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Biomedical subjects

K Laitinen

Publications and source records attributed to K Laitinen.

At least 73 records · Page 4Linked to original sources
PubMed1994

Familial high serum concentrations of the carboxyl-terminal propeptide of type I procollagen.

We describe a family with an apparently autosomal-dominant trait that caused extremely high circulating concentrations of the carboxyl-terminal propeptide of type I procollagen (PICP). All family members examined had normal values for other biochemical markers of bone formation and degradation and no related clinical abnormalities. Furthermore, their serum concentrations of the amino-terminal propeptide of type I procollagen (PINP) were normal. Although PINP and PICP are released from the same precursor molecule, PINP is cleared from the circulation via the scavenger receptor in liver endothelial cells, whereas PICP is cleared via the mannose receptor of these cells. We thus hypothesize that the clearance of circulating PICP is compromised in the affected subjects of this family, the result of either a defective mannose receptor function or an abnormal molecular structure of their PICP.

Adolescent↗
PubMed1993

Experimental infection of Chlamydia pneumoniae in mice.

NIH/S, Swiss Webster, and BALB/c mice were infected intranasally with three Chlamydia pneumoniae isolates, Kajaani 6, Helsinki 12, and TW-183. C. pneumoniae could be isolated from the lung homogenates and bronchoalveolar lavage fluids up to the third week post-infection. Specific serum IgG antibodies against C. pneumoniae reached high levels in the third week and remained elevated until the end of the 6-week follow-up period. Serum IgM levels were highest in the third week post-infection and started to decrease thereafter. In spite of these signs of ongoing infection, the mice did not show any symptoms of disease. NIH/S mice could be readily and uniformly infected, while BALB/c mice were the most resistant and developed the weakest antibody response. The greatest histological changes were detected in NIH/S mice as well. The inflammatory infiltrate, which consisted of lymphocytes and plasma cells throughout the study, was restricted to the peribronchial and perivascular space and to the interstitium of the lung parenchyma.

Animals↗
PubMed1993

Is alcohol an osteoporosis-inducing agent for young and middle-aged women?

The effects of alcohol abuse on the bone of women have scarcely been investigated, although women are more prone than men to osteoporosis. We studied 19 noncirrhotic female alcoholics (aged 24 to 48 years) hospitalized for 2 weeks for withdrawal and three groups of control women (n = 182). Sixteen patients and all control subjects had regular menstrual cycles. Forearm bone mineral content (BMC) and axial bone mineral density (BMD) were measured by single-photon absorptiometry and dual-energy x-ray absorptiometry, respectively. Parameters of bone metabolism were analyzed at the beginning and end of the withdrawal period. BMC and BMD did not differ between patients and controls at any of the five measurement sites. On admission, bone formation of the alcoholics was depressed as reflected by osteocalcin levels (-48%, P < .01); it normalized during abstention (P < .01). Urinary hydroxyproline, a parameter of bone resorption, and serum intact parathyroid hormone were at the control level throughout the observation period. Serum ionized calcium level increased by 4% (P < .0001), and serum free fatty acid (FFA) levels decreased by 30% (P < .05) during withdrawal; there was an inverse correlation between changes in these two parameters (r = -.49, P < .05). On admission, serum concentrations of 25-hydroxyvitamin D3 [25-OH-D3] and 1,25-dihydroxyvitamin D3 [1,25-(OH)2-D3] were reduced by 46% (P < .001) and 16% (P = .16); these did not normalize during abstention. In conclusion, provided that liver cirrhosis and gonadal dysfunction are not contributing, even heavy drinking does not seem to decrease bone mass in young and middle-aged women.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

High density lipoprotein subfractions, apolipoprotein A-I containing lipoproteins, lipoprotein (a), and cholesterol ester transfer protein activity in alcoholic women before and after ethanol withdrawal.

