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  • 1.
    Bengtsson, D
    et al.
    Kalmar Cty Hosp, Sweden.
    Brudin, L
    Kalmar Cty Hosp, Sweden.
    Wanby, Pär
    Kalmar Cty Hosp, Sweden.
    Carlsson, Martin
    Kalmar Cty Hosp, Sweden.
    Previously unknown thyroid dysfunction in patients with acute ischemic stroke.2012In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 126, no 2, p. 98-102Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Opinions differ regarding the clinical significance of subclinical thyroid disorders. The aim of the present study was to evaluate the prevalence and influence of previously unknown overt or subclinical thyroid dysfunction in patients with acute ischemic stroke and to look for differences between cardio-embolic and non-embolic ischemic stroke.

    MATERIAL AND METHODS: A total of 153 Swedish patients diagnosed with first-time acute ischemic stroke were included in the study and categorized for suspected cardio-embolic (n = 30) or non-embolic (n = 123) ischemic stroke depending on the presence of atrial fibrillation (AF). Blood samples were taken 48 h or earlier after onset of stroke symptoms.

    RESULTS: Previously, unknown overt or subclinical thyroid dysfunction was found in 12%. Previously, unknown overt or subclinical hyperthyroidism was more common in the AF group (13%) compared to the non-AF group (3%), P = 0.048. Patients with AF had slightly higher concentrations of free T4 (15 vs 14 pm; P < 0.001), but there was no significant difference in concentrations of S-TSH or prevalence of thyroperoxidase (TPO) antibodies between the groups.

    CONCLUSIONS: In patients with first-time acute ischemic stroke, unknown thyroid dysfunction is common, and unknown overt or subclinical hyperthyroidism is associated with cardio-embolic stroke.

  • 2.
    Carlsson, Martin
    et al.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Kalmar County Hospital.
    Brudin, Lars
    Kalmar County Hospital;Univ Hosp Linköping.
    Wanby, Pär
    Kalmar County Hospital.
    Directly measured free 25-hydroxy vitamin D levels show no evidence of vitamin D deficiency in young Swedish women with anorexia nervosa2018In: Eating and Weight Disorders, ISSN 1124-4909, E-ISSN 1590-1262, Vol. 23, no 2, p. 247-254Article in journal (Refereed)
    Abstract [en]

    Purpose Anorexia nervosa (AN) is an eating disorder characterized by low fat mass complicated by osteoporosis. The role of circulating vitamin D in the development of bone loss in AN is unclear. Fat mass is known to be inversely associated with vitamin D levels measured as serum levels of total, protein-bound 25-hydroxyvitamin D, but the importance of directly measured, free levels of 25(OH)D has not been determined in AN. The aim of this study was to investigate vitamin D status, as assessed by serum concentrations of total and free serum 25(OH)D in patients with AN and healthy controls. Methods In female AN patients (n = 20), and healthy female controls (n = 78), total 25(OH)D was measured by LC-MS/MS, and free 25(OH)D with ELISA. In patients with AN bone mineral density (BMD) was determined with DEXA. Results There were no differences between patients and controls in total or free S-25(OH)D levels (80 +/- 31 vs 72 +/- 18 nmol/L, and 6.5 +/- 2.5 vs 5.6 +/- 1.8 pg/ml, respectively), and no association to BMD was found. In the entire group of patients and controls, both vitamin D parameters correlated with BMI, leptin, and PTH. Conclusions The current study did not demonstrate a vitamin D deficiency in patients with AN and our data does not support vitamin D deficiency as a contributing factor to bone loss in AN. Instead, we observed a trend toward higher vitamin D levels in AN subjects compared to controls. Measurement of free vitamin D levels did not contribute to additional information.

  • 3. Carlsson, Martin
    et al.
    Lindström, Torbjörn
    Nyström, Fredrik
    Nilsson, Ingela
    Brudin, Lars
    Wanby, Pär
    Region Kalmar län.
    Evidence of Daytime Variation of Asymmetric Dimethylarginine: An Intervention Study with Rosiglitazon in Type 2 Diabetes2011In: The Open Endocrinology Journal, no 5, p. 14-18Article in journal (Refereed)
    Abstract [en]

    Background: Asymmetric dimethylarginine (ADMA) has in some, but not all studies been associated with insulin resistance (IR). We wanted to challenge the hypothesis that plasma ADMA levels are associated with IR in an intervention study using an insulin sensitizing drug. Another aim of the study was to study daytime ADMA variation and if food intake influence ADMA concentration.

    Methods: Nine patients with diet treated type 2 diabetes were investigated with daytime profiles of ADMA (8 am-5 pm) before and during treatment with rosiglitazone for 8 weeks. A control group matched for age and sex underwent a similar investigation at baseline.

