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Biomedical subjects

I Räihä

Publications and source records attributed to I Räihä.

At least 19 recordsLinked to original sources

Hippocampal MRI volumetry in cognitively discordant monozygotic twin pairs.

OBJECTIVE: To investigate whether hippocampal atrophy, a proxy for incipient Alzheimer's disease, can be detected in non-demented monozygotic co-twins of demented twins by using volumetric magnetic resonance imaging (MRI). METHODS: Seven pairs of monozygotic female twins discordant for cognitive function (mean (SD) age 75 (4) years), and 10 age and education matched healthy controls (seven women, three men; mean age 73 (3) years) were studied with volumetric MRI. RESULTS: The mean normalised right hippocampal volume was 31% lower (p = 0.002) in the demented twins, and 6% lower (p = 0.45) in the non-demented twins than in the controls. In the left hippocampus, the mean normalised volume was 36% lower (p<0.001) in the demented twins, and 9% lower (p = 0.13) in the non-demented twins than in the controls. CONCLUSIONS: Significant hippocampal atrophy was detected in the demented twins compared with the controls. This is in line with previous imaging and pathological studies, with hippocampus showing the early changes in Alzheimer's disease. In the non-demented twins, only a minor, non-significant reduction was observed in the hippocampal volumes compared with the controls. This could reflect gene-environment interactions that have protected the non-demented twins longer than their demented co-twins and contributed to the relative preservation of their hippocampal volumes, or it could be a sign of preclinical Alzheimer's disease in the non-demented twins.

Aged↗

Poor performance in the mini-mental state examination due to causes other than dementia.

OBJECTIVE: The aim of this study was to examine the extent to which causes other than dementia contribute to poor performance on the Mini-Mental State Examination (MMSE). DESIGN: Cross-sectional population-based study. SETTING: Municipality of Lieto, Finland. SUBJECTS: The study population consisted of all individuals residing in Lieto and born in or before 1926. A total of 1196 individuals, 93% of those eligible, participated. MAIN OUTCOME MEASURES: The MMSE was implemented following interviews and clinical examinations. Whenever an individual was unable to complete any individual item on the MMSE, the nurse recorded causes and assessed whether poor performance was mainly caused by dementia or other reasons. RESULTS: Poor test performance due to causes other than dementia was recorded in 122 (10.2%) individuals (4% of those in the 64-74 years group, 15% in the 75-84 years group and 42% in the group of 85 years of age or older). The most common causes were poor vision and hearing, deficient schooling and consequences of stroke. CONCLUSION: Ten percent of the elderly population had symptoms contributing to poor performance on the MMSE. Physicians should therefore consider and record co-morbidity in the testing situation, especially in very old individuals.

Aged↗

Increase in T-cell subsets of oral mucosa: a late immune response in patients with treated coeliac disease?