We studied 11 female alcoholics before and after ethanol withdrawal of 2 weeks and 10 healthy normolipidaemic, nonalcoholic women of similar age. In alcoholic women the HDL2 mass was increased by 63% (P < 0.01) on admission and normalized (P < 0.01) during abstention. The concentrations of HDL3 cholesterol and its mass remained unchanged throughout the study. Consistently with the fall of HDL2 gradient gel electrophoresis analyses also demonstrated decrease of the cholesterol concentration of HDL2b and HDL2a (P < 0.05) during alcohol withdrawal. On admission the apo A-II concentration was increased by 48% (P < 0.01) and it was normalized (P < 0.001) during abstention. Among apo A-I containing lipoproteins the most prominent change occurred in Lp A-I:A-II, which fell by 32% (P < 0.01) during 1 week's alcohol withdrawal. During abstention the lipoprotein (a) concentration increased in 10 out of 11 women. In patients cholesteryl ester transfer (CETP) activity increased by 35% (P < 0.01) during 1 week of ethanol withdrawal. On admission postheparin plasma lipoprotein (LPL) and hepatic lipase activities were increased by 25% (P = NS); during 1 week's abstention they both returned to the control level (P < 0.05- < 0.01). In conclusion, chronic alcoholic women display multiple changes of lipoprotein metabolism which are rapidly reversed during abstinence. In contrast to alcoholic men, studied previously by us using the same study design and methods, there was no significant elevation of HDL3 cholesterol and apo A-I. The data suggest that alcohol interferes with several regulatory steps of HDL metabolism which are partly gender dependent.

Adult↗
PubMed1993

Bone and the 'comforts of life'.

Coffee drinking, smoking and especially alcohol abuse are considered to be risk factors for fractures and osteoporosis. Caffeine causes acute increase in urinary calcium excretion, but epidemiological evidence for the effects of coffee consumption on the risk of fractures is contradictory. Many, (but not all) studies point to decreased bone mass or increased fracture risk in smokers. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density (BMD). These changes may also be produced by factors commonly associated with alcohol abuse, e.g. nutritional deficiencies, liver damage and hypogonadism. Alcohol, however, has clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcaemia and hypercalciuria. As assessed by serum osteocalcin levels, prolonged moderate drinking decreases the function of osteoblasts, the bone-forming cells. In addition, chronic alcoholics are characterized by low serum levels of vitamin D metabolites. Thus, alcohol seems to have a direct toxic effect on bone and mineral metabolism. In contrast, it has recently been reported that moderate alcohol consumption by postmenopausal women may have a beneficial effect on bone.

Animals↗
PubMed1992

Dual-energy X-ray absorptiometry in normal women: a cross-sectional study of 717 Finnish volunteers.

The bone mineral density (BMD) of the lumbar spine and proximal femur was measured using dual-energy X-ray absorptiometry in 717 healthy women aged 20-70 years. The maximal mean BMD was found at the age of 35-39 years in the spine and at the age of 20-24 in the femoral neck and Ward's triangle. No significant change in lumbar BMD was found from the age of 20 to 39 years. The spinal BMD values were relatively stable from age 20 to 39 years, whereas a linear decrease in BMD in the femoral neck and Ward's triangle was already apparent in the youngest age group (20-24 years). The major fall in BMD in all sites was related to the menopause. The overall decreases in BMD from the peak values to those at age 65-70 years were 20.4%, 19.0% and 32.6% in the lumbar spine, femoral neck and Ward's triangle, respectively. The correlation of trochanteric BMD with age was poor. BMD was positively correlated with weight in all measurement sites. Nulliparity was found to be a risk factor for osteoporosis. The present study confirmed that the menopause has a significant effect not only on spinal BMD but also on femoral BMD. Lumbar BMD was lower and BMDs in the proximal femur were higher in Finnish women than in white American women. This emphasizes the importance of national reference values for BMD measurements.

Absorptiometry, Photon↗
PubMed1992

Bone mineral density and abstention-induced changes in bone and mineral metabolism in noncirrhotic male alcoholics.

