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| 4. |
- Adami, HO, et al.
(författare)
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Time to abandon early detection cancer screening
- 2019
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Ingår i: European journal of clinical investigation. - : Wiley. - 1365-2362 .- 0014-2972. ; 49:3, s. e13062-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Akrawi, Delshad Saleh, et al.
(författare)
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Heritability of glomerulonephritis : A Swedish adoption study
- 2019
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 49:8
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Tidskriftsartikel (refereegranskat)abstract
- Background: Glomerulonephritis clusters in families. However, infections are common inducers of glomerulonephritis and may also cluster in families. Studies of adoptees and their biological and adoptive parents may disentangle genetic from environmental causes of familial clustering. This is the first adoption study aimed to estimate the genetic contribution to the familial transmission of glomerulonephritis. Materials and methods: We performed a family study for Swedish-born adoptees (born 1945–2000) and their biological and adoptive parents. The Swedish Multi-Generation Register was linked to the Hospital Inpatient Register for the period 1964–2012 and the Hospital Outpatient Register for 2001–2012. Odds ratio (OR) for glomerulonephritis was determined for adoptees with a biological parent with glomerulonephritis compared with adoptees without an affected biological parent. Similarly, the OR for glomerulonephritis was also determined in adoptees with an affected adoptive parent compared with adoptees without an affected adoptive parent. Heritability was estimated to be twice the observed tetrachoric correlation among adoptees and biological parents, under the assumption that only additive genetic factors contribute to the similarity between biological parents and adoptees. Results: The OR for glomerulonephritis was 4.08 in adoptees (95% confidence interval [CI] 1.79-9.27, P-value = 0.001) of biological parents diagnosed with glomerulonephritis. The OR for glomerulonephritis was 1.67 in adoptees (95% CI 0.53-5.26, P-value = 0.380) of adoptive parents diagnosed with glomerulonephritis. The heritability was 48%. Conclusion: Family history of glomerulonephritis in a biological parent is a risk factor for glomerulonephritis. The present study indicates that genetic factors play an important role in the aetiology of glomerulonephritis.
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| 7. |
- Al-Ani, Amer, et al.
(författare)
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Low bone mineral density and fat free mass in young and middle-aged patients with a femoral neck fracture
- 2015
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 45:8, s. 800-806
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundReduced bone mineral density (BMD) together with muscle wasting and dysfunction, that is sarcopenia, emerges as a risk factor for hip fracture. The aim of this study was to examine body composition and BMD and their relationship with trauma mechanisms in young and middle-aged patients with femoral neck fracture.Materials and methodsAltogether, 185 patients with femoral neck fracture aged 20–69 were included. BMD, body composition and fat-free mass index (FFMI) were determined by dual-X-ray absorptiometry (DXA), and trauma mechanisms were registered.ResultsNinety per cent of the whole study population had a femoral neck BMD below the mean for age. In the young patients (< 50 years), 27% had a Z-score of BMD ≤ −2 SD. More than half of the middle-aged patients (50–69 years) had osteopenia, that is T-score −1 to −2·5, and 35% had osteoporosis, that is T-score < −2·5, at the femoral neck. Patients with low-energy trauma, sport injury or high-energy trauma had a median standardised BMD of 0·702, 0·740 vs. 0·803 g/cm2 (P = 0·03), and a median FFMI of 15·9, 17·7 vs. 17·5 kg/m2 (P < 0·001), respectively. FFMI < 10th percentile of an age- and gender-matched reference population was observed in one-third.ConclusionsA majority had low BMD at the femoral neck, and one-third had reduced FFMI (i.e. sarcopenia). Patients with fracture following low-energy trauma had significantly lower femoral neck BMD and FFMI than patients with other trauma mechanisms. DXA examination of both BMD and body composition could be of value especially in those with low-energy trauma.
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| 8. |
- Al-Ani, Amer N., et al.
