[Palliative medicine--physician's responsibility]. / Palliativmedizin--Eine ärztliche Verpflichtung.

When caring for patients with an incurable progressive disease, the physician experiences a feeling of powerlessness because there is no curative treatment that he can offer. The reaction to this must not be resignation, but active palliative medicine to achieve the best possible quality of life for the remaining time. Palliative medicine is a holistic concept of treatment in an outpatient or inpatient setting, integrating physical, psychological, social and spiritual aspects. Palliative medicine started in Germany in the 1980s with a manifest delay compared to Great Britain and the Scandinavian countries and developed in the 90s with a growing dynamic. Even so, we are still a long way from a satisfactory situation in the field of palliative medicine in Germany. This is true for the practical implementation of palliative medicine in the outpatient or inpatient setting, for the training of physicians and nurses and for teaching and research at universities. The decision-makers in our health care system are called upon to support palliative medicine and ensure access to palliative care all over the country. Palliative medicine was started to ease suffering, preserve or restore autonomy and maintain dignity. As an active life aid it is, in our opinion, an alternative to any demand for euthanasia.

Effects of a low selenium state in patients with phenylketonuria.

Eighty-seven participants of the German Collaboratory Study for Children with Phenylketonuria (PKU) presented low plasma, whole blood and hair selenium (Se) values, reduced urinary selenium excretion, and decreased plasma and erythrocyte glutathione peroxidase activity in comparison with a healthy reference group (all figures p < 0.001). Aspartate amino transferase and thyroxine (T4) concentrations in plasma were inversely correlated with the selenium blood values of the PKU children. Somatic measurements showed a negative standard deviation score of body height in the PKU children compared with reference values. Despite the different Se supply, the infants did not present any specific Se deficiency symptoms.

Selenium and glutathione peroxidase activity in Hungarian children.

Selenium (Se) in plasma, whole blood and erythrocytes as well as glutathione peroxidase (GSH-Px) activity in plasma and erythrocytes were investigated in 161 healthy Hungarian children aged 1-15 years. Se was determined by AAS with hydride generation. The estimation of GSH-Px activity was performed in plasma with tertbutyl-hydroperoxide (t-BOOH) and in erythrocytes with hydrogen peroxide (H2O2) as acceptor substrates. The Se content in plasma (0.63 +/- 0.12 mumol/L), whole blood (0.81 +/- 0.14 mumol/L) and erythrocytes (1.14 +/- 0.26 mumol/L, the GSH-Px activity in plasma (87 +/- 19 U/L) and erythrocytes (5.93 +/- 1.04 U/gHb) was low in Hungarian children in comparison to values for children from other European countries. Samples from a rural area in southeast Hungary showed even lower Se content than samples from an industrial city in the northwest or from the capital. The Se in plasma and whole blood as well as GSH-Px activity in the plasma exhibited a clear age dependency. There was a good correlation between plasma Se and GSH-Px activity in all children (r = 0.633, p < 0.001). In addition, in children from the northwestern city and from the capital a correlation was found between Se content and GSH-Px activity of erythrocytes (r = 0.625, p < 0.001). There is no indication that the high mortality in young Hungarian adults from cardiovascular diseases is mainly caused by a low Se supply because there are no corresponding findings in the surrounding countries of southeastern or central eastern Europe with similar low Se states.

Treatment of primary mixed hyperlipidemia with etophylline clofibrate: effects on lipoprotein-modifying enzymes, postprandial lipoprotein metabolism, and lipoprotein distribution and composition.

In 17 patients with primary mixed hyperlipidemia we studied levels and composition of lipoproteins in fasting plasma, lipoprotein-modifying enzymes, and postprandial lipoprotein metabolism after an oral fat-tolerance test supplemented with vitamin A before, and 12 weeks after treatment with etophylline clofibrate. With treatment, fasting plasma cholesterol, triglycerides, and the levels of very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), and low density lipoproteins (LDL) decreased significantly; high density lipoprotein (HDL) cholesterol increased significantly. Treatment caused also an increase in the protein content of IDL, a decrease in the triglyceride content of LDL, and an increase in the size of LDL as assessed by gradient gel electrophoresis. Concentrations of triglycerides, chylomicrons, and chylomicron remnants after an oral fat load supplemented with vitamin A decreased by 33%, 30% and 6%, respectively (P < 0.005; P < 0.01; and P < 0.05). The activity of lipoprotein lipase and hepatic lipase in postheparin plasma increased by 51% and 45%, respectively (P < 0.01; P < 0.05). We found a decrease in the mass concentration of cholesteryl ester transfer protein (P < 0.05). Stepwise multiple regression analysis showed that the triglyceride content of LDL is determined primarily by fasting triglycerides (r = + 0.53, P < 0.05;baseline) and cholesteryl ester transfer protein (r = + 0.49, P < 0.05; 12 weeks); in contrast, the triglyceride content of HDL3 is determined exclusively by accumulation of postprandial triglycerides (r = + 0.67; P < 0.05; baseline) and postprandial chylomicrons (r = +0.87; P < 0.005; 12 weeks). We conclude that hypolipidemic treatment with etophylline clofibrate favorably affects the cardiovascular risk factor profile in primary mixed hyperlipidemia.

