bluuebunny/crossref_metadata_2025_split huggingface dataset:
Geographical pattern of female deaths from myocardial infarction in an urban population: fatal outcome out‐of‐hospital related to socio‐economic deprivation
Authors: Tydén P. , Engström G. , Hansen O. , Hedblad B. , Janzon L. 
Published: March 2003

Abstract. Tydén P, Engström G, Hansen O, Hedblad B, Janzon L (Malmö University Hospital, Lund University, Malmö, Sweden). Geographical pattern of female deaths from myocardial infarction in an urban population: fatal outcome out‐of‐hospital related to socio‐economic deprivation. J Intern Med 2001; 250: 201–207. Objective. This study of myocardial infarction (MI) amongst urban women has sought to assess whether there are differences in fatal outcome, in‐hospital respectively out‐of‐hospital, between residential areas defined in terms of socio‐economic circumstances. Design. Register‐based surveillance study 1986–95. Setting. Seventeen residential areas in the city of Malmö, Sweden. Subjects. Women 20–74 years of age. Main outcome measures. Differences in fatal outcome, in‐hospital respectively out‐of‐hospital, between residential areas were expressed in terms of age‐adjusted odds ratios (ORs), calculated by means of logistic regression. Socio‐economic circumstances in the areas were expressed in terms of a composite score. Results. Between residential areas there were marked and statistically significant differences in incidence (range 124–328/105, P < 0.001, d.f.=16) and mortality (range 38–132/105, P < 0.005, d.f.=16). Area rates of mortality covaried with incidence (r=0.85, P < 0.001) and with odds ratios of fatal outcome out‐of‐hospital (r=0.52, P=0.031) but not in‐hospital. The odds ratios of fatal outcome out‐of‐hospital decreased in a statistically significant stepwise fashion from areas in the lowest socio‐economic quintile (reference) to areas in the highest socio‐economic quintile (OR: 0.67, 95% CI: 0.48–0.94). There was no corresponding association with the odds ratios of fatal outcome in‐hospital. Conclusions. The high rate of mortality from MI amongst women in areas with deprived socio‐economic circumstances was related to deaths occurring out‐of‐hospital. In order to assess the preventive potential there is a need for further studies that may clarify to what extent the association with socio‐economic circumstances can be explained by other factors and conditions known to influence the probability of survival.
The NciI polymorphism in the cyclin D1 gene and sporadic primary hyperparathyroidism
Authors: Correa P. , Lundgren E. , Rastad J. , Åkerström G. , Westin G. , Carling T. 
Published: March 2003

Abstract. Correa P, Lundgren E, Rastad J, Åkerström G, Westin G, Carling T (Uppsala University Hospital, Uppsala, Sweden). The NciI polymorphism in the cyclin D1 gene and sporadic primary hyperparathyroidism. J Intern Med 2001; 250: 516–520. Objectives. The cell cycle regulator cyclin D1 plays an important role in parathyroid tumourigenesis. The NciI polymorphism in exon 4 has recently been associated with early onset of hereditary nonpolyposis colorectal cancer and is a prognostic indicator of nonsmall cell lung cancer and squamous cell carcinomas. Furthermore, a limited study of 28 primary hyperparathyroidism (pHPT) patients displayed a tendency of NciI influence on HPT development. We hypothesized that the NciI polymorphism may relate to a risk of developing pHPT. Design, setting and subjects. We genotyped 182 patients with sporadic pHPT and matched controls for the cyclin D1 polymorphism. A total of 88 pHPT patients and controls were recruited via a health‐screening. Results. The frequency distribution of the NciI genotypes NN, Ni, and ii were in pHPT patients and controls 22, 44 and 34%, and 26, 49 and 25%, respectively. The calculated allele frequencies were A=0.56; G=0.44 in cases and A=0.49; G=0.51 in controls. The frequency distributions did not differ comparing cases and controls when subgrouped after age and menopausal status. The NciI genotypes were not significantly associated with age of the individuals, serum (s)‐calcium, s‐parathyroid hormone (PTH), bone mineral density (BMD) or parathyroid tumour weight in any of the groups of pHPT patients or controls. Conclusions. No significant differences in distribution of the genotypes could be detected between the groups, suggesting that the polymorphism has minor or no pathogenic importance in the development of pHPT. Our results suggest that determination of the NciI polymorphism in the cyclin D1 gene is not a clinically useful tool for prediction of pHPT.
Oral oestradiol/trimegestone replacement reduces procarboxypeptidase U (TAFI): a randomized, placebo‐ controlled, 12‐week study in early postmenopausal women
Authors: Post M. S. , Hendriks D. F. , Van Der Mooren M. J. , Van Baal W. M. , Leurs J. R. , Emeis J. J. , Kenemans P. , Stehouwer C. D. A. 
Published: March 2003