BACKGROUND AND AIMS: In coeliac disease, the gut involvement is gluten-dependent. Following the introduction of a gluten-free diet, inflammatory cell infiltration decreases in the small intestinal mucosa. Our hypothesis was that the oral mucosa might mirror the changes found in coeliac disease similarly to the mucosa of the small intestine. Thus, the number of inflammatory cells in the oral mucosa would decrease in patients with coeliac disease on a gluten-free diet. METHODS: The distribution CD45RO+ and CD3(+) T cells, T-cell subpopulations (CD4(+), CD8(+), T-cell receptor (TCR)alpha beta+ and TCR gamma delta+ cells) and HLA DR expression were studied in the buccal mucosa of 15 untreated and 44 gluten-free diet treated coeliac disease patients, and of 19 controls. All 15 patients with untreated coeliac disease were immunglobulin (Ig)A endomysial antibody positive and all 44 patients on gluten-free diet except one were endomysial antibody negative, as were all control subjects. RESULTS: Untreated coeliac disease patients did not differ from controls in the densities of CD45RO+ cells, CD3(+) cells or of T-cell subsets. In contrast, in treated coeliac disease patients, a significant increase in the numbers of mast cells, CD3(+) and CD4(+) lymphocytes was found in the lamina propria of oral mucosa as compared with patients with untreated coeliac disease and controls. The increase in CD3(+) T cells was in part owing to an increase in lymphocytes expressing no TCR. No differences were found in the expression of human leucocyte antigen (HLA) DR in the epithelium or in the lamina propria in the patient groups studied or in the controls. In treated coeliac disease patients only a few TCR gamma delta+ T cells were found intraepithelially and in the lamina propria, but these cells were not detected in the lamina propria of oral mucosa of patients with untreated coeliac disease or in the controls. CONCLUSIONS: The infiltration of T cells into oral mucosa was increased in treated coeliac disease patients in spite of adherence to a gluten-free diet. Because the CD3(+) T cell count was higher than those of the TCR alpha beta+ and TCR gamma delta+ T cells, there must be other cells involved, probably natural killer (NK) cells. The increase in T-cell subsets in the treated coeliac disease patients seems not to result from poor dietary compliance, but might occur as a late immune response in coeliac disease and reflect chronic immunologic stimulation followed by regeneration of memory T cells.

Adult↗

Local challenge on oral mucosa with an alpha-gliadin related synthetic peptide in patients with celiac disease.

OBJECTIVE: Gluten-derived peptides (e.g., amino-acids 31-49 of alpha-gliadin) have been shown to cause changes typical of celiac disease in the gut. Gluten-derived peptides have mostly been used in in vitro studies. The easiest access to the gastrointestinal system may be the mouth. In the present study we were interested to see whether a synthetic peptide corresponding to amino-acids 31-49 of alpha-gliadin could induce inflammatory changes in the oral mucosa after a local challenge in celiac disease patients. METHODS: The challenge was made by injecting the peptide solution at a concentration of 10 microg/ml submucosally into the oral mucosa of 10 celiac disease patients after a gluten-free diet (GFD) and 12 healthy control subjects. B and CD45RO+ T cells, mast cells, CD3+, CD4+, CD8+ lymphocytes, and alphabeta and gammadelta T-cell receptor-bearing (TcR alphabeta, TcR gammadelta) lymphocytes were counted and HLA DR expression was determined. The expression of CD25 and Ki-67 antigen was also examined. RESULTS: The peptide significantly increased the total number of T cells in the lamina propria of the celiac disease patients. The expression of T-cell activation marker CD25 (IL-2 receptor), but not that of cell proliferation marker Ki-67, was also significantly increased in the lamina propria after peptide challenge. Such a reaction was not observed in the controls. The numbers of CD3+ and CD4+ T cells in the lamina propria were also increased in celiac disease patients after the challenge. The count of TcR gammadelta+ cells was very small in the oral mucosa in celiac disease and showed no increase when the oral mucosa was challenged with the peptide. The expression of HLA DR staining was enhanced after the submucosal peptide challenge in celiac disease; however, the difference was not statistically significant. CONCLUSIONS: The results show that in the celiac disease patients after the peptide challenge the oral mucosal lamina propria responds with a nonproliferative increase of lymphocytes. Thus, submucosal challenge with the peptide 31-49 can be used as an aid in the diagnosis of celiac disease. However, further studies with optimized methodology, including various concentrations of the peptide, adjuvants, other peptides, etc., are warranted, especially because the oral mucosa provides the easiest access to an in vivo peptide challenge in celiac disease.

Adult↗

Salivary antigliadin and antiendomysium antibodies in coeliac disease.