    Results: After treatment with rosiglitazone, ADMA (0.63- 0.64 mmol/L; p=0.26) and homocysteine (10.3 -10.6 mol/L; p=0.61) concentrations did not change. Postprandial (10 am – 5 pm) ADMA concentrations were 10% higher than fasting morning levels (p=0.006) and this difference was similar for controls and diabetes patients both pre and post treatment with rosiglitazone.

    Conclusions: Treatment with rosiglitazone aiming to improve insulin sensitivity did not affect ADMA concentration in type 2 diabetes patients. The ADMA daytime variation and the relation to food intake appear to be a novel finding and should be considered in future studies.

  • 4.
    Carlsson, Martin
    et al.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Kalmar County Hospital.
    Nilsson, Ingela
    Kalmar County Hospital.
    Brudin, Lars
    Kalmar County Hospital ; Linköping University Hospital.
    Von, Siv-Ping
    Kalmar County Hospital.
    Wanby, Pär
    Kalmar County Hospital.
    Erythrocyte fatty acid composition does not influence levels of free, bioavailable, and total 25-hydroxy vitamin D2017In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 77, no 1, p. 45-52Article in journal (Refereed)
    Abstract [en]

    In vitro, mono- and polyunsaturated fatty acids (FAs) may decrease the binding affinity of vitamin D metabolites for vitamin D-binding protein, which in turn may influence their bioavailability. FAs incorporated as phospholipids in erythrocyte (ery-) cell membranes reflect dietary intake. The purpose of this study was to investigate ery-FA composition in relation to markers for vitamin D. In healthy females (age 22.6 +/- 2.0 years) total 25(OH)D was measured by LC-MS/MS (n=78), free 25(OH)D with ELISA (n=64 of 78), and bioavailable 25(OH)D was calculated. Analysis of ery-FA composition was by gas chromatography (n=56 of 78). A strong correlation between total 25(OH)D and free 25(OH)D was seen (r=.66, p<.001), and between total-25(OH)D and bioavailable 25(OH)D (r=.68, p<.001). No correlations between 25(OH)D fractions and specific fatty acids were found, and in particular, no associations with mono- and poly-unsaturated FA compositions. All 25(OH)D fractions were correlated with leptin (total 25(OH)D (r=-.33, p<.003); bioavailable 25(OH)D (r=-.47, p<.001); free 25(OH)D (r=-.44, p<.001). Associations were found between PTH and total 25(OH)D (r=-.35, p=.002) and weaker between bioavailable 25(OH)D (r=-.35, p=.040) and free 25(OH)D (r=-.28, p=.079). All fractions of 25(OH)D appear to correlate in a similar way to PTH, BMI and body fat (leptin). No association was found between ery-FA composition and free/bioavailable 25(OH)D. It is unlikely that FAs are a strong uncoupling factor of DBP-bound 25(OH)D.

  • 5.
    Carlsson, Martin
    et al.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Kalmar County Hospital.
    Wanby, Pär
    Kalmar County Hospital.
    Brudin, Lars
    Linköping University;Kalmar County Hospital.
    Lexne, Erik
    Kalmar County Hospital.
    Mathold, Karin
    Kalmar County Hospital.
    Nobin, Rebecca
    Kalmar County Hospital.
    Ericson, Lisa
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry.
    Nordqvist, Ola
    Kalmar County Council.
    Petersson, Göran
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry.
    Older Swedish Adults with High Self-Perceived Health Show Optimal 25-Hydroxyvitamin D Levels Whereas Vitamin D Status Is Low in Patients with High Disease Burden2016In: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 8, no 11, article id 717Article in journal (Refereed)
    Abstract [en]

    Controversy pervades the definition of adequate and optimal vitamin D status. The Institutes of Medicine have recommended serum 25(OH) D levels above 50 nmol/L based upon evidence related to bone health, but some experts, including the Endocrine Society and International Osteoporosis Foundation, suggest a minimum serum 25(OH) D level of 75 nmol/L to reduce the risk of falls and fractures in older adults. In a cross-sectional study, we compared vitamin D status in people >= 75 years selected from four groups with a frailty phenotype, combined with a control group free from serious illness, and who considered themselves completely healthy. Only 13% of the 169 controls were vitamin D deficient (S-25(OH) D) < 50 nmol/L), in contrast with 49% of orthopedic patients with hip fractures (n = 133), 31% of stroke patients (n = 122), 39% of patients visiting the hospital's emergency department >= 4 times a year (n = 81), and 75% of homebound adult residents in long-term care nursing homes (n = 51). The mean vitamin D concentration of the healthy control group (74 nmol/L) was similar to a suggested optimal level based on physiological data and mortality studies, and much higher than that of many officially recommended cut-off levels for vitamin D deficiency (< 50 nmol/L). The present study provides a basis for planning and implementing public guidelines for the screening of vitamin D deficiency and vitamin D treatment for frail elderly patients.