Abstract. Post MS, Hendriks DF, van der Mooren MJ, van Baal WM, Leurs JR, Emeis JJ, Kenemans P, Stehouwer CDA (VU university medical center, Amsterdam, The Netherlands; University of Antwerp, Wilrijk, Belgium; and Gaubius Laboratory, TNO‐PG, Leiden, The Netherlands). Oral oestradiol/trimegestone replacement reduces procarboxypeptidase U (TAFI): a randomized, placebo‐controlled, 12‐week study in early postmenopausal women. J Intern Med 2002; 251: 245–251. Objective. To investigate the effects of short‐term postmenopausal oral hormone administration on plasma levels of procarboxypeptidase U (proCPU, thrombin‐activatable fibrinolysis inhibitor, EC 3.4.17.20), an inhibitor of fibrinolysis, in healthy early postmenopausal women. Design. A prospective, randomized, placebo‐controlled study. Setting. Outpatient clinic of the Department of Obstetrics and Gynaecology. Subjects. Seventy‐seven healthy early postmenopausal women were screened of whom 65 were randomized. Analyses were based on 60 participants. Interventions. The women received oral micronized oestradiol 2 mg either alone (E2 group, n=16), or sequentially combined with dydrogesterone 10 mg (E2 + D group, n=14) or trimegestone 0.5 mg (E2 + T, n=14), or placebo (n=16) for 12 weeks. Main outcome measure. ProCPU concentrations at baseline, and at 4 and 12 weeks of treatment. Results. Four weeks of E2 + T was associated with a significant decrease in the fasting proCPU concentration, which was sustained after 12 weeks [t=0: 636 ± 57 U L–1 (mean ± SD); t=4: 583 ± 63 U L–1; t=12: 589 ± 48 U L–1; ANCOVA versus placebo: P=0.011]. The percentage change from baseline versus placebo in this group was –8.4% [95% confidence interval (CI) –15.7 to –1.1] after 4 weeks and –5.9% (95% CI –11.7 to –0.1) after 12 weeks. There were no significant changes versus placebo in the E2 group nor in the E2 + D group. Conclusion. Short‐term treatment with E2 + T, but not E2 alone or E2 + D, lowers proCPU concentration. These findings add to accumulating evidence suggesting that different progestagens added to oestrogen replacement may differentially affect the risk of arterial and venous disease.
Primary and secondary prevention in cardiovascular disease: an old‐fashioned concept?
Authors: VAN VENROOIJ F. V. , STOLK R. P. , BANGA J. D. , ERKELENS D. W. , GROBBEE D. E. 
Published: March 2003

Abstract. van Venrooij FV, Stolk RP, Banga JD, Erkelens DW, Grobbee DE (Julius Centre for General Practice and Patient Oriented Research, University Medical Center, Utrecht, The Netherlands). Primary and secondary prevention in cardiovascular disease: an old‐fashioned concept? (Review). J. Intern Med 2002; 251: 301–306. Objective. Is the concept of primary and secondary cardiovascular prevention an old‐fashioned concept that needs to be re‐defined? Design. Discussion paper. Results. Cardiovascular prevention means reduction of absolute risk for cardiovascular disease (CVD), irrespective of clinical stage. Conclusion. For the calculation of an individual probability to develop CVD all factors that contribute to the risk must be taken into account, including previous CVD events.
Lipoprotein lipase polymorphisms and responses to long‐term overfeeding
Authors: UKKOLA O. , TREMBLAY A. , BOUCHARD C. 
Published: March 2003