The definitive diagnosis of coeliac disease is based on typical changes in the small intestine biopsy specimens. To screen individuals for coeliac disease serum IgA and IgG antigliadin (AGA), IgA antireticulin (ARA) and IgA antiendomysium (EmA) antibodies are used. The aim of this study was to investigate whether these antibodies can also be detected in saliva as diagnostic markers of coeliac disease. The study population comprised 30 patients with coeliac disease treated with a gluten-free diet, 14 patients with untreated coeliac disease and 13 healthy control subjects. Sera and saliva were tested simultaneously for the presence of IgA and IgG AGA and IgA EmA. None of patients studied had a selective IgA deficiency. There was no significant difference in salivary IgA AGA levels between the three groups tested and there was no correlation between the individual serum and salivary values of IgA AGA. Salivary IgG AGA levels were very low or undetectable. Serum IgA AGA showed a low sensitivity (36.4%) to detect an untreated patient with coeliac disease. All salivary samples, regardless of the study group were negative for IgA EmA. Serum IgA EmAs were universally detected in the sera of patients with newly diagnosed coeliac disease and also in the sera of five of 30 patients with treated coeliac disease. No IgA EmA was detected in the sera of controls. None of the patients studied had a selective IgA deficiency either. Serum IgA EmA is the most sensitive, and IgA and IgG AGA are good indicators for coeliac disease, but salivary IgA or IgG AGA and salivary IgA EmA are not helpful for the diagnosis or follow-up of coeliac disease patients.

Adolescent↗

Lifestyle, stress, and genes in peptic ulcer disease: a nationwide twin cohort study.

BACKGROUND: The familial accumulation of peptic ulcer disease observed in several studies may be attributable to genetic effects, aggregation of environmental exposure (shared environment), or both. The intrafamilial spread of Helicobacter pylori infection has raised the question whether shared environment could explain the familial aggregation of peptic ulcer disease rather than genetic similarity of family members. OBJECTIVE: To examine the contribution of genetic and environmental factors to the pathogenesis of peptic ulcer disease in a nationwide population-based cohort of adult twins. METHODS: The Finnish Twin Cohort consists of all same-sexed twin pairs born before 1958 with both twins alive in 1975. The total number of twin pairs is 13888, of whom 4307 are monozygotic (MZ) and 9581 are dizygotic (DZ) twins. Questionnaire surveys of twins were carried out in 1975, 1981, and 1990, including medical and psychosocial questions. One question asked whether a physician had ever made a diagnosis of gastric or duodenal ulcer. In addition, hospital discharge data from 1972 to 1991 were linked with the twin cohort to obtain those twin individuals who had been treated for gastric or duodenal ulcer. The prevalence of and concordance for peptic ulcer disease were examined in MZ and DZ twins. Model-fitting analysis was used to specify the relative roles of genetic and environmental factors. The contribution of lifestyle factors and stress was examined prospectively in an incidence study and by comparison of discordant pairs. RESULTS: The prevalence of peptic ulcer disease was 6.2% in men and 2.8% in women in 1975. There were 63 MZ and 86 DZ pairs concordant for peptic ulcer disease. Concordance for disease was significantly higher in MZ than in DZ twin pairs; the probandwise concordance rate was 23.6% (95% confidence interval [CI], 20.9%-26.3%) in MZ twins and 14.8% (95% CI, 13.3%-16.3%) in DZ twins. In the model-fitting analysis, a model with both additive genetic and unshared environmental effects had the best goodness-of-fit. Thirty-nine percent (95% CI, 32%-47%) of the liability to peptic ulcer disease was explained by genetic factors and 61% (95% CI, 53%-68%) by individual environmental factors. In the incidence study (logistic regression analysis of the entire cohort initially free of peptic ulcer disease, with subjects diagnosed as having peptic ulcer after 1975 as cases), current smoking (relative risk, 2.2; 95% CI, 1.5-3.2) and high stress levels (relative risk, 3.2; 95% CI, 1.4-7.6) in men and regular use of analgesics (relative risk, 3.3; 95% CI, 1.3-8.1) in women predicted peptic ulcer disease during the follow-up from 1976 to 1991. In the analysis of discordant pairs, smoking in men and regular use of analgesics in both sexes were predictors of peptic ulcer disease. CONCLUSIONS: The questionnaire and hospital usage data on peptic ulcer disease in the population-based twin cohort suggest that the familial aggregation of the disease is modest, and attributable almost solely to genetic factors. Environmental effects not shared by family members were significant predictors of disease, and they were attributable to smoking and stress in men and the use of analgesics in women. The minor effects of shared environment to disease liability do not support the concept that the clustering of risk factors, such as H pylori infection, would explain the familial accumulation of peptic ulcer disease.

