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A 64-year-old woman presented with a hemorrhagic perifollicular rash on her legs while taking warfarin. After biopsy, vitamin C deficiency was suggested as the diagnosis, which ascorbic acid assays later confirmed. Clinical resolution of the rash followed supplementation with vitamin C. Patients on a vitamin K limited diet may also be limiting their intake of vitamin C. Physicians should be aware of this possible correlation, and consider checking vitamin C levels in patients with a perifollicular hemorrhagic rash or other signs of vitamin C deficiency while on warfarin.

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Las enfermedades gingivales son una amplia familia de patologías diferentes y complejas, que se encuentran confinadas a la encía y son el resultado de diferentes etiologías. El interés por las alteraciones gingivales se basa no tanto en su gravedad, sino en su enorme prevalencia entre la población. Las enfermedades gingivales forman un grupo heterogéneo, en el que se pueden ver problemas de índole exclusivamente inflamatoria, pero también alteraciones de origen genético, traumático o asociadas a alteraciones sistémicas. En el Simposio Internacional de la American Academy of Periodontology, en 1999, se acordó incluir una categoría que hiciera alusión a los problemas únicamente localizados a nivel gingival. En el presente artículo se pretende recopilar toda la información necesaria para entender en qué consisten estos cuadros, en qué mecanismo etiopatogénico se basan y qué estrategias de tratamiento podemos poner en marcha para solucionarlos (AU)

Gingival diseases are a broad family of different and complex pathologies confined to the gingivae and which head from different aetiologies. Interest put on gingival alterations is based not so much on its severity but on its enormous prevalence among the population. Gingival diseases form an amorphous group in which not only problems of exclusively inflammatory nature can be seen, but also alterations of either genetic or traumatic origin or associated with systemic alterations. In 1999, at the International Symposium of the American Academy of Periodontology, it was agreed to include a category which made reference to problems located in the gingivae solely. The present review focuses on a compilation of all the information necessary to understand the meaning of these patterns, which ethiopathogenic mechanisms lay behind them and which strategies can be started up in order to solve them (AU)

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The author studied 99 epileptic patients in whom 5-10 years ago anticonvulsants had caused side-effects. In 10% of the patients, a stable remission of the paroxysmal manifestations and an improvement of the mental status was achieved after controlling the complications. The majority of the patients exhibited slow progression of the epileptic process following a reduction of disturbances induced by intoxication and folic acid deficiency. Severe toxic, metabolic and allergic complications (30%) were followed by further considerable progression of the paroxysmal and psychopathological symptomatology. The degree of progression and severity of the organic brain lesion in epileptic patients is an important factor affecting the manifestation of the side-effects associated with anticonvulsants and the efficiency of further anticonvulsive therapy. In 4% of the patients the author observed repeated drug-induced complications. The prophylaxis of repeated complications of the anticonvulsant treatment prevents epilepsy aggravation.

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The universal solvent dimethylformamide (DMFA) administered to guinea-pigs in a dose of 400 mg/kg bw per os for 14 days produced a considerable decrease in the content of total and reduced ascorbic acid (AA) in the liver, in all forms of AA in the adrenals, and lowering of vitamin C excretion with daily urine. The liver showed an increase in the concentration of dehydroascorbic acid and diminution of the concentration of cytochrome P-450 detected in liver homogenates. Additional administration of AA (50 mg/day) recovered the lowered level of the vitamin in the liver and adrenals but did not make the daily excretion of AA with urine return to normal. Additional administration of vitamin C to guinea-pigs recovered the level of cytochrome P-450 in liver homogenates, which was reduced during DMFA poisoning. One of the reasons for the development of vitamin C deficiency during DMFA poisoning is likely to be high oxidation of AA.

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Administration of the herbicide 2,4-DN (amine salt of 2,4-dichlorphenoxyacetic acid) to weanling rats in a dose of 1/20.000 and 1/2000 of the LD50 for 3 months brought about a 40-50% reduction of thiamine content in the organs and tissues of experimental animals as compared with control. The herbicide was introduced into a balanced formula diet. In the liver of rats given 2,4-DA, there was a 2-fold decrease in the content of flavine adeninedinucleotide, whereas the content of flavine mononucleotide showed a 2-fold rise. Besides, the rats given a lesser herbicide dose manifested a reduced excretion of riboflavine with urine, and an inhibition of liver succinate dehydrogenase. The same animals demonstrated an increase in the relative mass of the adrenals with a concurrent diminution in them of ascorbic acid content.

