[Folic acid and the risk of neural tube defects].
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Biomedical subjects
Publications and source records attributed to L Söderhjelm.
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The involvement of folic acid in the aetiology of neural tube defects (NTDs) has been discussed for decades. Both observational and controlled intervention trials have shown periconceptional folic acid supplementation (PFAS) to significantly reduce the incidence both of first-time and recurrent NTDs. PFAS may also be associated with reduction in the incidence of certain other congenital malformations, preterm delivery, and intra-uterine growth retardation. However, the mechanism whereby folic acid exerts its protective effect remains unclear. Thermolabile 5,10-methyl-enetetrahydrofolate reductase was the first folate-related enzyme to be associated with an increased risk of NTDs. This genetic variant may result in increased plasma homocysteine levels, which have been linked to an increased risk of NTDs. The folate-dependent genetic variants known today can explain no more than 30-50 per cent of the observed protective effect of folate. However, available evidence suggests low maternal folate status itself to be the major determinant of NTD risk. Since the vast majority of NTDs are first occurrences, and in Sweden a large proportion of fetuses with spina bifida remain undetected at routine ultrasonography during pregnancy, primary prevention by means of PFAS represents a major potential public health asset, capable of reducing both mortality and morbidity due to NTDs. Accordingly, implementation of a national strategy to reduce the incidence of NTDs, and promote awareness among health care providers and women of reproductive age of the benefits of PFAS is strongly to be recommended. Although supplemental folic acid tablets are the best proven means of improving folate status, compliance may be a problem, which emphasises the importance of considering a nutrient fortification programme as a complementary strategy for reducing the incidence of NTDs.
Packaging samples for many kinds of foodstuffs were received from manufacturers together with basic information about the materials used in their production. Half of the 29 samples studied contained phthalates in amounts exceeding 5 mg/kg. Two types of paper bag intended for sugar and exceptionally high phthalate contents although they were flexo printed. The maximum contents of di-isobutylphthalate (DIBP) and dibutylphthalate (DBP) were 450 and 200 mg/kg, respectively. The phthalates found originated from adhesives used in the joints of the packaging. In other packagings manufactured at the same time, DIBP concentrations varied from 92 to 193 mg/kg. Phthalates were also determined in sugar before and after packaging. Migration of phthalates ranged from 57 to 74% of the original content in the packaging after 4 months storage. Packed sugar contained DIBP 2.2-2.6 mg/kg and DBP 0.5-1 mg/kg. The sugar packagings were also tested using Tenax as a food stimulant. The results indicated that 69-91% of the original content of the phthalates migrated into Tenex after 10 days at 40 degrees C. The major drawback with migration testing using Tenax is its high cost; it is not practical to fill the whole 1 kg packaging with Tenax, and smaller samples of packaging must be used instead. However, the distribution of substances in the packaging might be non-uniform. In the sugar packagings studied here, the difference between phthalate concentrations in two samples taken from the same packaging was nearly 100-fold.
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A study of 116 patients admitted on the suspicion of myocardial infarction is presented. Twenty three of the patients were found to have infarction. For the diagnosis of infarct the most reliable biochemical analyses at present appear to be serum creatine kinase (S-CK, E.C.2.7.3.2.) with its isoenzyme S-CKMB and serum lactate dehydrogenase (S-LD, E.C.1.1.1.27.) with its isoenzyme S-LD-1. If an organization with blood samples at fixed intervals after the appearance of symptoms could be arranged, this would be most recommendable. In many hospitals this is, however, difficult and the blood samples have to be drawn at specified hours. In the four hospitals in the county of Västernorrland, Sweden, this latter procedure has been introduced. Blood is drawn at the arrival of the patient, at 8 am and 8 pm the first day, and at 8 am the next two days of the stay in hospital. In the first two samples S-CK and S-LD are determined, in the third S-CK, in the fourth S-CK and S-LD and in the fifth S-CK. If the values are elevated, S-CKMB and S-LD-1 are determined. S-Myoglobin has been found valuable in the early exclusion of the diagnosis of infarction.
Plasma pyridoxal phosphate (PLP) was determined in 10 newborn infants (two pairs of twins), their 8 mothers, and in addition in the mothers' breast milk. Mothers who did not take extra vitamin B-6 during pregnancy had lower levels of PLP both in plasma and in their milk. The infants' PLP decreased during the first two weeks of life when receiving only their mothers' milk. None of the mothers nor the infants showed any clinical signs of vitamin B-6 deficiency.
Forty patients with diabetes mellitus and a reference group of forty-five healthy controls have been studied. Significantly increased serum concentrations of parathyroid hormone and calcitonin were found in the diabetics as well as increased levels of alkaline phosphatase activity and phosphate independent of the duration of the diabetic state. No difference was found in serum calcium levels when compared with the healthy controls. Since these results cannot be explained by diabetes nephropathy an altered balance between parathyroid hormone and calcitonin in diabetes mellitus is postulated.
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In a material of 74 elderly patients with cerebral symptoms, most of them on account of atherosclerosis, deficiency of pyridoxal phosphate is uncommon: only ten had extremely low plasma levels. Nine of the patients had rather high levels of serum tryptophan. This might depend upon poor metabolization when pyridoxal phosphate is available in insufficient supply. In addition mean values are given for tryptophan, tyrosin and serotonin in this group of patients.
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