Activities of Daily Living↗

Oral mucosal changes in coeliac patients on a gluten-free diet.

Oral mucosal lesions or dental enamel defects may be the only presenting features of coeliac disease. A series of 128 patients with coeliac disease (CD) on a gluten-free diet (GFD), 8 patients with a newly diagnosed CD, and 30 healthy controls participated in a clinical and histopathological study of their oral mucosa. Oral mucosal lesions occurred in 71/128 GFD-treated CD patients. in 4/8 untreated and in 10/30 controls, and oral symptoms in 85/128, in 6/8 and in 10/30, respectively. Five CD patients had aphthous ulcers. Moderate to severe lymphocytic inflammation occurred in 36/117 and in 14/117 of the biopsy specimens of GFD-treated CD patients, in 1/8 and 2/8 of untreated CD patients, and in 3/30 and in 1/30 of controls, respectively. Intraepithelial T-cells were significantly more frequent in GFD-treated CD patients than in controls. There was no difference between untreated CD patients and controls. In the lamina propria of the GFD-treated CD patients, T-cells were more frequent than in the other groups. Mast cells were significantly more frequent in patients with GFD-treated CD. Nine GFD-treated CD patients had raised serum endomysium IgA antibody titres, although five of them reported to follow a strict GFD. A lack of strict compliance with a GFD may be related to the high prevalence of oral changes and symptoms. In addition, T-cell infiltration in the oral mucosa tends to increase with a longer duration of CD, independent of GFD-treatment. Clinically, it is important to study the oral cavity of patients suspected of having CD where the only clue to the disease may reside, since no less than 66% of the patients in this study had oral symptoms.

Adolescent↗

Characteristics of Helicobacter pylori-negative and -positive peptic ulcer disease.

OBJECTIVE: To examine histological and other features of patients with Helicobacter pylori-positive (HP+) and -negative (HP-) peptic ulcers and characterize typical features of peptic ulcer in elderly patients. METHODS: 137 consecutive patients with peptic ulcer and 70 patients with dyspepsia were studied over 24 months. Endoscopy and a structured personal interview were carried out in all patients. Three histological specimens were obtained from the antral mucosa. RESULTS: The mean age of ulcer patients was 62.4 (SD 15.7) years and that of dyspepsia patients was 56.9 (SD 18.1) years (P=0.026). Of patients with HP- ulcers, 80.6% were aged 65 years or over; the corresponding proportion of patients with HP+ ulcer was 33.7% (P=0.0001). The use of non-steroidal anti-inflammatory analgesics was more common among those whose ulcer was HP- (69.4% vs 33%, P=0.0002). The occurrence of antral inflammation, atrophy and intestinal metaplasia did not differ between those with HP- and HP+ ulcers, but activity of gastritis was more common in HP+ than in HP- patients (94.9% vs 47.1%, P=0.0001). In the logistic regression analysis, HP- peptic ulcer disease was independently associated with older age, bile reflux, the use of non-steroidal anti-inflammatory analgesics and intestinal metaplasia, while HP+ ulcer disease was associated with active inflammation of the antral mucosa and tendency to ulcer recurrence. CONCLUSION: HP+ and HP- peptic ulcers have well-defined characteristics which probably reflect their different pathogenesis. Peptic ulcer disease of elderly people is mostly HP-.

Adult↗

Blood vitamins, mineral elements and inflammation markers as risk factors of vascular and non-vascular disease mortality in an elderly population.

