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J Lindemans

Publications and source records attributed to J Lindemans.

At least 19 recordsLinked to original sources

Validation of the assessment of folate and vitamin B12 intake in women of reproductive age: the method of triads.

OBJECTIVE: To validate the folate and vitamin B12 intakes estimated by a food-frequency questionnaire (FFQ) designed to be used in a case-control study on the association between maternal dietary intake and the risk of having a child with a congenital heart defect. DESIGN AND SUBJECTS: The FFQ was filled out by 53 women of reproductive age. Immediately thereafter, blood samples were taken to determine serum folate, red blood cell (RBC) folate and serum vitamin B12 concentrations. Subsequently, three dietary 24-h recalls (24HR) were completed during a period of three successive weeks and used as a reference method. The recalls comprised two weekdays and one weekend day. Using the method of triads, validity coefficients were calculated by comparing nutrient intakes derived from the FFQ and 24HR with the corresponding nutritional biomarkers in blood. The validity coefficient is the correlation between the dietary intake reported by the FFQ and the unknown 'true' dietary intake. RESULTS: The comparison of B-vitamin intakes reported by the FFQ and the mean of the 24HR revealed deattenuated correlation coefficients of 0.98 for folate and 0.66 for vitamin B12. The correlation coefficients between the B-vitamin intakes estimated by the FFQ and concentrations of serum folate, RBC folate and serum vitamin B12 were 0.20, 0.28 and 0.21, respectively. The validity coefficients for serum folate, RBC folate and serum vitamin B12 were 0.94, 0.75 and 1.00, respectively. The estimated folate and vitamin B12 intakes were comparable with the results of the most recent Dutch food consumption survey. CONCLUSIONS: The adapted FFQ is a reliable tool to estimate the dietary intake of energy, macronutrients, folate and vitamin B12 in women of reproductive age. Therefore, this FFQ is suitable for the investigation of nutrient-disease associations in future. SPONSORSHIP: Funding was provided by the Netherlands Heart Foundation (Grant 2002.B027).

Adult↗

Maternal hyperhomocysteinaemia is a risk factor for congenital heart disease.

OBJECTIVE: To investigate the inter-relation between mother and infant homocysteine, folate and vitamin B12 status and the risk of a child with congenital heart disease (CHD). DESIGN: Case-control study. SETTING: Erasmus MC, University Medical Centre, Rotterdam, the Netherlands. POPULATION: Participants were 149 case-mothers and their children with CHD (n = 151) and 183 control-mothers with their children (n = 175). METHODS: Approximately 17 months after the index-pregnancy maternal fasting, children's random venous blood samples were drawn to measure plasma total homocysteine, serum and red blood cell (RBC) folate, and serum vitamin B12 concentrations. Data were compared between cases and controls using the Mann-Whitney U test. The biochemical parameters were dichotomised according to the cutoff value of the 10th percentile of vitamin concentrations and the 90th percentile of homocysteine concentrations based on control data. Risk estimates for the association between CHD and the biochemical parameters were estimated in a logistic regression model. MAIN OUTCOME MEASURES: Medians (minimum-maximum) and odds ratios (OR) (95% confidence intervals [CI]). RESULTS: The OR (95% CI) of having a child with CHD was 2.9 (1.4-6.0) for maternal hyperhomocysteinaemia (>14.3 micromol/l). This finding is substantiated by a significant concentration-dependent risk (Ptrend = 0.004). Hyperhomocysteinaemic case-mothers showed significantly lower serum folate and vitamin B12 concentrations than normohomocysteinaemic case-mothers. Serum and RBC folate concentrations were significantly higher in case-children than that in control-children. CONCLUSIONS: Maternal hyperhomocysteinaemia is associated with an increased risk of CHD, partially due to low folate and vitamin B12 status. The folate status of children warrants further investigation.

Adult↗

Acute and concomitant deterioration of hyponatremia and renal dysfunction associated with heart and liver failure.