  • 6.
    Ericson, Lisa
    et al.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry.
    Hovstadius, Bo
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry.
    Carlsson, Martin
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Kalmar County Hospital.
    Petersson, Göran
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry.
    Wanby, Pär
    Kalmar County Hospital.
    A cost analysis of systematic vitamin D supplementation in the elderly versus supplementation based on assessed requirements2017In: Journal of Aging Research and Healthcare, ISSN 2474-7785, Vol. 2, no 2, p. 13-22Article in journal (Refereed)
    Abstract [en]

    Hypovitaminosis D is common among older people and treatment with vitamin D is associated with reduced risk of falls and fractures. This paper provides a cost analysis of assessing the vitamin D status of and providing the pharmaceuticals for elderly citizens in Kalmar County, Sweden (population approximately 230,000). Four hypothetical interventions were analyzed: (a) systematic vitamin D/calcium supplementation to all elderly (≥75 years), (b) assessment of vitamin D status in elderly and supplementation to those with insufficient levels, (c) systematic vitamin D/calcium supplementation to all nursing-home residents, and (d) assessment of vitamin D status in nursing-home residents and supplementation to those with insufficient levels. The calculations were based on an estimated reduction in overall costs due to the assessed number of hip fractures after vitamin D/calcium supplementation. The annual net economic benefit of vitamin D/calcium supplementation was estimated at (a) €304,000, (b) €860,000, (c) €755,000, and (d) €740,000. The provision of systematic vitamin D supplementation to nursing-home residents would provide a substantial net economic benefit to society and assessment of the vitamin D status before starting supplementation does not seem to be necessary. Although assessment of all elderly citizens would be more comprehensive, the true proportion with insufficient vitamin D levels in the general population is uncertain and to reaching consensus on the most advantageous daily vitamin D intake, vitamin D blood levels are necessary. Also, systematic supplementation to all elderly would result in other outcomes that could be worth the cost, but that remains to be evaluated.

  • 7. Fava, C
    et al.
    Montagnana, M
    Rosberg, L
    Burri, P
    Almgren, P
    Jönsson, A
    Wanby, Pär
    Region Kalmar län.
    Lippi, G
    Minuz, P
    Hulthèn, L U
    Aurell, M
    Melander, O
    Subjects heterozygous for genetic loss of function of the thiazide-sensitive cotransporter have reduced blood pressure.2008In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 17, no 3, p. 413-418Article in journal (Refereed)
    Abstract [en]

    Gitelmańs syndrome (GS) is an inherited recessive disorder caused by homozygous or compound heterozygous loss of function mutations of the NaCl cotransporter (NCCT) gene encoding the kidney-expressed NCCT, the pharmacological target of thiazide diuretics. An observational study estimated the prevalence of GS to 19/1,000,000, in Sweden, suggesting that approximately 1% of the population carries one mutant NCCT allele. As the phenotype of GS patients, who always carry two mutant alleles, is indistinguishable from that seen in patients treated with high-dose thiazide diuretics, we aimed at investigating whether subjects carrying one mutated NCCT allele have a phenotype resembling that of treatment with low-dose thiazide diuretics. We screened first-degree relatives of 18 of our patients with an established clinical end genetic diagnosis of GS for NCCT loss of function mutations and identified 35 healthy subjects carrying one mutant allele (GS-heterozygotes). Each GS-heterozygote was assigned a healthy control subject matched for age, BMI and sex. GS-heterozygotes had markedly lower blood pressure (systolic 103.3 +/- 16.4 versus 123.2 +/- 19.4 mmHg; diastolic 62.5 +/- 10.5 versus 73.1 +/- 9.4 mmHg; P < 0.001) than controls. There was no significant difference between the groups either in plasma concentration or urinary excretion rate of electrolytes, however, GS-heterozygotes had higher fasting plasma glucose concentration. Similar to patients being treated with low-dose thiazide diuretics, GS-heterozygotes have markedly lower blood pressure and slightly higher fasting plasma glucose compared with control subjects. Our findings suggest that GS-heterozygotes, the prevalence of which can be estimated to 1%, are partially protected from hypertension through partial genetic loss of function of the NCCT. However, as our study had a case-control design, it is important to underline that any potential effects on population blood pressure and risk of future cardiovascular disease need to be examined in prospective and population-based studies.