(författare)
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Low bone mineral density and fat-free mass in younger patients with a femoral neck fracture
- 2015
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 45:8, s. 800-806
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Tidskriftsartikel (refereegranskat)abstract
- Background Reduced bone mineral density (BMD) together with muscle wasting and dysfunction, that is sarcopenia, emerges as a risk factor for hip fracture. The aim of this study was to examine body composition and BMD and their relationship with trauma mechanisms in young and middle-aged patients with femoral neck fracture. Materials and methods Altogether, 185 patients with femoral neck fracture aged 20-69 were included. BMD, body composition and fat-free mass index (FFMI) were determined by dual-X-ray absorptiometry (DXA), and trauma mechanisms were registered. Results Ninety per cent of the whole study population had a femoral neck BMD below the mean for age. In the young patients (<50years), 27% had a Z-score of BMD-2 SD. More than half of the middle-aged patients (50-69years) had osteopenia, that is T-score -1 to -25, and 35% had osteoporosis, that is T-score<-25, at the femoral neck. Patients with low-energy trauma, sport injury or high-energy trauma had a median standardised BMD of 0702, 0740 vs. 0803g/cm(2) (P=003), and a median FFMI of 159, 177 vs. 175kg/m(2) (P<0001), respectively. FFMI<10th percentile of an age- and gender-matched reference population was observed in one-third. Conclusions A majority had low BMD at the femoral neck, and one-third had reduced FFMI (i.e. sarcopenia). Patients with fracture following low-energy trauma had significantly lower femoral neck BMD and FFMI than patients with other trauma mechanisms. DXA examination of both BMD and body composition could be of value especially in those with low-energy trauma.
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| 10. |
- Almquist, T., et al.
(författare)
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Lipid-lowering treatment and inflammatory mediators in diabetes and chronic kidney disease
- 2014
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 44:3, s. 276-284
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Tidskriftsartikel (refereegranskat)abstract
- Background: Inflammation may contribute to the high cardiovascular risk in diabetes mellitus (DM) and chronic kidney disease (CKD). Monocyte chemoattractant protein-1 (MCP-1) facilitates the recruitment of monocytes into atherosclerotic lesions and is involved in diabetic nephropathy. Interferon gamma (IFNγ) is important in atherosclerosis and increases the synthesis of chemokines including MCP-1. Lipid-lowering treatment (LLT) with statins may have anti-inflammatory effects, and ezetimibe cotreatment provides additional cholesterol lowering. Methods: After a placebo run-in period, the effects of simvastatin alone (S) or simvastatin + ezetimibe (S+E) were compared in a randomized, double-blind, cross-over study on inflammatory parameters. Eighteen DM patients with estimated glomerular filtration rate (eGFR) 15-59 mL/min × 1·73 m2 (CKD stages 3-4) (DM-CKD) and 21 DM patients with eGFR > 75 mL/min (DM only) were included. Results: At baseline, monocyte chemoattractant protein 1 (MCP-1) (P = 0·03), IFNγ (P = 0·02), tumour necrosis factor-α (TNFα) (P < 0·01) and soluble vascular adhesion molecule (sVCAM) (P = 0·001) levels were elevated in DM-CKD compared with DM-only patients. LLT with S and S+E reduced MCP-1 levels (P < 0·01 by anova) and IFNγ levels (P < 0·01) in DM-CKD patients but not in DM-only patients. Reductions were most pronounced with the combination treatment. Conclusions: DM patients with CKD stages 3-4 had increased inflammatory activity compared with DM patients with normal GFR. Lipid-lowering treatment decreased the levels of MCP-1 and IFNγ in DM patients with concomitant CKD, which may be beneficial with regard to the progression of both atherosclerosis and diabetic nephropathy.
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| 19. |
- Axelsen, Mette, 1965, et al.
(författare)
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Suppression of the nocturnal free fatty acid levels by bedtime cornstarch in NIDDM subjects.