BACKGROUND: Although hyponatremia with concomitant renal dysfunction has been described anecdotally, little is known about how these two conditions are related, which type of renal dysfunction usually occurs, and which patients are at risk. METHODS: From 3029 measured serum sodium (S(Na)) concentrations in 3 months, patients with at least one S(Na) < or =125 mmol/l were selected, and divided in patients with at least 1 S(Creat) > or =125 micromol/l (study group, n=20), and patients whose S(Creat) remained normal (control group, n=50). RESULTS: During the first 5 days of hospitalization, S(Creat) almost doubled in the study group from 125 +/- 40 micromol/l to 207 +/- 72 micromol/l, while S(Na) decreased concurrently from 130 +/- 2 mmol/l to 122 +/- 3 mmol/l. The peak S(Creat) and S(Na) values coincided, and the average courses were highly correlated (r = 0.88, p < 0.001). The study group more often had heart failure (10/20 vs. 1/50, p < 0.001) and liver failure (7/20 vs. 4/50, p = 0.009), and received more often loop diuretics (13/20 vs. 12/50, p = 0.002), spironolactone (11/20 vs. 7/50, p = 0.001), and/or angiotensin-converting enzyme inhibitors (5/20 vs. 2/50, p = 0.02). Four patients were admitted to the intensive care (10 in control group, p = 1.0), and 5 patients died (10 in control group, p = 0.7). CONCLUSIONS: Renal dysfunction is common in severe hyponatremia and usually develops in an acute-on-chronic fashion with concomitant deterioration of both conditions. This concourse is associated with heart failure, liver failure, and/or a renal drug regimen. Given the recent results of clinical trials, this patient group may be especially suitable for treatment with vasopressin antagonists.

Adult↗

A shift to a peripheral Th2-type cytokine pattern during the carcinogenesis of cervical cancer becomes manifest in CIN III lesions.

BACKGROUND: A shifted balance between T helper 1 (Th1)-type and Th2-type cytokines has been hypothesised in cervical dysplasia. AIMS: To evaluate possible deregulation of the cytokine network by estimating the expression of peripheral cytokines in different stages of cervical disease and in relation to the presence or absence of high risk human papillomavirus (HR-HPV). METHODS: Twenty one HR-HPV positive women with high grade cervical intraepithelial neoplasia (CIN II-III) and 12 patients with invasive cervical carcinoma formed the study groups. Two control groups consisted of 10 HR-HPV positive and 11 HR-HPV negative women without CIN. Differences in leucocyte subgroups were evaluated by a differential leucocyte count. Plasma concentrations of tumour necrosis factor alpha (TNFalpha), TNFalpha receptors TNFRI and TNFRII, interferon gamma (IFNgamma), interleukin 2 (IL-2), IL-12, IL-4, and IL-10 were determined by enzyme linked immunosorbent assays. RESULTS: Leucocyte counts in patients with CIN III and carcinoma were significantly higher than in controls. Plasma IFNgamma concentrations were significantly lower in patients with CIN III and carcinoma than in women with CIN II or controls. Plasma concentrations of IL-12, IL-2, IL-4, and TNFalpha did not differ significantly between groups, but significantly lower plasma concentrations of TNFRII were found in CIN III and carcinoma compared with CIN II. IL-10 was detected with increased frequency in the plasma of patients with CIN III and carcinoma. CONCLUSIONS: These results indicate that a shift to a Th2-type cytokine pattern during the carcinogenesis of cervical cancer occurs in women with CIN III lesions.

Adult↗

New approach for the identification of folate-related pathways in human embryogenesis.

The role of natural folate intake and synthetic folic acid supplementation in the prevention of some congenital malformations is known, but on a molecular biological level poorly understood. In a first approach to identify folate-regulated pathways in human embryogenesis, tryptic digests of Epstein Barr Virus-immortalized B-lymphoblasts proteins from 6 cleft lip and/or palate patients and 2 controls were compared using matrix assisted laser desorption ionisation--time of flight (MALDI-TOF) mass spectrometry. After immortalisation, the lymphoblasts were cultured for 22 days in folate-rich, i.e. 5-methyltetrahydrofolate (5-mTHF), or folate-free medium. On day 22, 5-mTHF was added to the folate-free cultures and the profiles on day 22 and 23 were compared. After background correction for the peptide profiles of the folate-rich cultures, we found in the folate-free mediaseveral differentially expressed peptide peaks upon addition of 5-mTHF. These peptide peaks were mass annotated and matched withthe MSDB human database. The results suggest some folate-regulated protein candidates as Frizzled and the Rho GTP-ases WRCH and Chp that are known in human embryogenesis. Differential folate expressed proteins in patients and controls, however, have to be further investigated.

B-Lymphocytes↗

Automated counting of white blood cells in synovial fluid.

