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  • 1.
    Emilsson, Louise
    et al.
    Örebro University, School of Medicine, Örebro University, Sweden. Primary Care Res Unit, Värmlands Nysäter, Värmland County Council, Karlstad, Sweden.
    James, Stefan
    Department of Medical Sciences, Cardiology and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ischaemic heart disease in first-degree relatives to coeliac patients2014In: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 44, no 4, p. 359-364Article in journal (Refereed)
    Abstract [en]

    Objective: Coeliac disease (CD) has been linked to an increased risk of ischaemic heart disease (IHD). We examined the risk of IHD in first-degree relatives and spouses to coeliac patients to ascertain the genetic contribution to IHD excess risk.

    Study design and setting: Coeliac disease was defined as having a biopsy-verified villous atrophy (Marsh grade 3) in 1969-2008 (n=29096). Coeliac patients were matched to 144522 controls. Through Swedish registers, we identified all first-degree relatives and spouses to coeliac patients and their controls, in total 87622 unique coeliac relatives and 432655 unique control relatives. Our main outcome measure was IHD defined according to relevant international classification of disease codes in the Swedish Inpatient Registry or in the Cause of Death Registry. Hazard ratios (HR) and confidence intervals (CI) were estimated through Cox regression adjusted for sex, age-group and calendar year at study entry of the relative.

    Result: During a median follow-up of 108 years, 2880 coeliac relatives and 13817 control relatives experienced IHD. First-degree relatives of coeliac patients were at increased risk of IHD (HR=105; 95% CI=100-109, P-value=004), while spouses were at no increased risk (HR=099; 95% CI=087-112). The excess risk of IHD in coeliac first-degree relatives aged 40-59years was 70/100000 person-years.

    Conclusion: First-degree relatives to coeliac patients seem to be at an increased risk of IHD but the excess risk is so small that it has little clinical relevance.

  • 2.
    García-Diz, Luis
    et al.
    Department of Nutrition I, Complutense of Madrid University, Madrid, Spain.
    Murcia, M. Antonia
    Department of Food Science, Murcia University, Murcia, Spain.
    Gris, Jose L.
    Department of Food Science, Murcia University, Murcia, Spain.
    Pons, Antoni
    Department of Biology and Health Sciences, Islas Baleares University, Palma de Mallorca, Spain.
    Monteagudo, Celia
    Department of Food Science, Murcia University, Murcia, Spain.
    Martínez-Tomé, Magdalena
    Department of Food Science, Murcia University, Murcia, Spain.
    Jiménez-Monreal, Antonia M.
    Department of Food Science, Murcia University, Murcia, Spain.
    Assessing nutritional status of acute intermittent porphyria patients2012In: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 42, no 9, p. 943-952Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Acute intermittent porphyria (AIP) is a metabolic disease of haem synthesis, whose haem precursors may accumulate in the body. A well-balanced diet may prevent the symptoms, so that porphyric patients should be monitored closely during therapy for possible complications concerning any progression of acute porphyria. The aim was to evaluate the nutritional status of patients with AIP and to assess their compliance with nutritional recommendations, comparing the findings with a control group and assessing any possible nutritional deficiency.

    MATERIAL AND METHODS: Sixteen patients with AIP and a control group were evaluated by means of a lifestyle questionnaire, the Nutrition Screening Initiative checklist and a dietary questionnaire. The following diet quality indicators were calculated: animal and vegetal proteins, protein quality index, PUFA/SFA and MUFA + PUFA/SFA ratios, insoluble dietary fibre (DF)/total DF, soluble DF/total DF and insoluble DF/soluble DF ratios, thiamine, riboflavin and niacin density and the vitamin B6/protein ratio.

    STATISTICAL METHODS: Differences in continuous variables were compared using the unpaired Student's t-test and the chi-square test for nonparametric variables. The odds ratio (OR) of malnutrition was also used.

    RESULTS: Our patients showed a low intake of carbohydrates, a high lipid intake and very high protein intake, and accompanied by an inadequate intake of zinc, folic acid and tocopherol, increasing the risk of malnutrition for energy, Ca, Fe, Mg, K, folic acid and tocopherols.

    CONCLUSIONS: The patients with AIP studied individually show an increased risk of malnutrition and, given the potential increase of oxidative stress in patients with porphyria, it is recommended that they should increase their intake of carbohydrates, minerals and antioxidant nutrients.

  • 3. He, T.
    et al.
    Venema, K.
    Priebe, M. G.
    Welling, G. W.
    Brummer, Robert
    Örebro University, School of Health and Medical Sciences.
    Vonk, R. J.
    The role of colonic metabolism in lactose intolerance2008In: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 38, no 8, p. 541-547Article in journal (Refereed)
    Abstract [en]

    Lactose maldigestion and intolerance affect a large part of the world population. The underlying factors of lactose intolerance are not fully understood. In this review, the role of colonic metabolism is discussed, i.e. fermentation of lactose by the colonic microbiota, colonic processing of the fermentation metabolites and how these processes would play a role in the pathophysiology of lactose intolerance. We suggest that the balance between the removal and production rate of osmotic-active components (lactose, and intermediate metabolites, e.g. lactate, succinate, etc.) in the colon is a key factor in the development of symptoms. The involvement of the colon may provide the basis for designing new targeted strategies for dietary and clinical management of lactose intolerance.

  • 4.
    Strålberg, Towe
    et al.
    School of Medical Sciences, Örebro University, Örebro, Sweden.
    Nordenskjöld, Anna M.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Cardiology.
    Cao, Yang
    Örebro University, School of Medical Sciences. Örebro University Hospital. Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Kublickiene, Karolina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Nilsson, Erik
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Proprotein convertase subtilisin/kexin type 9 and mortality in patients starting hemodialysis2019In: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 49, no 7, article id e13113Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cardiovascular events are the leading cause of death in end stage renal disease (ESRD), but traditional markers of dyslipidemia are not clearly associated with cardiovascular risk in this population. Proprotein Convertase Subtilsin/Kexin type 9 (PCSK-9) could be of interest as a novel cardiovascular risk marker in ESRD due to the emergence of lipid lowering therapy based on PCSK-9 inhibition. The aim of the present study was to investigate if the convertase PCSK-9 is a potential risk marker for mortality among patients starting hemodialysis treatment.

    MATERIALS AND METHODS: This is a cohort study of 265 patients starting hemodialysis between 1991-2009, with three years follow-up. The association between baseline PCSK-9 levels and mortality was assessed using Cox proportional hazards- and quantile regression models, with adjustment for potential confounders.

    RESULTS: PCSK-9 levels at initiation of hemodialysis were associated to mortality in multivariable adjusted analysis. PCSK-9 levels exhibited an U-shaped association to mortality. Inclusion of the quadratic term of PCSK-9 in regression modeling optimized model performance. At baseline, PCSK-9 levels had positive correlations to Davies comorbidity score, hemoglobin and C-reactive protein while negative correlations were found for high-density lipoprotein and total cholesterol. PCSK-9 levels were higher in statin users and patients with a history of cardiovascular disease.

    CONCLUSIONS: This study shows, for the first time, that the level of PCSK-9 is associated with all-cause mortality in hemodialysis patients, independently of a number of potential confounders.

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