- 1997
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Ingår i: European journal of clinical investigation. - 0014-2972. ; 27:2, s. 157-63
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to examine the effects of a large dose of slow-release carbohydrates (CHOs) at bedtime on the nocturnal glucose, insulin and free fatty acid (FFA) levels, and to assess the putative effects on morning fasting and post-prandial glucose levels in patients with moderately controlled non-insulin-dependent diabetes mellitus (NIDDM). Unheated cornstarch (106 g of CHO) or a mixed equicaloric meal (58 g of CHO) was given at 22.00 hours to 10 NIDDM patients. For comparison, the patients were also given a smaller mixed meal at 22.00 hours on a third occasion (17 g of CHO). Compared with the mixed meals, cornstarch led to a slightly elevated early-morning plasma insulin level and a suppression of the nocturnal FFA level (P < 0.05), as well as to a reduced incremental glucose level (IAUC) after breakfast the next morning by approximately 30% (P < 0.05). There was a significant and linear relationship between the nocturnal FFA level and the glucose IAUC after breakfast (r = 0.44, P < 0.02), indicating that the effect may have been mediated by the suppressive effect of cornstarch on nocturnal lipolysis. In summary, bedtime intake of unheated cornstarch in NIDDM subjects is associated with a suppression of the nocturnal FFA levels and a reduced glucose IAUC after breakfast. As the treatment did not improve overall glucose control, studies of the effects of an individually titrated amount of cornstarch are proposed to further explore the putative favourable effects of bedtime cornstarch in the treatment of NIDDM.
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| 20. |
- Barathan, Muttiah, et al.
(författare)
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Increased frequency of late-senescent T cells lacking CD127 in chronic hepatitis C disease
- 2015
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 45:5, s. 466-474
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundHepatitis C virus (HCV) causes persistent disease in similar to 85% of infected individuals, where the viral replication appears to be tightly controlled by HCV-specific CD8+ T cells. Accumulation of senescent T cells during infection results in considerable loss of functional HCV-specific immune responses. Materials and methodsWe characterized the distinct T-cell phenotypes based on the expression of costimulatory molecules CD28 and CD27, senescence markers PD-1 and CD57, chronic immune activation markers CD38 and HLA-DR, and survival marker CD127 (IL-7R) by flow cytometry following activation of T cells using HCV peptides and phytohemagglutinin. ResultsHCV-specific CD4+ and CD8+ T cells from chronic HCV (CHC) patients showed increased expression of PD-1. Furthermore, virus-specific CD4+ T cells of CHC-infected subjects displayed relatively increased expression of HLA-DR and CD38 relative to HCV-specific CD8+ T cells. The CD4+ and CD8+ T cells from HCV-infected individuals showed significant increase of late-differentiated T cells suggestive of immunosenescence. In addition, we found that the plasma viral loads positively correlated with the levels of CD57 and PD-1 expressed on T cells. ConclusionsChronic HCV infection results in increased turnover of late-senescent T cells that lack survival potentials, possibly contributing to viral persistence. Our findings challenge the prominence of senescent T-cell phenotypes in clinical hepatitis C infection.
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| 21. |
- Barathan, Muttiah, et al.
(författare)
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Peripheral loss of CD8(+)CD161(++)TCRV7 center dot 2(+) mucosal-associated invariant T cells in chronic hepatitis C virus-infected patients
- 2016
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Ingår i: European Journal of Clinical Investigation. - : WILEY-BLACKWELL. - 0014-2972 .- 1365-2362. ; 46:2, s. 170-180
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundMucosal-associated invariant T (MAIT) cells play an important role in innate host defence. MAIT cells appear to undergo exhaustion and are functionally weakened in chronic viral infections. However, their role in chronic hepatitis C virus (HCV) infection remains unclear. Materials and methodsWe investigated the frequency of CD8(+)CD161(++)TCR V7.2(+) MAIT cells in a cross-sectional cohort of chronic HCV-infected patients (n = 25) and healthy controls (n = 25). Peripheral blood mononuclear cells were investigated for circulating MAIT cell frequency, liver-homing (CCR5 and CD103), biomarkers of immune exhaustion (PD-1, TIM-3 and CTLA-4), chronic immune activation (CD38 and HLA-DR), and immunosenescence (CD57) by flow cytometry. ResultsThe frequency of MAIT cells was significantly decreased, and increased signs of immune exhaustion and chronic immune activation were clearly evident on MAIT cells of HCV-infected patients. Decrease of CCR5 on circulating MAIT cells is suggestive of their peripheral loss in chronic HCV-infected patients. MAIT cells also showed significantly increased levels of HLA-DR, CD38, PD-1, TIM-3 and CTLA-4, besides CD57 in chronic HCV disease. ConclusionsImmune exhaustion and senescence of CD8(+)CD161(++)TCR V7.2(+) MAIT cells could contribute to diminished innate defence attributes likely facilitating viral persistence and HCV disease progression.