  • 8. Fava, Cristiano
    et al.
    Montagnana, Martina
    Rosberg, Lena
    Burri, Philippe
    Jönsson, Anders
    Wanby, Pär
    Region Kalmar län.
    Wahrenberg, Hans
    Hulthén, U Lennart
    Aurell, Mattias
    Guidi, Gian Cesare
    Melander, Olle
    Novel mutations in the SLC12A3 gene causing Gitelman's syndrome in Swedes.2007In: DNA Sequence, ISSN 1042-5179, E-ISSN 1029-2365, Vol. 18, no 5, p. 395-399Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Gitelman's syndrome (GS) is an inherited autosomal recessive disorder due to loss of function mutations in the SLC12A3 gene encoding the Na-Cl co-transporter (NCCT), the target of thiazide diuretics. The defective function of the NCCT, which normally is expressed in the apical membrane of the distal convolute tubule in the kidney, leads to mild hypotension, hypokalemia, hyperreninemic hyperaldosteronism, mild metabolic alkalosis, hypomagnesemia and hypocalciuria. Up to now, more than 100 mutations of the SLC12A3 gene have been described in GS patients.

    METHODS: We have collected 30 patients from Sweden with a clinical diagnosis of GS and undertaken a mutation screening by SSCP and successive sequencing of the 26 exons and intronic boundaries. Both mutations were identified in most (n = 28, 93%) and at least one mutation was identified in all patients.

    RESULTS: We found 22 different mutations evenly distributed throughout the gene, 11 of which have not been described previously. The new variants include 8 missense mutations (Glu68Lys, His69Asn, Argl45His, Vall53Met, Gly230Asp, Gly342Ala, Val677Leu and Gly867Ser), 1 insertion (c.834_835insG on exon 6) and 2 splice-site mutations (c.2667 + lT>G substitution in splicing donor site after exon 22, c.1569-1G>A substitution in the splicing acceptor site before exon 13).

    CONCLUSION: In Swedish patients with the clinical features of GS, disease-causing mutations in the SLC12A3 gene were identified in most patients. The spectrum of GS mutations is wide making full mutation screening of the SLC12A3 gene necessary to confirm the diagnosis.

  • 9.
    Mathold, K.
    et al.
    Kalmar County Hospital.
    Wanby, Pär
    Kalmar County Hospital.
    Brudin, Lars
    Kalmar County Hospital.
    Von, S. P.
    Kalmar County Hospital.
    Carlsson, Martin
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Kalmar County Hospital.
    Alterations in bone turnover markers in patients with noncardio-embolic ischemic stroke2018In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 11, article id e0207348Article in journal (Refereed)
    Abstract [en]

    Background The major cause of ischemic stroke is unstable or thrombogenic atherosclerotic plaques. Vascular calcification, a process that appears crucial for plaque stability, shares common features with bone formation. Many bone turnover proteins exhibit metabolic properties, but the evidence is conflicting regarding their possible involvement in vascular disease. Antibodies against sclerostin and dickkopf-1 are currently being evaluated as potential therapy for treating bone disorders. It is important to carefully assess the cardiovascular and metabolic effects of these proteins. The aim of the present study was to explore serum levels of bone turnover markers in patients with acute noncardio-embolic ischemic stroke in comparison with healthy controls. Methods In a cross-sectional study, we compared 48 patients aged. 75 years with noncardio-embolic ischemic stroke and 46 healthy controls. Serum levels of dickkopf-1, sclerostin, osteoprotegerin, osteopontin and osteocalcin were determined by Luminex technique. Results We found clearly increased serum levels of osteoprotegerin, sclerostin, dickkopf-1 and osteopontin in patients with stroke compared with healthy controls. No difference was seen in serum levels of osteocalcin between the two groups. Conclusion Our findings strengthen the hypothesis of bone turnover markers being involved in vascular disease. Whether these proteins can be used as candidate markers for increased stroke risk or prognostic biomarkers remains to be further elucidated.

  • 10.
    Nordqvist, Ola
    et al.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. Region Kalmar County, Sweden.
    Lönnbom Svensson, Ulrika
    Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences.
    Brundin, Lars
    County Hospital Kalmar, Sweden;Linköping university, Sweden.
    Wanby, Pär
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. County Hospital Kalmar, Sweden.
    Carlsson, Martin
    Linnaeus University, Faculty of Health and Life Sciences, Department of Medicine and Optometry. County Hospital Kalmar, Sweden.
    Adherence to risk management guidelines for drugs which cause vitamin D deficiency – big data from the Swedish health system2019In: Drug, Healthcare and Patient Safety, ISSN 1179-1365, E-ISSN 1179-1365, Vol. 11, p. 19-28Article in journal (Refereed)
    Abstract [en]

