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Folates in megaloblastic anaemia.

The importance of deficiency of the folic acid group of compounds (folates) in the pathogenesis of nutritional anaemias is receiving increasing recognition. There is evidence that the megaloblastic anaemias, due to either vitamin B(12) or folate deficiency, may be the cause of widespread morbidity in malnourished populations. It was therefore considered timely to review certain aspects of the role of folates in megaloblastic anaemia, with special reference to the dietary intake in relation to human requirements, and the recognition of folate deficiency in man.

Anemia↗

Destructive, granulating lesion in the temporal bone after elevated plasma homocysteine.

OBJECTIVE: This is a presentation of a seemingly new otolaryngologic disease. SETTING: This study was conducted at a tertiary referral center. CASE REPORT: A 38-year-old healthy man developed left-sided sudden deafness with vertigo and temporary left facial palsy. A granulating and destructive lesion in the left temporal bone was discovered; repeated histologic examination only showed simple granulation tissue. After 6 months, a part of the bony cochlea was extruded. With approximately 8 months' delay and after the patient had had postoperative lung embolism, plasma homocysteine was found to be significantly elevated, a condition known as an independent risk factor for thromboembolic lesions. In the acquired form, it is most often caused by nutritional deficiency of vitamin B cofactors. Accordingly, the patient was treated with folic acid, which rapidly normalized plasma homocysteine. Subsequently, the granulation tissue in the temporal bone gradually disappeared, clinically and radiologically, and the lesion healed, obviously without cochlea function. CONCLUSIONS: Thromboembolic lesion in the left temporal bone, probably in the thin end artery a. labyrintina, i.e., an avascular osteonecrosis. During the latest years, an association between avascular osteonecrosis (most often in the hip) and conditions with increased risk of thrombosis such as hyperhomocystinemia has been established but, to the best of our knowledge, it is never with a lesion in the temporal bone.

Adult↗

[Obstetric problems followed by stroke].

Obstetrical problems sometimes portend manifestations of atherosclerosis, as illustrated by two case reports. The first patient had the combination of hyperhomocysteinaemia due to chronic vitamin deficiencies in the diet, and smoking. The second was also a smoker and had a genetically determined mild hyperhomocysteinaemia, aggravated by chronic vitamin deficiencies resulting from poor dietary habits; she also had an increased folic acid requirement because of use of anti-epileptic drugs in combination with a familial predisposition for premature atherosclerotic manifestations. The first patient had four pregnancies, two of which ended in intrauterine foetal death due to placental infarction, and one in the birth of a dysmature boy. The second patient's four pregnancies ended twice in abortion and twice in the birth of a dysmature child; in one of the latter cases placental infarction was observed. Both women subsequently suffered cerebrovascular accidents while in addition, older cerebral infarctions were found to be present. Women with recurrent abortion, pre-eclampsia, placental infarction, placental detachment and foetal growth retardation should be examined, even if other risk factors are also present, for (mild) hyperhomocysteinaemia, and treated for it with vitamin suppletion (folic acid, vitamins B6 and B12), even although admittedly more research is necessary to make certain that such treatment has a preventive effect on the manifestations of this disorder.

Abortion, Habitual↗

The bioavailability of folic acid added to wine.

Folate deficiency is a frequent cause of anemia in alcoholics, but little attention has been paid to its prevention. Folic acid was readily soluble in wines of high ethanol content at concentrations of 10 microgram/ml. Lactobacillus casei folate activity of folic acid added to wines was well maintained during a month's storage at room temperature and fell to 61% to 66% of original activity after 3 months. Pteroylglutamic acid, 10 microgram/ml, added to wines and given in doses of the beverages (4 ml/kg body weight that caused inebriation, was well absorbed by six normal human volunteers (mean maximal increment in serum folate concentration +/- SEM, 71 +/- 8 ng/ml) and by seven recently intoxicated chronic alcoholics (mean increment, 94 +/- 4 ng/ml). Folate deficiency in alcoholics could be prevented by the fortification of alcoholic beverages with the vitamin.

Adult↗

Nutritional deficiency in oral candidosis.

A retrospective study of 108 patients was carried out to investigate the possible relationship between infection of the mouth with Candida albicans and blood levels of iron, folic acid and vitamin B12. The patients were separated into two groups--those with hyperplastic and those with atrophic candidal lesions--and compared with separate control groups. Twenty-one patients had chronic hyperplastic candidosis and seven were iron deficient. Comparison with an age- and sex-matched control group showed the differences to be significant only at the p less than 0.1 level. Seven of the patients with hyperplastic lesions had folic acid deficiency and the difference between patients and controls was statistically significant (less than 0.05). However, no significant differences in iron or folic acid deficiency were noted between 87 patients with atrophic candidosis and 65 conttrols, and vitamin B12 deficiency was not statistically significant for either the hyperplastic or the atrophic group. It is concluded that deficiency of iron, folic acid or vitamin B12 alone does not promote growth of Candida albicans on the oral mucous membrane but that in some susceptible individuals, iron or folic deficiency may facilitate epithelial invasion by hyphae of Candida albicans.

Atrophy↗

Dietary folic acid and the activity of brain cholinergic and gamma-aminobutyric acid (GABA) enzymes.

Charles River CD male rats were randomly divided into 3 groups of five each and placed on folate deficient, folate excess, and control diets respectively. glutamate decarboxylase GAD gamma-amino-butyrate aminotransferase (GABA-T), choline acetltransferase (ChAc), and acetylcholinesterase (AChE) were assayed in the rat brains after 6 weeks of dietary treatment. Neither folate deficiency nor folate supplementation influenced the enzymes associated with GABA and acetylcholine metabolism.

Acetylcholinesterase↗