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| 22. |
- Barros, H, et al.
(författare)
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Arachidonic acid absorption in human jejunum in organ culture : effects of ethanol
- 1990
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972. ; 20:5, s. 10-506
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Tidskriftsartikel (refereegranskat)abstract
- Human jejunal tissue obtained by peroral biopsy was cultured in control medium and in medium containing 100 mmol l-1 ethanol. Subsequently, the incorporation and metabolism of [3H]-arachidonic and [14C]-linoleic acid were evaluated. Of the two fatty acids a significantly higher amount of [3H]-arachidonic acid was incorporated into phospholipids and more [14C]-linoleic acid was incorporated into triacylglycerols. This preferential distribution of the labelled fatty acids was not affected by ethanol, but when ethanol was present in the tissue culture medium, there was a significant decrease in the incorporation of both fatty acids into tissue phospholipids. The study thus shows that ethanol in moderate concentrations can affect human jejunal absorption and metabolism of polyenoic fatty acids, contributing to a decrease in the amount of eicosanoid precursors available in jejunal tissue.
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| 23. |
- Belfrage, Per, et al.
(författare)
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Alterations of lipid metabolism in healthy volunteers during long-term ethanol intake
- 1977
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 7:2, s. 127-131
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Tidskriftsartikel (refereegranskat)abstract
- Nine young, healthy male volunteers were given ethanol (75 g/day) for 5 weeks. The ethanol was divided into five daily doses and taken so that blood ethanol levels never exceeded 0.04% (w/v). During the latter part of the ethanol intake period, there was a significant, transient increase of plasma triglyceride (TG) concentrations followed by reduction to normal levels. A three-fold increase of lipoprotein lipase activity (LLA) occurred in biopsy specimens of adipose tissue. An increase of alpha-lipoprotein concentrations, which correlated significantly with the decrease in plasma TG levels and the increase in adipose LLA, was also observed during the ethanol intake period. No changes were observed in plasma cholesterol and beta-lipoprotein levels. A transient, three-fold increase of TG concentrations occurred in liver biopsy specimens. Ultrastructural and cytochemical examinations of the biopsy specimens showed hyperplasia of the smooth endoplasmic reticulum, and increased canallicular activity of gamma-glutamyl transferase (gamma-GT) activity in most subjects towards the end of and after the ethanol intake period. Serum gamma-GT levels also increased significantly.
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| 29. |
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| 30. |
- Bovo, Roberto, et al.
(författare)
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Hearing impairment in the Sturge-Weber syndrome
- 2009
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Ingår i: European Journal of Clinical Investigation. - Oxford, UK : Wiley-Blackwell Publishing Inc.. - 0014-2972 .- 1365-2362. ; 39:9, s. 837-838
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Tidskriftsartikel (refereegranskat)
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| 31. |
- Brinck, Jonas W., et al.