Abstract. Ukkola O, Tremblay A, Bouchard C (Louisiana State University, Baton Rouge, LA, USA; University of Oulu, Oulu, Finland; and Laval University, Ste‐Foy, Quebec, Canada). Lipoprotein lipase polymorphisms and responses to long‐term overfeeding. J Intern Med 2002; 251: 429–436. Objectives. The role of the lipoprotein lipase (LPL) gene Hind III, S447X, Bam HI and Pvu II polymorphisms on body composition and lipid and lipoprotein changes in response to long‐term overfeeding was studied. Subjects. Twelve pairs of male monozygotic twins ate a 4.2 MJ day−1 energy surplus, 6 days a week, during a period of 100 days. Results. Overfeeding induced a decrease in high‐density lipoprotein 2 cholesterol (HDL2‐C) and HDL2‐C to HDL3‐C ratio in the H2H2 (n = 12) subjects of the LPL Hind III polymorphism. In contrast, the H1H1/H1H2 (n = 12) subjects experienced increases both in the HDL2‐C and HDL2‐C to HDL3‐C ratio (P = 0.009 and 0.007, respectively, for differences in percentage changes between H2H2 and H1H1/H1H2). In addition, the H2H2 genotype was associated with higher levels of very‐low‐density lipoprotein triglyceride (VLDL‐TG) (P < 0.03) and VLDL‐C (P < 0.05) before and after overfeeding and higher HDL‐TG levels (P < 0.003) after overfeeding. Postheparin lipoprotein lipase (PH‐LPL) activity tended to increase in H1H1/H1H2 and decrease in H2H2 subjects. The H2H2 subjects had lower total HDL‐C than those with the genotype H1H1/H1H2 4 months and 5 years after overfeeding (P = 0.04 and 0.10, respectively). The plasma lipid differences were similar amongst subjects with the S447S (n = 4) genotype of the S447X and H2H2 genotype of the Hind III polymorphisms. Body composition changes in response to overfeeding were not different between the Hind III genotypes. LPL Pvu II and Hind III polymorphisms were associated weakly with body weight gain (P = 0.015–0.039) but strongly with adipose tissue LPL activity (P < 0.01) after the caloric surplus. Conclusions. We conclude that the H2H2 subjects of the LPL gene Hind III polymorphism experience a decrease in the concentration of antiaterogenic lipoproteins when they are exposed to long‐term positive energy balance. This may have been partly caused by a diminished catabolism of TG‐rich particles in H2H2 subjects. LPL Pvu II and Bam HI polymorphisms were associated with body weight gain and adipose tissue LPL activity. Genetic variation at the LPL locus could thus be one of the factors responsible for the inter‐individual differences observed in plasma lipid and lipoprotein responses to chronic positive energy balance. It must be kept in mind that the sample size for this study was small. Nonetheless, it provides useful information on the genes and pathways that should be further explored.
Inhibitory effects of N‐acetylcysteine on scavenger receptor class A expression in human macrophages
Authors: SVENSSON L. , NORÉN K. , WIKLUND O. , LINDMARK H. , OHLSSON B. , HULTÉN L. Mattsson 
Published: March 2003