BACKGROUND: The need for protecting agents against degenerative processes of the body has been proposed to be especially high in elderly people. In order to evaluate the prognostic value of various biochemical factors in ageing the associations of blood concentrations of several vitamins, mineral elements and some other suggested risk factors with vascular and non-vascular mortality were studied in an elderly population. METHODS: A large health survey with complete clinical evaluation was carried out in the City of Turku in 1982-1983. A random sample of 344 community-living elderly individuals aged 65 years or older, stratified into four age groups, was studied. During the 13 years follow-up 225 subjects had died. Calcium, magnesium, copper, ceruloplasmin, zinc, selenium, iron, ferritin, transferrin, alpha-tocopherol, retinol, folate, vitamin B12, malondialdehyde, orosomucoid and insulin levels were analysed from the blood specimens. The relations between the compounds measured and relative mortality risks during the 13-year follow-up were analysed by Cox proportional hazards model adjusting for other known risk factors. RESULTS AND CONCLUSIONS: High concentrations of serum copper, orosomucoid and insulin were associated with increased risk of vascular mortality. The relative risks within the subjects of the highest tertile of serum concentrations were 2.2 for copper, 1.8 for orosomucoid, and 1.8 for insulin when adjusted for many confounding risk factors. Low serum vitamin B12 concentrations appeared to be significantly (P = 0.01) associated with increased vascular mortality. The associations were essentially not more significant when adjusted only for age. Contrary to earlier observations concentrations of serum magnesium, selenium, alpha-tocopherol, iron and its binding proteins or plasma and erythrocyte folate were not associated with increased mortality risk when adjusted for confounding risk factors. The authors suggest that in elderly subjects these elements and compounds are at the most weak, and probably non-independent risk factors for vascular mortality.

Aged↗

Cerebrospinal fluid tau protein as a biochemical marker for Alzheimer's disease: a community based follow up study.

OBJECTIVES: Biochemical markers for Alzheimer's disease would be of great value, especially to help in diagnosis early in the course of the disease. A pronounced increase in CSF tau protein (CSF-tau) is found in most patients with Alzheimer's disease. However, the specificity has to be further studied, as an increase in CSF-tau has also been found in other dementias, especially in vascular dementia. As most previous CSF studies have been based on selected inpatients, it was considered of special interest to examine the diagnostic potential of CSF-tau in a community population based sample of consecutive patients with dementia. Such patient material has been examined at the Piteå River Valley Hospital in Northern Sweden since 1986, and includes all those with memory disturbances in the community. The aim was also to study if an increase in CSF-tau is found early in the disease process, and whether CSF-tau changes during the progression of disease. METHODS PARTICIPANTS: Community population based sample of 75 demented patients (43 with Alzheimer's disease, 21 with vascular dementia, and 11 with mixed Alzheimer's disease/vascular dementia), 18 healthy subjects, and 18 neurological controls. A follow up investigation (including analysis of a new CSF sample) was performed in all patients after about one year. MAIN OUTCOME MEASURES: Concentrations of total (both normal tau and PHF-tau) tau in CSF, clinical measures (duration and severity of dementia), and apoE polymorphism. RESULTS: CSF-tau was markedly increased in Alzheimer's disease, 41/43 (95%) patients had values above the cut off level (mean+2 SD) in controls (306 pg/ml). High CSF-tau concentrations were also found in most patients with vascular dementia, preferentially in patients with vascular dementia without progressive leukoaraiosis on CT, whereas patients with vascular dementia with progressive leukoaraiosis had normal CSF-tau. Concentrations of CSF-tau were stable at one year follow up in both patients with Alzheimer's disease and patients with vascular dementia, and there was no correlation between CSF-tau and either duration or severity of dementia. CONCLUSIONS: The findings confirm the high sensitivity of CSF-tau for the diagnosis of Alzheimer's disease, but high CSF-tau was also found in vascular dementia, resulting in a lower specificity. However, high CSF-tau is preferentially found in patients with vascular dementia without progressive leukoaraiosis, which may constitute a group with concomitant Alzheimer's disease pathology. High CSF-tau may be present during the whole course of the disease in Alzheimer's disease. Possibly, therefore, the same high CSF-tau concentrations may be present before the onset of clinical dementia. Follow up studies on such patients will tell whether analysis of CSF-tau is useful as a biochemical marker for early Alzheimer's disease.