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The effect of certain drugs on nutrient metabolism is discussed. Antituberculotic drugs such as INH and cycloserine interfere with vitamin B6 metabolism and may produce a secondary niacin deficiency. Oral contraceptives interfere with the metabolism of folic acid and ascorbic acid, and in cases of deficient nutrition, they also seem to interfere with riboflavin. Anticonvulsants can act as folate antagonists and precipitate folic acid deficiency. Therefore, in some cases, supplementation with folate has been recommended simultaneously with anticonvulsant therapy. Cholestyramine therapy has been associated with malabsorption of vitamins; several reports suggest that cholestyramine affects absorption of the fat-soluble vitamins K and D and, in addition, may alter water-soluble vitamins, including folic acid. The study of the interaction of drugs and nutrients is an area that deserves a greater attention in the future, especially in groups where nutrient deficiencies may be prevalent.

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During the past 10 to 20 years it has become increasingly clear that a certain number of drugs may lead to increased vitamin requirements. However, it is unusual for symptomatic avitaminosis to develop, and then only when circumstances are present which in themselves increase the risk of vitamin deficiency. Therapeutic doses of drugs will interfere with the vitamin status only to a restricted degree, provided they are administered for brief periods and to patients receiving a normal supply of vitamins. Most cases of vitamin deficiency have in fact been described in connection with drugs usually taken for a longer period of time by patients who were already in negative vitamin balance as a result of disease or marginal supply of the necessary vitamins. This review describes some of the more important articles covering this topic.

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An absorption screen was performed in 10 chronic alcoholic patients within a few days of admission due to an acute alcoholic episode. Impaired absorption of d-Xylose was noted in three patients and low leucocyte ascorbic acid and serum folate levels in five. No abnormality was detected in jejunal histology. The absorption of water and electrolytes from the jejunum was studied in these patients using a triple-lumen tube perfusion system. The mean rate of absorption of water in the alcoholic subjects (50-0 +/- 2-3 ml/h) was significantly lower (P less than 0-001) than the mean value in 14 healthy control subjects (205 +/- 15-9 ml/h). A significant reduction of Na+ and Cl-absorption was also demonstrated in the alcoholic subjects. These results indicate that patients with acute-on-chronic alcoholism may have a function impairment of water and electrolyte absorption from the jejunum. This may, in part, account for some of the nutritional deficiencies in such patients and for symptoms such as diarrhoea which may be present.

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Plasma, leukocyte, and platelet ascorbic acid levels are decreased in women ingesting oral contraceptive steroids. Studies have shown that it is the estrogenic component of the oral contraceptive agents that is associated with the decresased ascorbic acid concentrations. Urinary excretion of ascorbic acid does not appear to be increased by the steroids. Although serum levels of copper are increased by estrogens and oral contraceptives, ascorbic acid catabolism does not appear to be increased (unpublished). Our preliminary data on tissue uptake of ascorbic acid suggest that changes in tissue distribution are one possible answer for the observed effects of the steroids on blood levels of ascorbic acid.

PIP: Plasma, leukocyte and platelet ascorbic acid levels have been shown to decrease in in women using oral contraceptives (OC). Supplemental ascorbic acid therapy ranging from 50-200 mg/day showed no difference between the values for supplemented and nonsupplemented OC use. Measurement of plasma ascorbic acid after supplementation with 500 mg ascorbic acid/day for 14 days showed that adequate supplementation to reach tissue saturation and maximum fasting plasma levels occurred in control subjects but not in OC users. Other studies indicated that when women were maintained for 75 days on high ascorbic acid intake, the plasma levels in OC users were lower than in controls. Studies in humans and animals suggest that the estrogen in OCs cause decreased plasma and tissue levels of ascorbic acid. Women taking oral progestin (.35 mg daily norethisterone) and depot progestin (150 mg medroxyprogesterone acetate im every 3 months) had similar leukocyte plasma and platelet levels of ascorbic acid to controls. 625 mg daily of conjugated estrogens showed lower plasma and leukocyte levels than controls. Whereas increase of urinary excretion of ascorbic acid during OC therapy has not been shown, an increase in serum copper levels has been shown under OC use and estrogen influence. It is suggested that an increased catabolism of ascorbic acid accounts for the decreased plasma and tissue levels in humans and animals with estrogen or OC steroids. Other unconfirmed or disputed suggestions include decreased absorption, changes in tissue distribution and decreased levels of reducing compounds. Tissue uptake patterns in steroid-treated animals appear altered suggesting that changes in tissue distribution may be associated with observed changes in ascorbic acid blood levels in OC users.

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