Abstract. Svensson L, Norén K, Wiklund O, Lindmark H, Ohlsson B, Mattsson Hultén L (Wallenberg Laboratory for Cardiovascular Research, The Sahlgrenska Academy at Göteborg University, Göteborg; and AstraZeneca, Mölndal, Sweden). Inhibitory effects of N‐acetylcysteine on scavenger receptor class A expression in human macrophages. J Intern Med 2002; 251:. Objective. The formation of foam cells from monocyte‐derived macrophages involves the uptake of modified lipoproteins by scavenger receptors. Antioxidants inhibit lipoprotein oxidation and may also modulate gene expression. We investigated the effect of the antioxidant N‐acetylcysteine on the expression of the class A scavenger receptor (SR‐A) types I and II in human macrophages. Design. Monocytes and macrophages from healthy blood donors and plaque‐derived macrophages from patients undergoing carotid endartherectomy were used for experiments. SR‐A mRNA was analysed with quantitative and semiquantitative reverse transcription‐polymerase chain reaction, and ligand binding and uptake were assessed with 125I‐labelled acetylated low‐density lipoprotein (LDL). Results. Incubation of monocytes and monocyte‐derived macrophages with N‐acetylcysteine decreased both SR‐A I and II mRNA expression. N‐Acetylcysteine also reduced SR‐A mRNA in lesion‐derived cells. Binding and uptake of 125I‐acetylated LDL was decreased after brief incubation with N‐acetylcysteine. After longer periods of incubation with N‐acetylcysteine we observed an increased degradation of lipoproteins. Conclusions. Our results imply that N‐acetylcysteine leads to a decrease in SR‐A mRNA and initially also to an attenuated uptake of modified lipoproteins. This adds more to the knowledge about the cellular actions of this drug.
The enigma of increased non‐cancer mortality after weight loss in healthy men who are overweight or obese
Authors: NILSSON P. M. , NILSSON J.‐Å. , HEDBLAD B. , BERGLUND G. , LINDGäRDE F. 
Published: March 2003

Abstract. Nilsson PM, Nilsson J‐A, Hedblad B, Berglund G, Lindgärde F. (University Hospital, Malmö, Sweden). The enigma of increased non‐cancer mortality after weight loss in healthy men who are overweight or obese. J Intern Med 2002; 252: 70−78. Objective. To study effects on non‐cancer mortality of observational weight loss in middle‐aged men stratified for body mass index (BMI), taking a wide range of possible confounders into account. Design. Prospective, population based study. Setting. Male population of Malmö, Sweden. Participants. In all 5722 men were screened twice with a mean time interval of 6 years in Malmö, southern Sweden. They were classified according to BMI category at baseline (<21, 22−25, overweight: 26−30, and obesity: 30+ kg m−2) and weight change category until second screening (weight stable men defined as having a baseline BMI ± 0.1 kg m−2 year−1 at follow‐up re‐screening). Main outcome measures. Non‐cancer mortality calculated from national registers during 16 years of follow‐up after the second screening. Data from the first year of follow‐up were excluded to avoid bias by mortality caused by subclinical disease at re‐screening. Results. The relative risk (RR; 95% CI) for non‐cancer mortality during follow‐up was higher in men with decreasing BMI in all subgroups: RR 2.64 (1.46−4.71, baseline BMI <21 kg m−2), 1.39 (0.98−1.95, baseline BMI 22−25 kg m−2), and 1.71 (1.18−2.47, baseline BMI 26+ kg m−2), using BMI‐stable men as reference group. Correspondingly, the non‐cancer mortality was also higher in men with increasing BMI, but only in the obese group (baseline BMI 26+ kg m−2) with RR 1.86 (1.31−2.65). In a subanalysis, nonsmoking obese (30+ kg m−2) men with decreased BMI had an increased non‐cancer mortality compared with BMI‐stable obese men (Fischer's test: P=0.001). The mortality risk for nonsmoking overweight men who increased their BMI compared with BMI‐stable men was also significant (P=0.006), but not in corresponding obese men (P=0.094). Conclusions. Weight loss in self‐reported healthy but overweight middle‐aged men, without serious disease, is associated with an increased non‐cancer mortality, which seems even more pronounced in obese, nonsmoking men, as compared with corresponding but weight‐stable men. The explanation for these observational findings is still enigmatic but could hypothetically be because of premature ageing effects causing so‐called weight loss of involution.
Long‐lasting intestinal bleeding in an old patient with multiple mucosal vascular abnormalities and Glanzmann's thrombasthenia: 3‐year pharmacological management
Authors: Coppola A. , De Stefano V. , Tufano A. , Nardone G. , Amoriello A. , Cerbone A. M. , Di Minno G. 
Published: March 2003

