Taurine concentrations in serum of critically injured patients and age- and sex-matched healthy control subjects

Article Abstract:

Studies have shown that the processes involved in the production of taurine are not completely developed in the human newborn. Taurine is a derivative of the sulfur-containing amino acid cysteine, and is present in the bile in combination with bile acids. Taurine must be provided in the newborn diet to prevent taurine deficiency. Studies suggest that taurine deficiency may cause the development of cholestasis (cessation of bile excretion) during parenteral (intravenously administered) nutrition. Taurine deficiency may also cause inflammation of the gallbladder and the development of gall stones in adults. The association of decreasing levels of taurine and gallbladder inflammation soon after the start of parenteral nutrition would be consistent with previous reports of the effects of taurine deficiency. The levels of sulfur-containing amino acids, the elements that make up proteins, were measured in nine patients who suffered trauma, or injury. These patients received parenteral nutrition for seven days. The results were compared to measurements made in healthy subjects of the same age and sex. Blood levels of taurine were decreased by 60 percent in the patient group, compared with the healthy subjects. Blood levels of the amino acid methionine were higher in patients, but levels of cysteine were similar among patients and healthy subjects. The early decrease in taurine blood levels in trauma patients suggests that this amino acid may be important in the period following injury. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Wounds and injuries, Injuries, Amino acids, Taurine

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Selenium distribution in blood fractions of New Zealand women taking organic or inorganic selenium

Article Abstract:

The effects of supplementation with different forms of selenium (a trace mineral essential for humans) on its distribution in red blood cells and blood plasma were assessed. Selenium was given in either the organic form as selenium-enriched yeast (SeMet) or in the inorganic form as selenate. The study included three groups of 11 women: one group was given no selenium, one was treated with 200 micrograms of selenium as SeMet, and one was given 200 micrograms of selenium as selenate (supplements were taken daily for 32 weeks). Red blood cells and plasma were collected bimonthly and analyzed by gel filtration. The results showed differences in the distribution of selenium in the plasma between women given SeMet and those receiving selenate. In addition, selenium was associated mainly with hemoglobin, the oxygen-carrying pigment of red blood cells, in women taking SeMet. In contrast, selenium was distributed equally between the glutathione peroxidase and hemoglobin portions of red blood cells in women receiving the selenate form. The amount of selenium associated with the glutathione peroxidase portion was greater in the red blood cells and plasma of women taking selenate than the women taking SeMet. (Consumer Summary produced by Reliance Medical Information, Inc.)

Hemoglobin, Hemoglobins, Organometallic compounds, Glutathione

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Cardiomyopathy associated with nonendemic selenium deficiency in a Caucasian adolescent

Article Abstract:

Deficiency of specific nutrients can occur in patients who receive total parenteral nutrition (TPN) over the long term. TPN is the provision of calories and nutrients intravenously, and is administered to patients whose digestive systems are not functioning. Selenium is a trace element, meaning it is needed in tiny amounts to maintain physiological processes. Even though the amount required by the human body is small, a deficiency of selenium can have serious consequences, as illustrated by this case report. The patient had been on TPN for 17 months when she died of cardiac arrest caused by septic (infectious) shock. Seven months before she died, she was diagnosed with severe selenium deficiency and began treatment with supplemental selenium added to her TPN. While her blood levels of selenium increased, it was clear at autopsy that she had developed cardiomyopathy (disease of the heart muscle) due to prolonged selenium deficiency. This cardiomyopathy eventually led to the cardiac arrest. The chronic selenium deficiency may also have been related to the sepsis, which apparently triggered the cardiac arrest in the patient's diseased heart. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Cardiomyopathy, Myocardial diseases

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