BACKGROUND AND PURPOSE: Abuse of alcohol may derange bone metabolism and cause osteoporosis. Due to confounding factors associated with alcohol abuse, however, the effect of alcohol itself on bone loss remains obscure. The influence of alcohol intake on bone and mineral metabolism is rather well known, but how the metabolism normalizes during withdrawal has rarely been investigated. The aims of the present study were to evaluate the alcohol-induced changes of bone and mineral metabolism and their recovery during abstention, and to reassess any possible link between alcohol abuse and osteoporosis. PATIENTS AND METHODS: We studied 27 non-cirrhotic male alcoholics hospitalized for 2 weeks for withdrawal. For comparison, three groups of control subjects were examined. Serum and urinary parameters of bone and mineral metabolism as well as intestinal absorption of calcium were determined at the beginning and end of the treatment period. Bone mineral density (BMD) was measured by dual-energy x-ray absorptiometry at four axial sites (lumbar spine, femoral neck, Ward's triangle, trochanter). RESULTS: On admission, bone formation in the alcoholics was reduced as reflected by decreased serum levels of osteocalcin (-28%; p < 0.05) and procollagen I carboxyterminal propeptide (-17%; p < 0.05). Both parameters normalized within 2 weeks of abstention (p < 0.0001 and p < 0.01, respectively). Urinary hydroxyproline, a parameter of bone resorption, was at the control level on admission and increased slightly during abstention (p < 0.05). Serum ionized calcium increased by 3% (p < 0.0001) during withdrawal. Concomitantly, serum free fatty acids (FFA) decreased by 38% (p < 0.001), and there existed an inverse correlation (r = -0.50, p < 0.05) between changes in ionized calcium and FFA. Serum levels of intact parathyroid hormone and vitamin D metabolites were similar in patients and controls throughout the whole observation period. Intestinal absorption of calcium measured by stable strontium was 37% higher in alcoholics than in controls (p < 0.001); it decreased to nearly normal toward the end of the treatment period. Mean axial BMD did not differ between patients and controls at any of the four measurement sites. However, BMD decreased parallel with duration of drinking history in the alcoholics at all axial sites (p < 0.05 to < 0.01, analysis of covariance with age and weight as covariates). CONCLUSIONS: Decreased bone formation, which is uncoupled from ongoing bone resorption, recovers completely during 2 weeks of abstention. In the absence of confounding factors, the central BMD is normal in noncirrhotic male alcoholics, although the negative effect of alcohol on BMD is evident when duration of excessive drinking is taken into account.

Absorptiometry, Photon↗
PubMed1992

The dose-dependency of alcohol-induced hypoparathyroidism, hypercalciuria, and hypermagnesuria.

Ingestion of alcohol evokes hypoparathyroidism, hypercalciuria, and hypermagnesuria. The dose-dependency of these changes has not been assessed before. We measured the serum concentrations of intact parathyroid hormone (PTH), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of alcohol per kg of body weight. As compared with the control experiment the maximum reductions in the mean PTH concentration were 31% (P = 0.19), 31% (P = 0.20) and 45% (P = 0.01) with the three alcohol doses, respectively. After stopping drinking, the urinary excretion of calcium was 85%, 142% and 207% higher during the three alcohol experiments than during the control session (P < 0.05, < 0.01 and < 0.01, respectively), also urinary magnesium increased up to threefold. We conclude that in nonalcoholic subjects acute alcohol intake induces hypoparathyroidism, hypercalciuria, and hypermagnesuria, the latter two being dose-dependent. The direct renal effects of alcohol are the major mechanisms for hypercalciuria and hypermagnesuria, but hypoparathyroidism contributes to hypercalciuria at high levels of alcohol intoxication.

Adult↗
PubMed1992

Bone mineral density measured by dual-energy X-ray absorptiometry in normal men.

