Infants delivered at term by mothers smoking at least 10 cigarettes daily during pregnancy (n = 46) were found to be growth retarded compared to infants of non-smoking mothers (n = 49), birthweights 3,445 +/- 385 (SD) g and 3,667 +/- 392 g respectively (p less than 0.05) in the two groups. Cord serum thyrotropin (TSH) was significantly decreased (8.2 +/- 4.0 U/l vs. 10.3 +/- 4.9 U/l) and free thyroxine index (FT4I)/TSH ratio significantly increased (18.8 +/- 9.0 vs. 14.4 +/- 7.6) (p less than 0.05) in the smoking group compared to infants of non-smokers. Cord serum thyroxine (T4) and FT4I were higher in the smoking group (149.0 +/- 22.4 nmol/l and 125.5 +/- 14.9 respectively) compared to infants of non-smoking mothers (140.6 +/- 21.6 nmol/l and 120.0 +/- 16.5 respectively), with borderline statistical significance (0.05 less than p less than 0.10). The results indicate that infants of smoking mothers may have a hyperfunction of the thyroid gland at birth compared to infants of non-smokers, with a negative feed-back on TSH production from the pituitary gland. Increased metabolic rate and oxygen consumption caused by fetal thyroid hyperfunction may be pathogenetic factors for the fetal growth retardation caused by maternal smoking.

No abstract

The clinical and pathologic features of a male patient with generalized glutathione deficiency and pyroglutamic aciduria are presented. The patient died at the age of 28 years. He was mentally retarded from infancy and developed progressive tremor, retardation of movement, and ataxia as from the age of 16. Neuropathologic examination of the brain disclosed a selective atrophy of the granule cell layer of the cerebellum and focal lesions in the visual cortex and the thalamus. The type and distribution of the lesions resembled those seen after mercury intoxication. However, in our patient the damage was probably caused by the lack of protection of glutathione against oxidative damage in the brain. Possible treatment of this rare metabolic disorder might include external supply of an antioxidant, e.g., a thiol capable of penetrating the blood brain barrier.

A method for the determination of angiotensin-converting enzyme in serum (S-ACE; EC 3.4.15.1.) with use of 3-(2-furylacryloyl)-L-phenylalanyl-glycyl-glycine (FAPGG) as substrate has been adapted for the Cobas Bio microcentrifugal analyser. The method allows 24 determinations per hour in a sample volume of 28 microliters with a within run precision of less than 3% and a between run precision of less than 5%. The reaction is linear up to at least 470 U/l. The reference interval in 92 blood donors has been determined to 14-110 U/l. The method correlates well with the manual method of Hurst & Lovell-Smith (r = 0.982). We have found the method excellently suited for routine assay.