OBJECTIVES: To evaluate the performance of automated leucocyte (white blood cell; WBC) counting by comparison with manual counting. METHODS: The number of WBC was determined in heparinized synovial fluid samples by the use of (i) a standard urine cytometer (Kova) and a microscope (reference method) and (ii) a haematology analyser (Sysmex XE-2100; WBC/BASO and DIFF channels). Imprecision within and between days was determined by replicate analysis of a low (level A; WBC approximately 0.560 x 10(9)/l) and a high (level B; WBC approximately 1.081 x 10(9)/l) dedicated synovial fluid control (Quantimetrix). RESULTS: The WBC count of the DIFF channel was highly correlated with the WBC count of the microscopic reference method (r = 0.99; WBC analyser = 0.870 x WBC reference method + 0.413). In contrast, no agreement existed between WBC counts generated by the WBC/BASO channel of the analyser and the reference method (r = 0.52; WBC analyser = 0.008 x WBC reference method + 0.079). Within-day imprecision (4-7%) and between-day imprecision (10%) of the haematology analyser were smaller than the within-day imprecision (12%) and the between-day imprecision (20-22%) of the manual reference method. For manual counting, inter-observer coefficients of variation were 35.9% (control level A) and 21.0% (control level B). CONCLUSIONS: The WBC count in synovial fluid can be reliably determined using the DIFF channel of the Sysmex XE-2100. Automated counting of WBC in synovial fluid offers more precise and faster results than manual counting.

Arthritis↗

Significance of elevated cobalamin (vitamin B12) levels in blood.

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Hematologic disorders like chronic myelogeneous leukemia, promyelocytic leukemia, polycythemia vera and also the hypereosinophilic syndrome can result in elevated levels of cobalamin. Not surprisingly, a rise of the cobalamin concentration in serum is one of the diagnostic criteria for the latter two diseases. The increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases like acute hepatitis, cirrhosis, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. This phenomenon is predominantly caused by cobalamin release during hepatic cytolysis and/or decreased cobalamin clearance by the affected liver. Altogether it can be concluded that an observed elevation of cobalamin in blood merits the a full diagnostic work up to assess the presence of disease.

Animals↗

[The significance of an elevated cobalamin concentration in the blood].

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Diseases such as chronic myeloid leukaemia, promyelocytic leukaemia, polycythaemia vera and hypereosinophilic syndrome are often accompanied by markedly elevated levels of cobalamin in the blood. A rise in the serum cobalamin concentration is one of the diagnostic criteria for polycythaemia vera and hypereosinophilic syndrome. In haematological disorders, the increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases such as acute hepatitis, cirrhosis of the liver, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. In liver diseases, the increase in cobalamin is predominantly caused by cobalamin release during hepatic cytolysis and/or through decreased clearance of circulating cobalamin by the affected liver. Liver disorders are not an indication for determining the serum cobalamin concentration. However, a coincidentally observed elevated serum cobalamin concentration is reason for further investigation.

Hematologic Diseases↗

The effect of hormone replacement therapy on serum homocysteine levels in perimenopausal women: a randomized controlled trial.

Serum homocysteine levels may be lowered by hormone replacement therapy, but randomized controlled trial data are scarce. We performed a single center randomized placebo-controlled trial to assess the 6 months effect of hormone replacement therapy compared with placebo on fasting serum homocysteine levels in 121 perimenopausal women free of cardiovascular disease, and recruited from the general population. The trial was double-blind with respect to a sequential combined regimen of oral 17 beta-estradiol and desogestrel (17 beta E(2)-D) and the placebo group and open with respect to a combination of conjugated equine estrogens and norgestrel (CEE-N). At baseline and after 6 months, fasting serum homocysteine levels were measured. Differences in 6 months serum homocysteine levels from baseline between treatment and placebo groups were calculated, and expressed as a percentage of the 6 months placebo level. After 6 months, the difference in serum homocysteine levels between women receiving 17 beta E(2)-D and placebo was -6.3% (95% CI, -12.4%; 0.0%, P=0.06). The difference between women receiving CEE-N and placebo was -10.1% (95% CI, -16.7%; -2.9%, P<0.01). The difference between the combined group of both types of hormone replacement therapy users and placebo was -7.8% (95% CI, -13.2%; -2.0%, P=0.01). No significant difference was observed between the two active regimens. Our results indicate that hormone replacement therapy decreases homocysteine levels in perimenopausal women.

Adult↗

Does iron-deficient erythropoiesis in pregnancy influence fetal iron supply?

