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Biomedical subjects

L Pitkänen

Publications and source records attributed to L Pitkänen.

7 recordsLinked to original sources

Aetiology of congenital hypothyroidism in Finland.

In Finland a nationwide screening programme for congenital hypothyroidism (CHT) has operated since 1980 with complete coverage. Among the total of 307,000 newborns screened, the incidence per 100,000 was 24.6 for thyroid dysgenesis and 4.0 for dyshormonogenesis. We conclude that, when screening is based on cord serum TSH, the false-positive results are caused mainly by difficult delivery. The most important factors associated with dyshormonogenesis were CHT in the family, origin from a geographic risk area, and origin of both mother and father from the same community. These reflect the autosomal recessive inheritance. The risk factors for dysgenesis were female gender, CHT in the family, birth in a geographic risk area, and birth during a risk period of the year.

Congenital Hypothyroidism↗

Thyroid function tests in elderly Finnish men.

Serum total thyroxine (T4), triiodothyronine (T3) and thyrotrophin (TSH) levels were determined among 65-84-year-old Finnish men living either in eastern Finland (n = 309) or in southwestern Finland (n = 389). The mean value for serum total T4 was 112.2 +/- 23.0 nmol/l in eastern Finland and 111.3 +/- 21.9 nmol/l in southwestern Finland. The mean value for serum T3 was 1.76 +/- 0.30 nmol/l in eastern Finland and 1.75 +/- 0.46 nmol/l in southwestern Finland. Serum TSH values showed the mean for men from eastern Finland to be 3.25 +/- 2.29 mU/l and the mean for men from southwestern Finland to be 3.11 +/- 1.83 mU/l. No differences were found in the means of the thyroid function tests between the two areas. Serum T4 levels were not related to age. Serum T3 values fell with age. In both areas, serum TSH levels were highest among men 70-74 years of age.

Age Factors↗

Finnish national screening for hypothyroidism. Few false positives, early therapy.

National cord blood screening for congenital hypothyroidism has operated in Finland with complete coverage since 1980. A low frequency of false positives, 0.08%, was achieved by supplementing the TSH screen with a T4 determination in borderline samples. Among 175188 infants the incidence of (unconfirmed) hypothyroidism was 1/2637. The median age at start of therapy was 6 days. The programme imposed a 2-3 week therapy on the false positive cases. This did not appear to cause any adverse effects. A mechanism for masking congenital hypothyroidism was observed: two athyroid infants were euthyroid at birth because of feto-fetal transfusion.

Congenital Hypothyroidism↗

Acute effects of marathon running on levels of serum lipoproteins and androgenic hormones in healthy males.

The acute effects of marathon (42.2 km) running on serum lipid and lipoprotein levels, particularly high-density lipoprotein (HDL) subfractions HDL2 and HDL3, and on levels of serum androgenic hormones, luteinizing hormone (LH), and testosterone were studied in 20 healthy non- champion -class joggers participating in the First North Karelian Heart Marathon. Serum triglyceride and cholesterol levels were unchanged after the marathon, whereas the lipoprotein distribution of both lipids was significantly altered. Very-low-density lipoprotein triglyceride (VLDL-TG) and cholesterol (VLDL-C) levels decreased significantly, whereas low-density lipoprotein triglyceride (LDL-TG) but not cholesterol (LDL-C) levels were increased, suggesting an accumulation of VLDL remnants in the LDL density range. HDL cholesterol (HDL-C) level rose significantly owing to an increase in HDL2-C. HDL3-C level remained the same. Serum levels of apolipoproteins A-I and A-II, the main apolipoprotein constituents of HDL, did not change during the marathon but their distribution between the HDL subfractions differed, indicating a conversion of HDL3 to HDL2. Serum levels of LH, testosterone, and sex-hormone-binding globulin (SHBG) all decreased during the marathon. The changes in levels of serum lipoproteins and androgenic hormones were not interrelated. We concluded that the short-term regulation of HDL levels during acute exhaustive exercise is controlled not by changes in serum androgenic hormones but by enhanced degradation of triglyceride-rich lipoproteins.

Adult↗