Abstract. Coppola A, De Stefano V, Tufano A, Nardone G, Amoriello A, Cerbone AM, Di Minno G (Centro di Coordinamento Regionale per le Emocoagulopatie; Università‘Federico II’, Napoli; A.O.R.N. ‘A. Cardarelli’, Napoli; Italy). Long‐lasting intestinal bleeding in an old patient with multiple mucosal vascular abnormalities and Glanzmann's thrombasthenia 3‐year pharmacological management (Case report). J Intern Med 2002; 252: 271–275.A 75‐year‐old woman with Glanzmann's thrombasthenia was admitted because of persistent melaena. Endoscopic examination showed multiple angiodysplastic lesions, with active bleeding in small and large bowel. Electro‐coagulation of some lesions, octreotide, conjugated oestrogens and selective embolization of jejunal vessels did not change transfusion requirements. After 8 month‐transfusions, ethinylestradiol + norethisterone in association with octreotide was started, leading to no transfusion over the following 9 months. Bleeding recurred after withdrawing octreotide and substituting ethinylestradiol + norgestrel for the ethinylestradiol + norethisterone combination. Re‐introduction of octreotide did not improve bleeding; however, a reduction of transfusion requirement was observed when the ethinylestradiol + norethisterone pill was re‐administered. The association of octreotide and of an oestrogen–progesterone combination was helpful in the difficult management of recurrent bleeding in this patient with diffuse gastrointestinal vascular abnormalities and a severe condition predisposing to bleeding.
Recurrent deep venous thrombosis caused by congenital interruption of the inferior vena cava and heterozygous factor V Leiden mutation
Authors: Schneider J. G. , Eynatten M. V. , Dugi K. A. , Duex M. , Nawroth P. P. 
Published: March 2003

Abstract. Schneider JG, Eynatten MV, Dugi KA, Duex M, Nawroth PP (Ruprecht‐Karls‐University of Heidelberg, Heidelberg, Germany). Recurrent deep venous thrombosis caused by congenital interruption of the inferior vena cava and heterozygous factor V Leiden mutation (Case report). J Intern Med 2002; 252: 276–280.A case of a 44‐year‐old patient with recurrent deep venous thrombosis (DVT) caused by congenital dysgenesis of the inferior vena cava (IVC) in coincidence with heterozygous factor V Leiden mutation is presented. The IVC malformation was a fortuitous finding because the vascular malformation of the collateral draining thoracic veins were suspected to be a malignant mass in chest X‐ray. This vascular abnormality is a rare finding but recent epidemiological research suggests that there may be an association between the congenital absence of the IVC and DVT. In our case, the patient is even at higher risk combining the malformation probably affecting venous blood flow and the hypercoagulabilic state by heterozygous presence of the factor V Leidenmutation.
Cholesterol treatment forever? The first Scandinavian trial of cholesterol supplementation in the cholesterol‐synthesis defect Smith–Lemli–Opitz syndrome
Authors: Starck L. , Lövgren‐Sandblom A. , Björkhem I. 
Published: March 2003