    Purpose: Several medications are known to cause vitamin D deficiency. The aim of this study is to describe vitamin D testing and supplementation in patients using these “risk medications”, thereby assessing adherence to medical guidelines.Patients and methods: A database with electronic health records for the population in a Swedish County (≈240,000 inhabitants) was screened for patients prescribed the pre-defined “risk medications” during a 2-year period (2014–2015). In total, 12,194 patients were prescribed “risk medications” pertaining to one of the three included pharmaceutical groups. Vitamin D testing and concomitant vitamin D supplementation, including differences between the included pharmaceutical groups, was explored by matching personal identification numbers.Results: Corticosteroids were prescribed to 10,003 of the patients, antiepileptic drugs to 1,101, and drugs mainly reducing vitamin D uptake to 864. Two hundred twenty-six patients were prescribed >1 “risk medication”. Seven hundred eighty-seven patients (6.5%) had been tested during the 2-year period. There were no differences regarding testing frequency between groups. Concomitant supplements were prescribed to 3,911 patients (32.1%). It was more common to be prescribed supplements when treated with corticosteroids. Vitamin D supplementation was more common among tested patients in all three groups. Women were tested and supplemented to a higher extent. The mean vitamin D level was 69 nmol/L. Vitamin D deficiency was found in 24.1% of tested patients, while 41.3% had optimal levels. It was less common to be deficient and more common to have optimal levels among patients prescribed corticosteroids.Conclusion: Adherence to medical guidelines comprising testing and supplementation of patients prescribed drugs causing vitamin D deficiency needs improvement in Sweden.

  • 11.
    Wanby, Pär
    Kalmar County Hospital, Sweden.
    On certain genetic and metabolic risk factors for carotid stenosis and stroke2006Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    The present study evaluated genetic and metabolic factors influencing the risk of acute cerebrovascular disease (CVD) and internal carotid artery stenosis (ICA stenosis) in a Swedish community. The threonine (T) containing protein of the FABP2 A54T gene polymorphism has a greater affinity for long chain fatty acids (FFAs) than the alanine (A) containing protein. This altered affinity for FFAs has been shown to affect the intestinal absorption of fatty acids and consequently the fatty acid composition of serum lipids, in particularly postprandially. Endothelium derived NO is a potent vasodilator and antiatherogenic agent. Asymmetric dimethyl arginine (ADMA) is an endogenous competitive inhibitor of endothelial nitric oxide synthase (eNOS). ADMA has been shown to be involved in the pathogenesis of atherosclerotic disease, and ADMA inhibits eNOS by displacement of L-arginine from the enzyme, which in turn is believed to affect the amount of NO available within the endothelium.

    The FABP2 A54T gene polymorphism was analyzed in 407 patients with acute CVD and also in a subset of these patients whose carotids had been evaluated with ultrasound. Both the FABP2 polymorphism and a common polymorphism of the eNOS gene, Glu298Asp, were analyzed in a different population consisting of 54 matched pairs of patients with ICA stenosis and controls. ADMA levels were measured in both study populations.

    We found that the T54 allele was more frequent in patients with transient ischaemic attacks (TIA), and that the TT genotype was more prevalent in young, non-smoking patients with CVD than in controls.

    Increased concentrations of ADMA were observed in cardio-embolic infarction and TIA, but not significantly in non-cardio-embolic infarction nor in haemorrhagic stroke. In multivariate logistic regression models, CVD increased across quartiles of ADMA in all subgroups, but this association was only significant in the TIA group. A decreased arginine/ADMA ratio, a measure of NO availability was associated with CVD in the entire study population. Patients with severe carotid stenosis had significantly higher ADMA levels than the controls. Allele and genotype frequencies of the FABP2 and eNOS polymorphisms did not differ between patients with ICA stenosis and controls.

    Our results indicate that ADMA is a strong marker for TIA and severe ICA stenosis, and that relative defiency of arginine, measured as L-arginine/ADMA, is present in acute CVD.

    We also conclude that a common polymorphism of the FABP2 gene increases susceptibility to ischaemic stroke and TIA.

  • 12.
    Wanby, Pär
    et al.
    Kalmar County Hospital, Sweden.
    Berglund, J.
    University Hospital of Linköping, Sweden.
    Brudin, L.
    Kalmar County Hospital, Sweden.
    Hedberg, D.
    Kalmar County Hospital, Sweden.
    Carlsson, Martin
    Kalmar County Hospital, Sweden.
    Increased ferritin levels in patients with anorexia nervosa: impact of weight gain.2016In: Eating and Weight Disorders, ISSN 1124-4909, E-ISSN 1590-1262, Vol. 21, no 3, p. 411-417Article in journal (Refereed)
    Abstract [en]

    PURPOSE: A few recent studies have found elevated ferritin levels in patients with anorexia nervosa (AN), indicating ferritin as a potential biomarker of disease severity. The purpose of this study was to study how body mass index (BMI) and changes in BMI affect plasma ferritin concentrations in Swedish patients with eating disorders.