Aged↗

Environmental differences in twin pairs discordant for Alzheimer's disease.

The aim of this study was to examine the contribution of environmental factors to the pathogenesis of Alzheimer's disease by comparing environmental differences in twin pairs discordant for Alzheimer's disease. Seventy four twin pairs discordant for Alzheimer's disease were found by linking the Finnish twin cohort and the Hospital Discharge Register from years 1972-91. In 50 pairs (25 monozygotic and 25 dizygotic pairs), both co-twins had responded to a questionnaire survey in 1975. Exposure differences were compared between these pairs. A reduced risk of Alzheimer's disease was significantly associated with a higher level of schooling (relative risk 0.3; 95% confidence interval 0.1-0.9, p=0.029). In addition, a reduced risk was suggestively associated with ambidextrousness or left handedness (p=0.083) and an increased risk with marriage (p=0.052), widowhood (p=0.074), and a history of cholelithiasis (p=0.071). In conclusion, a reduced risk of Alzheimer's disease was associated with a higher level of schooling.

Aged↗

Information system for clinical resource management in a regional setting.

The Hospital District of Varsinais-Suomi consists of five hospitals for non-psychiatric diseases to deliver specialised health care for the population of 440,000 inhabitants in South-western Finland. We have applied an open regional information system to aid clinical resource management in such a complex expert organisation. The main areas of application have been assessment of inpatient care usage in different communities and in different diagnosis-related-groups (DRG), measurement of length of hospital stay in different DRGs and comparison of DRG unit weight costs of different hospitals. The open structure of the data base and its distribution to all parties of health care professionals has resulted in mutual decisions on structural changes and increased cost containment activities.

Aged↗

Alzheimer's disease in twins.

Besides familial Alzheimer's disease (AD), the genetic susceptibility has also been found in sporadic cases of AD, mostly related to the apolipoprotein E polymorphism. The penetrance of AD is determined by age and probably by environmental exposure. Gene-environment interaction of a disease can be examined through studies of twins. The relative roles of genetic and environmental influences can be estimated by comparing the concordance rates between monozygotic (MZ) and dizygotic (DZ) twins. Genetic models can be used to specify contributions both from genetic as well as shared and unique environmental effects. The role of environmental factors can be investigated in the co-twin control study, either by comparing environmental exposure in MZ twins discordant for a disease or by comparing MZ twins discordant for an exposure suspected of causing a particular disease. The sampling of twin pairs AD can be carried out using voluntary recruitment, linkage of twin and hospital discharge registries or screening of twin registry population. Potential sources of biases in sampling are discussed. The majority of the published twin studies on AD are case reports or based on selected materials. In MZ pairs, the concordance rates for AD have varied between 31% and 83%. Only one co-twin control study in twins discordant for AD has been published. Published twin studies on AD are briefly reviewed.

Alzheimer Disease↗

A marked increase in the incidence of colorectal cancer over two decades in southwest Finland.

The Finnish Cancer Registry's data on all colorectal cancer cases from 1971 to 1990 in southwest Finland, an area of mean population of 433,000, were analyzed. The age-adjusted incidence of colon cancer per 100,000 population increased in men from 8.5 in 1971-1980 to 13.5 in 1981-1990 and in women from 10.3 to 13.1. The incidence of male rectal cancer increased from 9.8 to 11.1 and in women from 6.4 to 7.1. The proportion of elderly patients clearly rose and, in 1981-1990, patients over 65 years of age had 68.4% of all colon cancers and 73.9% of all rectal cancers. There was a proximal shift in the site distribution of cancers: the proportion of rectal cancers decreased from 45.9% in 1971-1980 to 40.9% in 1981-1990. This change was most marked in men. There was no change in the spread and operability of colorectal cancers during the two decades. There was an increase in colon cancer mortality while the mortality of rectal cancer cancer slightly decreased.