A cross-sectional study of 222 healthy Finnish men aged 20-69 years was performed to establish reference values of bone mineral density (BMD) using dual-energy X-ray absorptiometry (DEXA). The effects of age, and of some physical and lifestyle factors on BMD of the lumbar spine and proximal femur (femoral neck, Ward's triangle and trochanter) were investigated. The maximal mean BMD was observed at the age of 20-29 years in all the measurement sites. Except for the trochanteric area, BMD diminished along with age, the over-all decrements being 4%, 11%, and 23% in the lumbar, femoral neck and Ward's triangle areas, respectively. BMD was in a positive relationship to weight and height in all the measurement sites. The adjusted (for age, height and weight) BMDs were higher (P less than 0.05) in the group of daily dietary calcium intake greater than 1200 mg as compared with the group of lowest calcium intake (less than 800 mg day-1) in the three femoral areas. Cigarette smoking or alcohol drinking had no obvious effect on BMD.

Absorptiometry, Photon↗
PubMed1992

Effect of calcitonin on the alcohol drinking of rats.

Previous work has shown that calcitonin inhibits eating by rats and that it affects several neurotransmitter systems suspected to play a role in alcohol consumption. The present study was an initial test of whether calcitonin does affect voluntary alcohol consumption by male Wistar rats with prolonged alcohol experience. Calcitonin (20 IU/kg) or saline was injected subcutaneously on 10 consecutive days when the rats (n = 20) had continual access to 10% (v/v) ethanol solution, and to food and water. Using a cross-over design, the effects of 40 IU/kg calcitonin vs. saline were then examined in a second 10-day treatment period. Similar patterns of effects were obtained with both calcitonin doses, but the patterns differed with alcohol, food, and water intake. Alcohol drinking showed biphasic changes with both doses, producing highly significant Treatment x Day interactions (p < 1E-10 and p = 6E-7): it was significantly reduced on the first day of calcitonin treatment and significantly increased on the last few days. Food intake was reduced on all calcitonin days although most markedly on the first. Water drinking was not altered on the first calcitonin day, but was greatly increased on the second, then gradually returned toward the baseline. In a second experiment, the animals were switched to 1 hr of alcohol access per day, and calcitonin (20 IU/kg) was administered periodically to one group 4 hr before the alcohol access. Alcohol drinking was significantly reduced in all cases when the calcitonin injection was preceded by at least 1 day without calcitonin.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1991

Transient hypoparathyroidism during acute alcohol intoxication.

BACKGROUND: Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however. METHODS: We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol. RESULTS: The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001). CONCLUSIONS: Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.

Adult↗
PubMed1991

Alcohol and bone.

Abuse of alcohol is considered to be an important risk factor for fractures and osteoporosis. Alcohol abuse is associated with deleterious changes in bone structure detected by histomorphometry, and with a decrease in bone mineral density. These changes may also be produced by factors commonly associated with alcohol abuse, e.g., nutritional deficiencies, liver damage, and hypogonadism. Thus the etiology of alcohol-associated bone disease is multifactorial. Alcohol has, however, clear-cut direct effects on bone and mineral metabolism. Acute alcohol intoxication causes transitory hypoparathyroidism with resultant hypocalcemia and hypercalciuria. Prolonged moderate drinking elevates serum parathyroid hormone (PTH) levels, whereas chronic alcoholics are characterized by low serum levels of vitamin D metabolites with resultant malabsorption of calcium, hypocalcemia, and hypocalciuria. Independently of whether alcohol consumption is of short duration, social, or heavy and chronic, it seems to suppress the function of osteoblasts, as evidenced by low serum levels of osteocalcin. It has recently been reported, however, that alcohol can also have a beneficial effect on bone. Among postmenopausal women, moderate alcohol consumption correlates positively with central and peripheral bone mineral density, and with serum estradiol levels.

Bone Density↗
PubMed1991

Bone mineral density measured by dual-energy X-ray absorptiometry in healthy Finnish women.