    MATERIALS AND METHODS: In a retrospective computer search from 2009 to 2014, 662 patients with an eating disorder were identified from more than 200,000 individuals with electronic medical records. Three hundred and eighty-nine patients (374 females and 15 males) were found to have at least one p-ferritin value with a corresponding BMI value. Patients with AN were compared to a combined group consisting of patients with bulimia nervosa (BN) and patients with an eating disorder not otherwise specified (EDNOS).

    RESULTS: Patients with AN had lower BMI compared to the combined group of patients with other eating disorders (BMI = 16.5 ± 1.5, n = 77 vs. 21.0 ± 4.7, n = 312, p < 0.001). Patients with AN also had higher plasma ferritin levels (median 42 μg/L (range 3.3-310) vs. 31 μg/L (range 2.8-280); p < 0.001). As BMI increased in patients with AN, ferritin levels decreased (from a median of 40 μg/L (7-400) to 26 (4-170), n = 47; p < 0.001).

    DISCUSSION: Measuring ferritin in patients with AN could be valuable in monitoring improvements of nutritional status, but the full clinical value of following ferritin in individual patients has yet to be determined. The study also shows how research can benefit from electronically captured clinical data using electronic health records.

  • 13.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Brattström, L
    Brudin, L
    Hultberg, B
    Teerlink, T
    Asymmetric dimethylarginine and total homocysteine in plasma after oral methionine loading.2003In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 63, no 5, p. 347-353Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Elevation of homocysteine (Hcy) and asymmetric dimethylarginine (ADMA) in plasma are believed to be involved in the pathogenesis of cardiovascular disease (CVD). In humans, oral methionine loading results in acute elevation of plasma Hcy. This is associated with impaired NO-dependent vasodilatation, a mechanism that may explain the relationship between elevated Hcy and risk of CVD. ADMA, an endogenous competitive inhibitor of NO-synthase, may be elevated in plasma of patients with CVD. It was proposed that ADMA is synthesized in a methionine-dependent reaction which also forms Hcy. In this study plasma total homocysteine (tHcy) and ADMA concentrations were measured before and after oral methionine loading of human subjects.

    METHODS: Plasma tHcy and ADMA levels were measured in 12 healthy males (age 32-58 years) before and after oral loading with L-methionine (100 mg/kg body weight in orange juice).

    RESULTS: At noon, 4 h after methionine loading, tHcy and ADMA levels (35.4 +/- 10.9 and 0.80 +/- 0.13 micromol/L, mean +/- SD) were significantly higher than the corresponding values obtained at noon the day before (15.6 +/- 7.4 and 0.63 +/- 0.10 micromol/L, both p<0.001). Noon values 4 h after methionine loading were also significantly higher than values obtained immediately before the methionine load (13.7 +/- 5.9 and 0.66 +/- 0.10 micromol/L, both p<0.001). Reinvestigation of 8 of 12 subjects showed that at 4 and 8 h after compared with levels immediately before methionine loading there was a significant increase in tHcy (28.4 +/- 10.2 and 33.45 +/- 11.1 vs. 10.8 +/- 3.3 micromol/L, both p<0.001). However, the corresponding ADMA levels did not increase (0.73 +/- 0.17 and 0.76 +/- 0.22 vs. 0.70 +/- 0.10 micromol/L, both not significant).

    CONCLUSIONS: No clear evidence was found to support the supposition that methionine-induced hyperhomocysteinaemia may be accompanied by elevated levels of ADMA, an endogenous competitive NO-synthase inhibitor that may represent an alternative pathogenic mechanism for homocysteine-associated impairment of endothelial NO-dependent functions.

  • 14.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Nilsson, I
    Brudin, L
    Nyhammar, I
    Gustafsson, I
    Carlsson, Martin
    Increased plasma levels of asymmetric dimethylarginine in patients with carotid stenosis: no evidence for the role of the common FABP2 A54T gene polymorphism.2007In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 115, no 2, p. 90-96Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Both asymmetric dimethylarginine (ADMA), which is an inhibitor of endothelial nitric oxide synthase and the fatty acid-binding protein 2 (FABP2) A54T gene polymorphism have been associated with cerebrovascular disease. The objective of the present study was to investigate the role of ADMA and the FABP2 A54T polymorphism in carotid atherosclerosis.