Aged↗

Clinical presentation of peptic ulcer in the elderly.

The aim of this study was to determine the age-related characteristics of peptic-ulcer patients. A total of 125 consecutive patients (63 men and 62 women) with peptic ulcer were studied prospectively. The ulcers were diagnosed at endoscopy. The mean age of patients was 62 years (57 years in men and 68 in women). Patients were asked about their use of nonsteroidal anti-inflammatory drugs (NSAIDs). The main symptom, the duration of symptoms, the ulcer location and size, and the presence of Helicobacter pylori (HP) from the histologic specimen were recorded. Ulcer complications such as bleeding or perforation were also noted. These parameters were compared in two age groups: 65 years or under (n = 65) and over 65 years (n = 60). In the older age group, duodenal ulcer was less common (42 vs. 66%, p = 0.008) and typical epigastric pain was rare (35 vs. 91%, p < 0.001). Ulcer bleeding was present more commonly in the older age group (50 vs. 14%, p < 0.001). The duration of symptoms was shortest in patients who used NSAIDs, especially among older patients. Elderly patients also had an atypical location more often (39 vs. 15%, p = 0.003). After adjustment for use of NSAIDs, these characteristics remained among the elderly. The presence of HP was less common in the older age group (56 vs. 92%, p < 0.001). Furthermore, in the group of elderly patients who did not use NSAIDs, 35% were HP-negative. In conclusion, the presentation of peptic ulcer in the elderly has distinct characteristics, which are not entirely related to the use of NSAIDs.

Adult↗

Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly.

The purpose of this study was to determine the effect of serum lipids, lipoprotein fractions, and apolipoprotein (apo) A-1, B and E on mortality from vascular and nonvascular causes in an unselected elderly population. The random sample of 347 community-living individuals aged 65 years or older was obtained in 1982. Serum total cholesterol, LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), triglyceride, and apo A-1, B and E were determined at baseline. After the 11-year follow-up, 199 of the participants had died, and 148 were still alive. Mortality data from vascular and nonvascular causes by the end of 1993 were obtained from official registers. In the univariate analysis, a low total cholesterol level was associated with death due to both vascular and nonvascular causes (P value for trend, .021 and .0027, respectively). After the adjustment for other risk factors, the inverse association between total cholesterol and vascular mortality disappeared, but low total cholesterol was still a significant predictor of death due to nonvascular causes. Adjusted relative risks (RRs) of death due to nonvascular causes for those with elevated total cholesterol (5.1 to 6.5, 6.6 to 8.0, and > 8.0 mmol/L) compared with the reference group (< or = 5.0 mmol/L) were 0.5 (95% confidence interval [CI], 0.2 to 1.2), 0.6 (0.2 to 1.0), and 0.2 (0 to 0.8), respectively. Neither concentrations of HDL-C, LDL-C, triglyceride, nor apo B were associated with vascular or nonvascular mortality. On the other hand, low concentration of apo A-1 predicted vascular death. The RR for the lowest tertile was 1.6 (1.1 to 2.5) compared with the highest tertile. Furthermore, the occurrence of the apo E e4 allele was associated with increased risk of vascular mortality (RR, 1.5; 95% CI, 1.0 to 2.2), but the risk was not related to the levels of lipids, lipoproteins, or other apolipoproteins at baseline. Nonvascular mortality also tended to be predicted by the presence of the e4 allele (RR, 1.5; 95% CI, 0.9 to 2.5). In an unselected elderly population, the allelic variation of apo E, i.e., the presence of the e4 allele, and a low concentration of apo A-1 were more accurate indicators of vascular mortality than total cholesterol or lipoprotein fractions. The risk associated with the apo E polymorphism is unrelated to dyslipidemia.

Aged↗