(författare)
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High-density lipoprotein from end-stage renal disease patients exhibits superior cardioprotection and increase in sphingosine-1-phosphate
- 2018
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 48:2
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Tidskriftsartikel (refereegranskat)abstract
- Background: Chronic kidney disease (CKD) exacerbates the risk of death due to cardiovascular disease (CVD). Modifications to blood lipid metabolism which manifest as increases in circulating triglycerides and reductions in high-density lipoprotein (HDL) cholesterol are thought to contribute to increased risk. In CKD patients, higher HDL cholesterol levels were not associated with reduced mortality risk. Recent research has revealed numerous mechanisms by which HDL could favourably influence CVD risk. In this study, we compared plasma levels of sphingosine-1-phosphate (S1P), HDL-associated S1P (HDL-S1P) and HDL-mediated protection against oxidative stress between CKD and control patients. Methods: High-density lipoprotein was individually isolated from 20 CKD patients and 20 controls. Plasma S1P, apolipoprotein M (apoM) concentrations, HDL-S1P content and the capacity of HDL to protect cardiomyocytes against doxorubicin-induced oxidative stress in vitro were measured. Results: Chronic kidney disease patients showed a typical profile with significant reductions in plasma HDL cholesterol and albumin and an increase in triglycerides and pro-inflammatory cytokines (TNF-alpha and IL-6). Unexpectedly, HDL-S1P content (P = .001) and HDL cardioprotective capacity (P = .034) were increased significantly in CKD patients. Linear regression analysis of which factors could influence HDL-S1P content showed an independent, negative and positive association with plasma albumin and apoM levels, respectively. Discussion: The novel and unexpected observation in this study is that uremic HDL is more effective than control HDL for protecting cardiomyocytes against oxidative stress. It is explained by its higher S1P content which we previously demonstrated to be the determinant of HDL-mediated cardioprotective capacity. Interestingly, lower concentrations of albumin in CKD are associated with higher HDL-S1P.
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| 32. |
- Börschel, Christin S., et al.
(författare)
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Risk prediction of atrial fibrillation and its complications in the community using hs troponin I
- 2023
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Ingår i: European Journal of Clinical Investigation. - : John Wiley & Sons. - 0014-2972 .- 1365-2362. ; 53:5
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Atrial fibrillation (AF) is becoming increasingly common. Traditional cardiovascular risk factors (CVRF) do not explain all AF cases. Blood-based biomarkers reflecting cardiac injury such as high-sensitivity troponin I (hsTnI) may help close this gap.Methods: We investigated the predictive ability of hsTnI for incident AF in 45,298 participants (median age 51.4 years, 45.0% men) across European community cohorts in comparison to CVRF and established biomarkers (C-reactive protein, N-terminal pro B-type natriuretic peptide).Results: During a median follow-up of 7.7 years, 1734 (3.8%) participants developed AF. Those in the highest hsTnI quarter (≥4.2 ng/L) had a 3.91-fold (95% confidence interval (CI) 3.30, 4.63; p <.01) risk for developing AF compared to the lowest quarter (<1.4 ng/L). In multivariable-adjusted Cox proportional hazards models a statistically significant association was seen between hsTnI and AF (hazard ratio (HR) per 1 standard deviation (SD) increase in log10(hsTnI) 1.08; 95% CI 1.01, 1.16; p =.03). Inclusion of hsTnI did improve model discrimination (C-index CVRF 0.811 vs. C-index CVRF and hsTnI 0.813; p <.01). Higher hsTnI concentrations were associated with heart failure (HR per SD 1.37; 95% CI 1.12, 1.68; p <.01) and overall mortality (HR per SD 1.24; 95% CI 1.09, 1.41; p <.01).Conclusion: hsTnI as a biomarker of myocardial injury does not improve prediction of AF incidence beyond classical CVRF and NT-proBNP. However, it is associated with the AF-related disease heart failure and mortality likely reflecting underlying subclinical cardiovascular impairment.
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| 33. |
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| 34. |
- Carlstedt, F., et al.
