the rat kidney; damage which is partially abrogated by the administration of CAR.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(1):E19.
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    ABSTRACT: Purpose: The purpose of this study was to investigate the effect of oral isotretinoin, a drug used in the treatment of acne vulgaris, on hearing function determined by serial audiology examinations. Methods: Forty patients with acne vulgaris were included in this study. Nine patients were excluded from the study because of inconsistent follow-up. The hearing of each participant was tested with pure tone audiometry and transient evoked autoacoustic emissions before and two and four weeks after treatment with isotretinoin (0.3-0.6 mg/kg/day) in the remaining 31 patients (62 ears). Results: The differences between the mean values of the pre-treatment and post-treatment pure tone hearing thresholds at 1000, 2000, 4000 and 6000 Hz frequencies were statistically significant (p < 0.05), but there was no significant difference between the pre-treatment and post-treatment values at 250 and 500 Hz frequencies (p > 0.05). The difference between the pre-treatment and post-treatment signal-noise ratio values of the transient evoked autoacoustic emissions was not significantly different (p > 0.05). Conclusion: Our results suggest that the use of isotretinoin may cause bilateral hearing threshold changes. Further animal and human studies are required to investigate and characterize isotretinoin-induced neurophysiological alterations in hearing.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E102.
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    ABSTRACT: Purpose: The purpose of this study was to analyze the effects of estrogen deficiency and hormone replacement therapy (HRT) on fibrinolytic activity in a rat mode of surgically-induced menopause. Methods: Twelve-week-old, sexually mature female Sprague-Dawley rats, each weighing 200-250 g, were randomly divided into four groups: (1) sham-operated group, (2) ovariectomy group, (3) ovariectomy group followed by oral administration of daily 17β-estradiol (0.02 mg/kg/day) (E2) + norethisterone acetate (0.01 mg/kg/day), and (4) ovariectomy group followed by oral administration of daily 17β-estradiol (0.01 mg/kg/day) + drospirenone (0.02 mg/kg/day). Tissue plasminogen activator (tPA) antigen, plasminogen activator inhibitor-1 (PAI-1) antigen, and PAI-1/tPA levels were measured as markers of fibrinolysis in plasma and liver and brain tissue. Results: Compared with sham-operated rats, ovariectomized rats showed higher levels of fibrinolytic activity; however, the increased fibrinolytic activity in plasma and liver tissue was significantly reduced by HRT regimens. No change was observed in the levels of fibrinolytic activity in brain tissue. Conclusions: HRT showed beneficial effects by decreasing fibrinolytic activity related to surgically-induced menopause. Short-term HRT treatment was associated with a shift in the procoagulant-anticoagulant balance toward a procoagulant state.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2014; 37(2):E85.
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    ABSTRACT: Several mechanisms for the development of depression have been proposed, and a comparative examination reveals considerable overlap. This paper begins by summarizing the conclusions drawn in the literature on the major biological theories: HPA-axis hyperactivity, the monoamine theory, the cytokine hypothesis/ macrophage theory, and structural changes to relevant brain regions and neurons. It then discusses the role of psychosocial stress as a bridge between the pathophysiology of depression and its predominantly psychosocial risk factors, touching upon theories offered in psychology and in population health. This paper further proposes a unifying framework which integrates the major theories. The multiple systems involved, and the directional complexity among them, likely help to explain the wide-ranging symptoms associated with depression, and the wide variety of comorbid medical conditions. They may also contribute to challenges in treatment, the diversity in symptoms and treatment outcomes among individuals, and the high rates of symptom persistence and relapse. The apparent bi-directionality of associations may suggest the existence of positive-feedback loops which aggravate symptoms; however, further bench research is required to confirm such phenomena. A better understanding of these interweaving associations is warranted. Additionally, given the significant influence of socioeconomic and psychosocial factors on the aetiology of depression, population-level interventions that address the social determinants of health are required. Current individual-level pharmacologic approaches are designed to treat pathophysiology once it is underway, and current individual-level non-pharmacologic interventions (such as talk therapy) are designed to moderate the relationship between psychosocial stress and pathophysiology. In contrast, a key strategy for primary prevention lies in population-level interventions that address the predominantly social causes of one of depression's most notable risk factors: chronic psychosocial stress.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2013; 36(4):E170.
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    ABSTRACT: A patient's ability to be cared for and to die at home is heavily dependent upon the efforts of family caregivers. Considerable stresses are associated with such caregiving, including physical, psychosocial and financial burdens. Research has shown that unmet needs and dissatisfaction with care can lead to negative outcomes for caregivers. While many family caregivers also report caregiving as life-enriching, some report that they would prefer alternatives to care at home, primarily because of these associated burdens. Little is known about which interventions are most effective to support family caregivers ministering palliative care at home. Well-designed studies to test promising interventions are needed, followed by studies of the best ways to implement the most effective interventions. Clinically effective practice support tools in palliative home care are warranted to identify family caregiver needs and to ensure that patients and their family caregivers have a choice about where care is provided.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2013; 36(3):E121.