BACKGROUND: It was investigated whether the iron status in newborns is negatively influenced by iron-deficient erythropoiesis of the mother during pregnancy. METHODS: The iron status is characterized by hemoglobin, erythrocyte zinc protoporphyrin and serum ferritin values. Iron-deficient erythropoiesis of the mother is characterized by erythrocyte zinc protoporphyrin values. Measurement of erythrocyte zinc protoporphyrin was performed in 103 non-anemic females within 24 hours after delivery. The iron status of their newborns was measured in cord blood. RESULTS: Erythrocyte zinc protoporphyrin concentrations were normal in 62% and elevated in 38% of the females, hence 39 women had iron-deficient erythropoiesis. There were no significant differences in mean values of the iron status parameters between neonates born to females with iron-deficient erythropoiesis and neonates born to females not having iron-deficient erythropoiesis. No correlation was found between maternal erythrocyte zinc protoporphyrin values and any of the neonatal parameters. CONCLUSION: It is concluded that fetal iron supply is not negatively influenced by iron-deficient erythropoiesis in the mother.

Anemia, Iron-Deficiency↗

Erythrocyte zinc protoporphyrin testing in pregnancy.

BACKGROUND: To compare the usefulness of serum ferritin, hemoglobin and erythrocyte zinc protoporphyrin estimations as indicators of the need of iron supplementation in pregnancy. METHODS: In 97 healthy pregnant women serum ferritin, hemoglobin and erythrocyte zinc protoporphyrin concentrations were measured at each trimester period. Iron supplementation was prescribed at hemoglobin values below 113 g/L. RESULTS: Neither in the first nor in the second trimester differences in serum ferritin and erythrocyte zinc protoporphyrin values have been found between women who got iron therapy prescribed and women who did not get iron therapy, whereas already in the first trimester hemoglobin values were lower in the group that got iron therapy. These results indicate that hemodilution rather than iron deficiency determined which women got iron therapy. In the third trimester 14 out of 80 women without iron supplementation had depleted iron stores and a significant erythrocyte zinc protoporphyrin increase, indicating evolving iron deficiency anemia. However, only five of them showed hemoglobin levels below 113 g/L and got iron therapy. Low serum ferritin levels were found in 23% of the women at booking and in 92% in the third trimester. Serum ferritin levels neither predicted the development of iron deficient erythropoiesis nor of anemia. CONCLUSIONS: Iron deficiency can neither be diagnosed nor predicted by serum ferritin or hemoglobin measurements at booking or later on in pregnancy. Erythrocyte zinc protoporphyrin measurements can be of help in determining which women have iron deficient erythropoiesis and may benefit by iron therapy.

Adult↗

Total homocysteine and cognitive decline in a community-based sample of elderly subjects: the Rotterdam Study.

Homocysteine has been associated with an increased risk of cardiovascular disease. Cardiovascular diseases have been related to cognitive decline. The authors investigated the association of homocysteine with concurrent cognitive impairment and subsequent cognitive decline in a random sample of 702 community-dwelling respondents aged 55 years or over to the prospective Rotterdam Study in 1990-1994. Multiple logistic regression was used to calculate odds ratios and 95 percent confidence intervals for the association between total homocysteine levels and cognitive impairment (Mini-Mental State Examination (MMSE) score <26) and cognitive decline (drop in MMSE score of >1 point/year). Mean duration of follow-up was 2.7 years. After adjustment for age, sex, and education, there was no relation between total homocysteine and cognitive impairment (highest vs. lowest tertile: odds ratio (OR) = 1.30, 95% confidence interval (CI): 0.50, 3.38) or cognitive decline (middle vs. lowest tertile: OR = 1.14, 95% CI: 0.67, 1.93; highest vs. lowest tertile: OR = 0.91, 95% CI: 0.52, 1.58). Subjects who were lost to follow-up due to death or nonresponse had slightly higher age-adjusted homocysteine levels and lower MMSE scores at baseline. Sensitivity analyses showed that selective loss to follow-up was not a likely explanation for the absence of an association in the participants. Although a relation between homocysteine and reduced cognitive function is biologically plausible, this study suggests no such association in a community-based sample of the elderly.

Aged↗

Homocysteine and short-term risk of myocardial infarction and stroke in the elderly: the Rotterdam Study.