    MATERIAL AND METHODS: 54 patients with severe carotid stenosis and 54 matched controls without significant carotid stenosis were compared. ADMA was analysed with an ELISA method. The FABP2 A54T polymorphism was determined with a polymerase chain reaction-restriction fragment length polymorphism technique.

    RESULTS: Patients with carotid stenosis had higher ADMA levels (0.76 +/- 0.16 micromol/l) than the controls (0.70 +/- 0.14 micromol/l, P < 0,01). Allele and genotype frequencies of the FABP2 polymorphism did not differ between patients and controls.

    CONCLUSIONS: ADMA levels in subjects with carotid stenosis are increased which emphasize the role of ADMA as a novel risk factor for atherosclerosis and future cardiovascular risk. The FABP2 A54T polymorphism is not associated with severe carotid stenosis.

  • 15.
    Wanby, Pär
    et al.
    Kalmar County Hospital, Sweden.
    Nobin, R
    Kalmar County Hospital, Sweden.
    Von, S-P
    Kalmar County Hospital, Sweden.
    Brudin, L
    Kalmar County Hospital, Sweden.
    Carlsson, Martin
    Kalmar County Hospital, Sweden.
    Serum levels of the bone turnover markers dickkopf-1, sclerostin, osteoprotegerin, osteopontin, osteocalcin and 25-hydroxyvitamin D in Swedish geriatric patients aged 75 years or older with a fresh hip fracture and in healthy controls.2016In: Journal of Endocrinological Investigation, ISSN 0391-4097, E-ISSN 1720-8386, Vol. 39, no 8, p. 855-863Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Bone turnover markers have a potential clinical use in describing bone remodeling and in predicting fractures.

    AIMS: In an elderly population ≥75 years with a fresh hip fracture, and in healthy controls, investigate bone turnover markers and their relation to each other, to vitamin D status and to bone mineral density (BMD).

    METHODS: In a cross-sectional study serum levels of dickkopf-1 (DKK-1), sclerostin (SOST), osteoprotegerin (OPG), osteopontin (OPN), osteocalcin, 25-hydroxyvitamin D (25(OH)D) were analyzed in 89 Swedish patients with a fresh hip fracture and in 82 healthy volunteers. Serum levels of bone markers were determined by Luminex technique.

    RESULTS: S-25-hydroxyvitamin D (S-25(OH)D) was decreased in patients compared to controls (48 ± 21 vs. 76 ± 25 nmol/L, p < 0.001). SOST, but none of the other bone turnover markers correlated with BMD (r = 0.50, p < 0.001). Compared with controls, higher levels of OPG (488 ± 1.4 vs. 191 ± 1.4 ng/L, p < 0.001), OPN (69 ± 1.7 vs. 19 ± 1.4 µg/L, p < 0.001), DKK-1 (273 ± 1.7 vs. 168 ± 1.7 ng/L, p < 0.001), and lower levels of osteocalcin (5.8 ± 3.5 vs. 9.5 ± 3.6 µg/L, p < 0.001), were found in the fracture group. Levels of OPG, DKK-1 and SOST in both groups were positively associated. S-25(OH)D concentration was not found to be strongly associated with any of the bone markers.

    CONCLUSIONS: In contrast to findings in other studies, we found no strong correlation between 25(OH)D and the investigated bone markers. Both in patients with a fresh hip fracture and in healthy elderly, DKK-1, SOST and OPG appear to be associated. This suggests a relevance in these relationships meriting further investigation.

  • 16.
    Wanby, Pär
    et al.
    Kalmar County Hospital, Sweden.
    Olsen, Björn
    Kalmar County Hospital, Sweden.
    Myocarditis in a patient with salmonella and campylobacter enteritis.2001In: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, E-ISSN 1651-1980, Vol. 33, no 11, p. 860-862Article in journal (Refereed)
    Abstract [en]

    Myocarditis associated with bacterial enteritis has only rarely been described and the pathogenesis is unclear. Herein we report a case where a young adult developed myocarditis during the acute stage of an infection with Salmonella heidelberg and Campylobacter jejunii/coli. The patient's troponin I value was elevated. We suggest that use of cardiac-sensitive troponins may be a useful tool for diagnosis of acute myocarditis in the context of bacterial enteritis. We also suggest the need for further investigation of the pathogenesis of myocarditis associated with enteric pathogens.

  • 17.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Palmquist, P
    Rydén, I
    Brattström, L
    Carlsson, Martin
    The FABP2 gene polymorphism in cerebrovascular disease.2004In: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404, Vol. 110, no 6, p. 355-360Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Earlier studies have shown that the fatty acid binding protein 2 (FABP2) T54 allele is associated with dyslipidemia, which in turn correlates with the incidence of cerebrovascular disease (CVD). To assess whether the FABP2 gene A54T polymorphism is associated with an increased risk of CVD we undertook a case-control study.