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    ABSTRACT: Purpose: Fetuin-A is a hepatokine that is linked to lipid metabolism, obesity, insulin resistance, type 2 diabetes and cardiovascular disease. Elevated thyroid-stimulating hormone (TSH) levels are associated with metabolic and cardiovascular disturbances. Our aim was to determine if TSH can regulate fetuin-A levels. Methods: Fetuin-A serum levels were examined in 26 subjects (19 women; previous thyroidectomy and radioactive iodine ablation) undergoing recombinant human TSH (rhTSH) stimulation to screen for thyroid cancer recurrence. Their age was 49±10 years, and body mass index (BMI) was 28±6 (both expressed as mean±SD). The patients received two doses of rhTSH (0.9 mg), administered 24 hours apart on days 1 and 2, without discontinuation of ongoing L-thyroxine therapy. Morning blood samples were obtained on days 1 (prior to the first dose of rhTSH), 3 and 5. Results: The baseline value of fetuin-A (mean±SD) for all participants was 527±186 mg/L. Values of fetuin-A did not change in response to rhTSH administration. The lack of response was not dependent on gender, age, baseline free thyroxine level or BMI. Conclusion: Fetuin-A has been implicated in metabolic and inflammatory conditions, but there have been no reports on whether fetuin-A is influenced by TSH. Within the context of rhTSH administration for surveillance of thyroid cancer recurrence, there was no effect on serum levels of fetuin-A.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2013; 36(5):E264.
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    ABSTRACT: Purpose: Obesity is associated with left ventricular diastolic dysfunction and altered heart rate variability, as well as pulmonary dysfunction. The relationship between asthma and cardiac dysfunction in severely obese subjects is unknown, although it has been hypothesized that cardiac dysfunction may contribute to increase airway hyper-responsiveness (AHR). This study aimed to determine if AHR is associated with left ventricular diastolic dysfunction and heart rate variability in severely obese subjects. Methods: Sixty-one subjects with severe obesity (BMI ≥35 kg/m2 with comorbidities) completed this study. All subjects completed respiratory questionnaires, spirometry, lung volume measurements, methacholine inhalation test, 24hour Holter monitoring and a complete echocardiography evaluation. Blood samples were obtained for measurement of metabolic markers. Subjects with AHR, defined by a provocative concentration of methacholine inducing a 20% fall in FEV1 (PC20) < 8 mg/ml, were compared with those with no AHR (PC20 ≥8 mg/ml). Results: According to these criteria, 32 subjects had AHR and 29 had no AHR(mean PC201.70 mg/ml and 15.3 mg/ml respectively, p < 0.001). The groups were similar for anthropometric data and comorbidities. Fasting glucose, Hb1Ac, total cholesterol, LDL, triglycerides, Apo-B, C-reactive protein (CRP) and pro-BNP levels were also comparable between groups (p > 0.05). CRP level correlated with PC20 (AHR, r=0.38, p=0.03). Indices of heart rate variability and overall cardiac function were similar in subjects with or without AHR but grade 2 left ventricular diastolic dysfunction was more prevalent in subjects with AHR (p=0.037). Conclusions: Altered cardiac function, dysglycemia and dyslipidemia do not seem to be significantly associated with AHR in severely obese subjects in contrast to systemic inflammation.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2013; 36(5):E255.
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    ABSTRACT: Chronic Obstructive Pulmonary Disease (COPD) is the most common cause of admission to acute care facilities in Canada. The burden of illness for patients, caregivers and the health care system is profound. Dyspnea in advanced COPD pervades all aspects of patients' lives. When increasing symptom burden limits patients to their homes, crucial primary care services become less accessible, and care of end-stage COPD becomes increasingly fragmented and reactive. Given the considerable physical and psychosocial consequences of advanced COPD, this phase can be devastating for patients and families. In this article we outline the need for clinical interventions and re-organized models of care designed for better continuity to achieve more favorable outcomes for these patients and their families. Outreach programs and use of personalized action plans that include advice on careful use of opioids can be remarkably effective. The move toward an integrated approach to COPD management with more effective advance care planning will help patients and their families make informed decisions throughout the illness trajectory. Intensive medical treatment focused on increasing survival can coexist with both holistic and palliative approaches to improve the quality of life of patients with severe end-stage COPD.
    Clinical and investigative medicine. Medecine clinique et experimentale 01/2013; 36(3):E114.