BACKGROUND: Elevated homocysteine level increases vascular disease risk. Most data are based on subjects younger than 60 years; data for the elderly are more limited. We examined the relationship of homocysteine level to incident myocardial infarction and stroke among older subjects in a nested case-control study. METHODS: Subjects were participants in the Rotterdam Study, a cohort study among 7983 subjects residing in the Ommoord district of Rotterdam, the Netherlands. Baseline examinations were performed from March 1, 1990, to July 31, 1993. The analysis is restricted to myocardial infarction and stroke that occurred before December 31, 1994. One hundred four patients with a myocardial infarction and 120 with a stroke were identified with complete data. Control subjects consisted of a sample of 533 subjects drawn from the study base, free of myocardial infarction and stroke. Nonfasting total homocysteine levels were measured. RESULTS: Results were adjusted for age and sex. The risk of stroke and myocardial infarction increased directly with total homocysteine. The linear coefficient suggested a risk increase by 6% to 7% for every 1-micromol/L increase in total homocysteine. The risk by quintiles of total homocysteine level was significantly increased only in the group with levels above 18.6 micromol/L (upper quintile): odds ratios were 2.43 (95% confidence interval, 1.11-5.35) for myocardial infarction and 2.53 (95% confidence interval, 1.19-5.35) for stroke. Associations were more pronounced among those with hypertension. CONCLUSIONS: The present study, based on a relatively short follow-up period, provides evidence that among elderly subjects an elevated homocysteine level is associated with an increased risk of cardiovascular disease.

Aged↗

Influence of iron deficiency anaemia on haemoglobin A2 levels: possible consequences for beta-thalassaemia screening.

Iron deficiency modulates the synthesis of HbA2, resulting in reduced HbA2 levels in patients with iron deficiency anaemia. The diagnosis heterozygous beta-thalassaemia is based on a raised HbA2 level. Patients with beta-thalassaemia and concomitant iron deficiency can show normal HbA2 levels. It is of clinical importance to know the quantitative effect of iron-deficient erythropoiesis on the levels of HbA2 in order to be able to determine which iron-deficient patients with normal HbA2 levels have to be retested after iron therapy in thalassaemia screening programmes. In this study, HbA2 levels in 150 patients with iron-deficiency anaemia and 71 healthy controls have been measured. A linear correlation is found in the patient group between HbA2 and Hb, HbA2 and MCV, and HbA2 and erythrocyte zinc protoporphyrin (ZPP). In future studies, the correlation between HbA2 and erythrocyte parameters in patients with heterozygous beta-thalassaemia and concomitant iron deficiency has to be examined. We recommend that ZPP be measured in these studies too, as ZPP levels may be a better indicator of concomitant iron deficiency than Hb or MCV in thalassaemic patients.

Adult↗

Serum ferritin and risk of myocardial infarction in the elderly: the Rotterdam Study.

BACKGROUND: Elevated body iron stores have been suggested to be a risk factor for ischemic heart disease. OBJECTIVE: We examined whether elevated serum ferritin concentrations, other indicators of iron status, and dietary iron affected the incidence of myocardial infarction (MI) in an elderly population. DESIGN: A nested, case-control study of 60 patients who had their first MI and 112 age- and sex-matched control subjects embedded in the population-based cohort of the Rotterdam Study. RESULTS: The age- and sex-adjusted risk of MI for subjects with serum ferritin concentrations > or = 200 microg/L was 1.82 (95% CI: 0.90, 3.69; P = 0.096). The odds ratio (OR) was 1.26 (95% CI: 0.98, 1.64; P = 0.078) for the highest tertile of serum ferritin and was only slightly altered in a multivariate model. Risk of MI associated with the highest tertile of ferritin was most evident in current or former smokers (OR: 1.68; 95% CI: 1.17, 2.47; P for trend = 0.008) and in subjects with hypercholesterolemia (OR: 1.43; 95% CI: 0.99, 2.11; P for trend = 0.056) or diabetes (OR: 2.41; 95% CI: 1.12, 7.67; P for trend = 0.027). No association with risk of MI was observed for tertiles of serum iron, serum transferrin, or total dietary iron. For dietary heme iron, risk of MI was significantly increased in a multivariate model in which dietary energy, fat, saturated fat, and cholesterol were adjusted for (OR: 4.01; 95% CI: 1.17, 15.87; P for trend = 0.031). CONCLUSION: In the presence of other risk factors, serum ferritin may adversely affect ischemic heart disease risk in the elderly.

Aged↗