A cross-sectional study of 351 healthy Finnish women aged 20-76 years was done to establish reference values of bone mineral density (BMD) using dual-energy X-ray absorptiometry (DEXA). The effects of age and of several physical and lifestyle factors on BMD of the lumbar spine and proximal femur (femoral neck, trochanter, and Ward's triangle area) were investigated. Altogether 58 women were excluded from the final analysis due to significant spinal osteoarthritis or other diseases or drugs known to influence calcium or bone metabolism. The precision of the method was 0.9, 1.2, 2.7, and 2.4% in the lumbar, femoral neck, Ward's triangle and trochanter area, respectively. Lumbar BMD was increased by 30% (P less than 0.001) in 15 patients with osteoarthritis (21% of women 50 years or older), but it was apparently unaffected in 5 cases with aortic calcification. Except for the trochanter area, BMD diminished along with age, and this was significant after the menopause. The peak of mean BMD was observed at the age of 31-35 years in the spine and at the age of 20-25 years in the femoral neck and Ward's triangle. BMD was in a positive relationship to weight both in premenopausal and postmenopausal women and to the use of oral contraceptives in premenopausal women and to that of estrogen replacement therapy in postmenopausal women. Labors and pregnancies had a weak positive effect on BMD in premenopausal women. As compared with nonusers premenopausal women who had used alcohol showed a slightly decreased BMD of Ward's triangle. In postmenopausal women there was a positive correlation between alcohol intake and BMD.

Adult↗
PubMed1991

The effect of moderate alcohol intake on serum apolipoprotein A-I-containing lipoproteins and lipoprotein (a).

Two main types of lipoprotein particles are identified within high-density lipoprotein (HDL): those containing both apolipoprotein (apo) A-I and apo A-II (Lp A-I:A-II) and those containing only apo A-I (Lp A-I). To study the effects of prolonged moderate alcohol intake on apo A-I-containing lipoproteins in serum, 60 g/d of ethanol was administered to 10 healthy male volunteers (age, 27 to 45 years) during 3 weeks. The drinking period was preceded and followed by an abstinence period of 3 weeks. The HDL3 cholesterol level increased by 17% (P less than .01) and decreased by 22% (P less than .001) on and off alcohol, respectively. The HDL2 cholesterol increased by 17% (P = NS) during ethanol intake and decreased by 14% during the following abstention (P less than .01). The serum concentration of apo A-I increased by 17% (P less than .001) during drinking and came back to the starting level after 2 weeks of abstention. Ethanol intake caused an increase in the serum levels of both Lp A-I and Lp A-I:A-II, the former explaining one third of the total increase of apo A-I. The Lp (a) concentration decreased by 33% (P less than .05) during the first week of ethanol intake, but increased back to the starting level until the end of drinking. These data suggest that the increment of the antiatherogenic Lp A-I may be one beneficial effect provided by ethanol with respect to coronary heart disease.

Adult↗
PubMed1991

Effects of 3 weeks' moderate alcohol intake on bone and mineral metabolism in normal men.

To study the effects of prolonged moderate alcohol intake on bone and mineral metabolism, 60 g/day of ethanol was administered to 10 healthy male volunteers during 3 weeks. The drinking period was preceded and followed by an abstinence period of 3 weeks. The serum level of osteocalcin decreased by 30% towards the end of the alcohol period (P less than 0.01), recovering by 25% after the termination of drinking (P less than 0.01). The serum level of intact parathyroid hormone increased to the end of the drinking period (P less than 0.05). After stopping drinking it came back to baseline (P less than 0.05) within a week. The serum levels of 25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, the serum and urinary levels of calcium, and the intestinal absorption of calcium measured by stable strontium remained practically unchanged throughout the whole observation period. We conclude that prolonged moderate alcohol intake impairs osteoblastic function, leading to lowered serum levels of osteocalcin, but it does not derange vitamin D metabolism.

Adult↗
PubMed1991

Life-threatening laryngeal edema in a pregnant woman previously treated for thyroid carcinoma.

A woman previously treated for papillary thyroid carcinoma developed life-threatening laryngeal edema during each of two pregnancies. The second episode led to tracheostomy. The laryngeal edema probably resulted from immobilization of the vocal cord(s), possibly caused by the thyroid carcinoma treatment combined with upper respiratory infection and the general tendency toward edema during pregnancy. Patients with a narrow upper respiratory airway must be adequately monitored during pregnancy because prompt intervention may be needed.

Adult↗