Objectives.  To investigate if exogenous cholesterol affects sterol turnover in the cholesterol‐synthesis defect Smith–Lemli–Opitz syndrome (SLOS) and if clinical effects justify long‐time supplementation. The SLOS is caused by a deficiency of the enzyme 7‐dehydrocholesterol‐7‐reductase with markedly reduced cholesterol levels and greatly increased levels of 7‐dehydrocholesterol (7‐DHC).Design.  Treatment with dietary cholesterol in patients with SLOS in a case series study.Setting.  All biochemical analyses were performed in one laboratory. The clinical follow‐up was carried out by one of the authors (LS), a paediatric neurologist.Subjects.  Seven patients with biochemically verified SLOS have been diagnosed in Sweden and all of them are included in the study.Interventions.  Six patients were treated for 0.5–6 years orally with cholesterol and the bile acid taurocholate and one patient was supplemented with cholesterol only.Main outcome measures.  In addition to cholesterol, 7‐ and 8‐DHC, lathosterol was used as a marker of endogenous cholesterol synthesis and the patients were followed clinically. Nerve conduction velocities (NCV) were measured before treatment in all patients and a UVA‐light test was performed in one of them.Results.  Lathosterol was initially increased by cholesterol supply in subjects with very low cholesterol levels with subsequent rise of 7‐ and 8‐DHC. Photosensitivity clinically improved in all, verified by UVA‐light testing in one. Progressive polyneuropathy improved, whilst stationary forms did not.Conclusion.  Dietary cholesterol can up‐regulate sterol turnover in severely affected patients. Although some specific features are treatable and verifiable by objective methods, data supporting life‐long treatment dietary cholesterol in all SLO patients are still lacking.
A plasma glucose concentration below 2.5 mmol L−1 is not an appropriate criterion to end the 72‐h fast
Authors: Wiesli P. , Brändle M. , Schwegler B. , Lehmann R. , Spinas G. A. , Schmid C. 
Published: March 2003

Abstract.  Wiesli P, Brändle M, Schwegler B, Lehmann R, Spinas GA, Schmid C (University Hospital, CH‐8091 Zurich, Switzerland). A plasma glucose concentration below 2.5 mmol L−1 is not an appropriate criterion to end the 72‐h fast. J Intern Med 2002; 252: 504–509.Context.  The classical end‐point to terminate the 72‐h fast in a patient evaluated for a hypoglycaemic disorder is the occurrence of hypoglycaemic symptoms in association with a low plasma glucose level. However, neither the symptoms nor the plasma glucose level have been exactly defined.Objective.  To determine whether a useful cut‐off plasma glucose concentration as criterion to end the prolonged fast in the absence of neuroglycopenic symptoms can be defined.Design.  Single centre case–control study.Setting.  Tertiary referral hospital in Switzerland.Subjects.  The 72‐h fast was prospectively performed in 23 consecutive patients (17 women and six men) following a standardized protocol between July 1999 and January 2002. All patients were referred to our clinic for evaluation of suspected hypoglycaemia. The criterion to end the fast before 72 h was defined by the occurrence of symptoms or signs typical for neuroglycopenia irrespective of plasma glucose levels.Main outcome measure.  Insulin levels and insulin to plasma glucose ratios in insulinoma patients and in individuals without insulin‐secreting tumours at termination of the fast and at plasma glucose levels ≤2.5 mmol L−1, prior to the occurrence of neuroglycopenic symptoms.Results.  In seven patients, the fast was terminated before 72 h because they developed neuroglyco‐penic symptoms. Insulin‐secreting tumours were found and successfully removed in these seven patients. Sixteen individuals developed no neuroglycopenic symptoms throughout the 72‐h fast and an insulin‐secreting tumour could be excluded in these 16 patients. Five of these 16 individuals had plasma glucose levels ≤2.5 mmol L−1 during the 72‐h fast. Insulin levels and insulin to glucose ratios in insulinoma patients and healthy individuals overlapped during as well as at termination of the fast. Prior to the occurrence of neuroglycopenic symptoms and at venous plasma glucose ≤2.5 mmol L−1, insulin to plasma glucose ratios dropped in insulinoma patients to values within the normal range on several occasions.Conclusions.  Terminating the fast at plasma glucose levels ≤2.5 mmol L−1 does not allow confirmation or exclusion of an insulin‐secreting tumour. Thus, the occurrence of symptoms or signs typical for neuroglycopenia is the prerequisite criterion to end the fast before 72 h.