    MATERIALS AND METHODS: A total of 407 patients diagnosed with acute CVD and 158 control subjects were genotyped for the A54T polymorphism using a PCR-RFLP method.

    RESULTS: Allele and genotype frequencies of the FABP2 A54T polymorphism did not differ between subjects with acute CVD (TT, 9.6%; TA, 41.0%; AA, 49.4%) and controls (TT, 7.6%; TA, 41.1%; AA, 51.3%; P = ns) or in the following subgroups of CVD compared with controls: non-cardioembolic infarction (n = 252), intracerebral hemorrhage (n = 23), and cardioembolic infarction (n = 91). In transient ischemic attacks (TIAs) (n = 41) the combined TT and TA genotype frequency (TT + TA, 65.9%) was more frequent than in controls (48.7%) (P = 0.05). Furthermore, the TT genotype was more frequent in non-smoking patients under the age of 70 (n = 77) with a non-cardioembolic infarction (TT, 18.2%) compared with controls (7.6%) (P = 0.024).

    CONCLUSIONS: Our findings suggest an involvement of the FABP2 (A54T) gene polymorphism in the pathogenesis of CVD. The FABP2 T54 allele appears to be a genetic susceptibility marker for TIA and non-cardioembolic infarction at younger onset.

  • 18.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Palmquist, Petter
    Brudin, Lars
    Carlsson, Martin
    Genetic variation of the intestinal fatty acid-binding protein 2 gene in carotid atherosclerosis.2005In: Vascular Medicine, ISSN 1358-863X, E-ISSN 1477-0377, Vol. 10, no 2, p. 103-108Article in journal (Refereed)
    Abstract [en]

    The alanine (A) to threonine (T) substitution at codon 54 of the intestinal fatty acid-binding protein 2 (FABP2) has been associated with dyslipidaemia and other characteristics of the metabolic syndrome, which in turn is a risk factor for cerebrovascular disease. The aim of this study was to investigate whether the A54T polymorphism in the FABP2 gene is associated with internal carotid artery (ICA) stenosis in stroke patients. Swedish subjects initially diagnosed with acute cerebrovascular disease (n=196) that had been assessed with ultrasound of the carotid arteries were identified and grouped depending on whether a stenosis was found. The subjects were genotyped for the A54T polymorphism using a PCR-RFLP method. In a multivariate logistic-regression analysis, where known risk factors for atherosclerosis were fixed (diabetes, systolic blood pressure, age and smoking), having the FABP2 T allele was a significant risk factor for ICA stenosis (odds ratio 2.9; 95% confidence interval, 1.1-7.7; p = 0.04) together with diabetes (odds ratio 4.9; 95% confidence interval, 1.8-14; p < 0.01). Age, smoking and blood pressure did not reach statistical significance. In conclusion, our result supports the hypothesis that the FABP2 A54T polymorphism is associated with ICA stenosis.

  • 19.
    Wanby, Pär
    et al.
    Region Kalmar län.
    Teerlink, T
    Brudin, L
    Brattström, L
    Nilsson, I
    Palmqvist, P
    Carlsson, Martin
    Asymmetric dimethylarginine (ADMA) as a risk marker for stroke and TIA in a Swedish population.2006In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 185, no 2, p. 271-277Article in journal (Refereed)
    Abstract [en]

    Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has been shown to be involved in the pathogenesis of atherosclerosis. The present study was initiated to investigate the role of ADMA as a risk marker of acute cerebrovascular disease (CVD). We examined 363 CVD patients and 48 controls. The ADMA concentration (mean+/-S.D., mumol/L) in controls was 0.50 +/- 0.06. Compared to controls, increased concentrations of ADMA were observed in cardio-embolic infarction (0.55 +/- 0.08; p < 0.001; n = 71), and TIA (0.54 +/-0 .05; p < 0.001; n = 31), but not in non-cardio-embolic infarction (0.51 +/- 0.07; p = 0.56; n = 239) and haemorrhagic stroke (0.51 +/- 0.11; p = 0.77; n = 22). In multivariate logistic regression models, CVD increased across quartiles of ADMA in all subgroups, but this association was only significant in the TIA group (odds ratio for highest versus lowest quartile 13.1; 95% CI: 2.9-58.6; p trend 0.001) A decreased arginine/ADMA ratio was significantly associated with CVD in the entire study population (p < 0.01). Our results indicate that ADMA is a weak independent marker for acute stroke and a strong marker for TIA and that relative arginine deficiency, measured as the l-arginine/ADMA ratio, is present in acute CVD.

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