(författare)
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Serum levels of parathyroid hormone are related to the mortality and severity of illness in patients in the emergency department
- 1997
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 27:12, s. 977-981
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Tidskriftsartikel (refereegranskat)abstract
- Hypocalcaemia is a common finding in intensive care patients. In addition, raised levels of parathyroid hormone (PTH) have been described. The explanation and clinical importance of these findings are yet to be revealed. To investigate the occurrence of hypocalcaemia and elevated PTH levels and their relationship to morality and the severity of disease, serum levels of PTH, ionized calcium (Ca2+) and the cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) were measured on arrival in the emergency department in a broad spectrum of 140 acutely ill patients patients suffering from common diseases such as stroke, acute abdominal disorders, obstructive lung diseases, heart failure, acute myocardial infarction, angina pectoris, trauma and infectious diseases. A score (APACHE II) was calculated to assess the severity of disease. Elevated PTH levels (> 55 pg ml-1) were seen in 16% of the patients, being most frequent in patients with myocardial infarction (28%) and congestive heart failure (42%). The levels were significantly correlated with the APACHE II score (r = 0.48, P < 0.0001) and with the length of stay in hospital (r = 0.26, P < 0.002). PTH was also significantly (P < 0.03) elevated in non-survivors compared with survivors and was found to be a stronger predictor of mortality (P < 0.01) than the APACHE II score (P < 0.02) in Cox's proportional hazard analysis. No close relationships were found between the cytokine levels and the indices of calcium metabolism. In conclusion, a rise in serum levels of PTH was common and related to the severity of disease and mortality in a mixed emergency department population.
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| 39. |
- Cretti, A., et al.
(författare)
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Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion
- 2001
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972. ; 31:5, s. 405-416
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Tidskriftsartikel (refereegranskat)abstract
- Objective To characterise the performance of beta -cell during a standard oral glucose tolerance test (OGTT). Design Fifty-six subjects were studied. A minimal analogic model of beta -cell secretion during the OGTT was applied to all OGTTs (see below). The amount of insulin secreted over 120' in response to oral glucose (OGTT-ISR; Insulin Units 120'(-1) m(-2) BSA) and an index of beta -cell secretory 'force' (beta -lndex; pmol.min(-2).m(-2) BSA) were computed with the aid of the model. In protocol A, 10 healthy subjects underwent two repeat 75 g OGTT with frequent (every 10(/)-15(/)) blood sampling for glucose and C-peptide to test the reproducibility of OGTT-ISR and beta -Index with a complete or a reduced data set. In protocol B, 7 healthy subjects underwent three OGTTs (50, 100 or 150 g), to test the stability of the beta -Index under different glucose loads. In protocol C, 29 subjects (15 with normal glucose tolerance, 7 with impaired glucose tolerance and 7 with newly diagnosed type 2 diabetes) underwent two repeat 75 g OGTT with reduced (every 30' for 120') blood sampling to compare the reproducibility and the discriminant ratio (DR) of OGTT-ISR and beta -index with the insulinogenic index (IG-Index: Delta Insulin (30' - Basal)/Delta Glucose (30' - Basal)). In protocol D, 20 subjects (14 with normal glucose tolerance, 5 with impaired glucose tolerance and 1 with newly-diagnosed type 2 diabetes) underwent a 75 g OGTT and an intravenous glucose tolerance test (IVGTT) on separate days to explore the relationships between acute (0'-10') insulin response (ATR) during the IVGTT and beta -index and OGTT-ISR during the OGTT. Results In all protocols, the minimal analogic model of C-peptide secretion achieved a reasonable fit of the experimental data. In protocol A, a good reproducibility of both beta -index and OGTT-ISR was observed with both complete and reduced (every 30') data sets. In protocol B, increasing the oral glucose load caused progressive increases in OGTT-ISR (from 2.63 +/- 0.70 to 5.11 +/- 0.91 Units.120'(-1).m(-2) BSA; P < 0.01), but the -index stayed the same (4.14 +/- 0.35 vs. 4.29 +/- 0.30 vs. 4.30 +/- 0.33 pmol.min(-2).m(-2) BSA). In protocol C, both OGTT-ISR and beta -index had lower day-to-day CVs (17.6 +/- 2.2 and 12.4 +/- 2.4%, respectively) and higher DRs (2.57 and 1.74, respectively) than the IG-index (CV: 35.5 +/- 6.3%; DR: 0.934). OGTT-ISR was positively correlated to BMI (P < 0.03), whereas -index was inversely related to both fasting and 2 h plasma glucose (P < 0.01 for both). In protocol D, -index, but not OGTT-ISR was significantly correlated to ATR (r = 0.542, P < 0.02). Conclusions Analogically modelling -cell function during the OGTT provides a simple, useful tool for the physiological assessment of beta -cell function.
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| 40. |
- Cunningham, Janet L., et al.
(författare)
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The biological hallmarks of ileal carcinoids
- 2011
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 41:12, s. 1353-1360
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Forskningsöversikt (refereegranskat)abstract
- Endocrine tumours derived from the small intestine, ileal carcinoids, produce and secrete the hormones tachykinins and serotonin, which induces the specific symptoms related to the tumour. Because of their low proliferation rate, they are often discovered at late stages when metastases have occurred. The biology that characterizes these tumours differs in many ways from what is generally recognized for other malignancies. In this overview, the current knowledge on the development and progression of ileal carcinoids is described.
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| 41. |
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| 42. |
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| 44. |
- Ding, Wern Yew, et al.
(författare)
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Impact of renal impairment on atrial fibrillation : ESC-EHRA EORP-AF Long-Term General Registry.
- 2022
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 52:6
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Atrial fibrillation (AF) and renal impairment share a bidirectional relationship with important pathophysiological interactions. We evaluated the impact of renal impairment in a contemporary cohort of patients with AF.METHODS: We utilised the ESC-EHRA EORP-AF Long-Term General Registry. Outcomes were analysed according to renal function by CKD-EPI equation. The primary endpoint was a composite of thromboembolism, major bleeding, acute coronary syndrome and all-cause death. Secondary endpoints were each of these separately including ischaemic stroke, haemorrhagic event, intracranial haemorrhage, cardiovascular death and hospital admission.RESULTS: A total of 9,306 patients were included. The distribution of patients with no, mild, moderate and severe renal impairment at baseline were 16.9%, 49.3%, 30.0% and 3.8%, respectively. AF patients with impaired renal function were older, more likely to be females, had worse cardiac imaging parameters and multiple comorbidities. Among patients with an indication for anticoagulation, prescription of these agents was reduced in those with severe renal impairment,p<0.001. Over 24 months, impaired renal function was associated with significantly greater incidence of the primary composite outcome and all secondary outcomes. Multivariable Cox regression analysis demonstrated an inverse relationship between eGFR and the primary outcome (HR 1.07[95% CI,1.01-1.14] per 10 mL/min/1.73m2 decrease), that was most notable in patients with eGFR <30mL/min/1.73m2 (HR 2.21[95% CI,1.23-3.99] compared to eGFR ≥90mL/min/1.73m2 ).CONCLUSION: A significant proportion of patients with AF suffer from concomitant renal impairment which impacts their overall management. Furthermore, renal impairment is an independent predictor of major adverse events including thromboembolism, major bleeding, acute coronary syndrome and all-cause death in patients with AF.
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| 45. |
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| 46. |
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| 47. |
- Ekström, Ulf, et al.
(författare)
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Mutations in the low-density lipoprotein receptor gene in Swedish familial hypercholesterolaemia patients: clinical expression and treatment response
- 1998
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972. ; 28:9, s. 740-747
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Familial hypercholesterolaemia, an autosomal co-dominant disorder caused by defects in the low-density lipoprotein receptor gene, is strongly associated with premature development of cardiovascular disease. METHODS: In this study, we have applied a gene screening method in a population of familial hypercholesterolaemia patients in order to describe the genetic background of the disease in southern Sweden. These patients were studied with the aim of relating the presence of the different mutations to the clinical expression of the disease and to the response to pharmacological treatment. RESULTS: In 16 out of 21 patients, potentially disease-causing low-density lipoprotein receptor gene defects were found, including five not previously described alterations (C240-->F, C122-->stop, C356-->Y, 785insG, 165delG). No defects in apolipoprotein B were found. One group of patients (n = 4) carried the mutation C122-->stop and another group of patients (n = 4) a mutation causing the substitution W66-->G. Patients in the two genotype subgroups were very similar with respect to lipid levels before treatment. CONCLUSION: A tendency towards differential susceptibility to treatment with statins was observed for the patient groups, encouraging further comparative studies of heterozygous FH patients.
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| 48. |
- Eliasson, Björn, 1959, et al.
(författare)
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Leptin levels in smokers and long-term users of nicotine gum
- 1999
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Ingår i: Eur J Clin Invest. - 0014-2972. ; 29:2, s. 145-52
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to examine the effects of cigarette smoking and other forms of long-term nicotine consumption on circulating leptin levels as well as the relationship between leptin levels and insulin sensitivity, measured with the euglycaemic hyperinsulinaemic clamp, in healthy middle-aged men. STUDY DESIGN: Samples from 73 subjects were analysed: 23 non-smokers, 31 smokers and 19 long-term nicotine gum chewers (NGCs) with similar ranges of age, body mass index (BMI) and per cent body fat. RESULTS: Leptin levels were higher in NGCs and smokers than in the non-smoking matched control subjects. Smoking cessation for 8 weeks further increased the leptin levels, probably due to the concomitant increase in body fat (mean +/- SD, 2.2 +/- 1.8 kg). Acute administration of one dose of nicotine nasal spray or smoking one cigarette did not significantly change the circulating leptin levels during the following 60 min. Plasma leptin concentrations were positively correlated with the proportion of body fat and negatively correlated with the degree of insulin sensitivity in each of the three subject groups. In a stepwise multiple linear regression analysis, plasma leptin concentrations were significantly correlated with the proportion of body fat, degree of insulin sensitivity and smoking status. CONCLUSION: These data show that long-term use of nicotine is associated with elevated circulating leptin levels. The increased leptin levels may be an important reason for the lower body weight in smokers. The results of this study also support the view that leptin is directly or indirectly related to insulin sensitivity in men.
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| 49. |
- Eliasson, Björn, 1959, et al.
(författare)
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No acute effects of smoking and nicotine nasal spray on lipolysis measured by subcutaneous microdialysis
- 1997
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Ingår i: Eur J Clin Invest. - 0014-2972. ; 27:6, s. 503-9
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Tidskriftsartikel (refereegranskat)abstract
- Smoking is associated with insulin resistance, dyslipidaemia and markers of the insulin resistance syndrome. This study investigated adipose tissue lipolysis in situ by subcutaneous microdialysis twice in 10 healthy, male smokers after smoking four cigarettes over 2 h and after the administration of an equal amount of nicotine given as nasal spray (NNS). Glucose and insulin levels, in situ lipolysis and adipose tissue blood flow were studied in the post-absorptive state and after a 75-g oral glucose tolerance test (OGTT). Post-absorptively, acute smoking and NNS increased neither subcutaneous adipose tissue glycerol production nor plasma free fatty acid (FFA) or glycerol levels. After the OGTT, plasma insulin and lactate levels were significantly higher after smoking, whereas FFA levels were higher after NNS. Normal smoking or the administration of a normal dose of NNS caused only minor metabolic changes. Thus, it does not seem likely that increased lipolysis is an important contributor to the dyslipidaemia seen in smokers.
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| 50. |
- Eliasson, Björn, 1959, et al.
(författare)
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Smoking cessation improves insulin sensitivity in healthy middle-aged men
- 1997
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Ingår i: Eur J Clin Invest. - 0014-2972. ; 27:5, s. 450-6
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Tidskriftsartikel (refereegranskat)abstract
- Cigarette smokers have recently been shown to exhibit insulin resistance, dyslipidaemia and markers of the insulin resistance syndrome (IRS). The aim of this study was to examine the effects of smoking cessation on insulin sensitivity and IRS. Forty male, non-obese healthy smokers participated in this open parallel study with 8 weeks of follow-up. Seventeen subjects were able to stop smoking, while 23 subjects continued to smoke and served as a controls group. Anthropometric and metabolic data were measured. Degree of insulin sensitivity was determined with the euglycaemic hyperinsulinaemic clamp technique. Smoking cessation increased insulin sensitivity and improved the lipoprotein profile in spite of a modest increase in body weight. Initial smoking habits correlated positively with the increase in BMI as well as the improvements in the metabolic variables after smoking cessation. These data support the view that smoking causes insulin resistance and IRS, and also demonstrate that the beneficial metabolic effects of smoking cessation override the effects of an accompanying modest increase in body weight.
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