Selenium in German infants fed breast milk or different formulas.

At birth and at 4 months of age, selenium (Se) values of 129 term infants on three different diets were determined: 50 infants were breast fed (HM), 44 received formula based on cow's milk (F) and 35 were fed "hypoallergenic formula" (PHF) (partially hydrolysed whey protein). The Se status of a group of twins (n = 12) fed "hypoallergenic formula" was compared with the respective group of singletons. All infants had low plasma Se values during early infancy. The plasma Se of breast-fed infants remained stable (plasma Se 43 +/- 8 ng/ml at birth and at 4 months), whereas plasma glutathione peroxidase (GSH-Px) decreased (birth: 107 +/- 29 U/l; 4 months: 62 +/- 11 U/l). The formula-fed infants showed a reduction in plasma Se levels from birth to 4 months (38 +/- 10 ng/ml and 29 +/- 9 ng/ml, respectively). The decrease was even more pronounced in infants fed the "hypoallergenic formula". This group presented the lowest Se values (plasma Se 39 +/- 9 ng/ml at birth; 20 +/- 6 ng/ml at 4 months). Renal excretion of Se was found to be lower in the formula-fed infants (F and PHF) compared with the HM group. There was a significant correlation between plasma and urinary Se (r = 0.62, p = 0.0001). Urinary Se (microgram Se/g creatinine) appeared to be a good indicator of Se intake. Measurements of urine Se might be used as a screening method for the estimation of the Se supply. Weight and length increases in all infants were within the normal range. There were no differences between the different feeding groups.

Trace mineral status of full-term infants fed human milk, milk-based formula or partially hydrolysed whey protein formula.

Plasma zinc, copper, and selenium concentrations were determined in 129 full-term infants at birth and at the age of four months by electrothermal or hydride generation atomic absorption spectrometry. Of these, 49 infants were exclusively breast-fed (HM), 45 received various commercially available cow's milk formulae (F) and 35 infants were fed partially hydrolysed whey protein formula (PHF). The results were correlated with hematological, biochemical and somatic data. Plasma zinc values decreased from birth to the age of four months in all three groups (p < 0.001). The plasma Zn level of the babies fed PHF were similar to those of breast-fed infants, whereas in F-fed children the zinc values were significantly lower (PHF, 807 +/- 106; HM, 794 +/- 112; F, 725 +/- 111 micrograms l-1; all the measurements were performed at the age of four months). In infants fed PHF formula there was a negative correlation between plasma zinc and weight or height increments. In agreement with the literature, plasma copper and ceruloplasmin increased significantly within the first four months of life. The plasma copper content was similar in either feeding group. Plasma selenium was low at birth (40 +/- 9 micrograms l-1) and remained constant in breast-fed infants. In infants on PHF there was a steeper decline of plasma Se (20 +/- 6 micrograms l-1) than in infants fed cow's milk formula (29 +/- 9 micrograms l-1). Other parameters of the Se status showed a similar pattern. Despite the different zinc, copper, and selenium supply, plus presumedly different bioavailability, all the infants thrived.(ABSTRACT TRUNCATED AT 250 WORDS)

Selenium status and lipoproteins in healthy and diabetic children.

Selenium and the selenium-dependent glutathione peroxidase (GSH-Px) were measured in healthy and diabetic children from Germany and Hungary. Hyperglycemia and hyperlipidemia are present in diabetes mellitus and they are associated with increased lipid peroxidation. The selenium content of erythrocytes, whole blood and plasma, as well as of plasma glutathione peroxidase activity, were found to be low in the healthy Hungarian children compared to the healthy Germans. Both groups of diabetics had significantly higher blood selenium (1.05 +/- 0.14 versus 0.86 +/- 0.1 mumol/L in Hungarians, 1.34 +/- 0.21 versus 1.12 +/- 0.22 mumol/L in Germans) and higher plasma selenium (0.89 +/- 0.15 versus 0.68 +/- 0.01 mumol/L in Hungarians and 1.01 +/- 0.2 versus 0.88 +/- 0.19 mumol/L in Germans) than the healthy children of the same countries. In all diabetic children the plasma glutathione peroxidase activity and triglycerides were higher and the plasma HDL-cholesterols (HDLC = high density lipoprotein-cholesterol) lower than those in healthy controls. The patients showed linear correlations between blood glucose and plasma glutathione peroxidase activity, as well as in erythrocyte glutathione peroxidase activity with triglycerides (TG) and an inverse correlation with HDL-cholesterol. Plasma selenium correlated only in healthy children with triglycerides, cholesterol and HDL-cholesterol. Irrespective of the geographical region diabetics had a higher selenium status than healthy children. In addition, we found correlations between selenium and lipoproteins in the reference group. The mode of glycation, oxidative procedures and the selenium binding to lipoproteins could explain the different associations in the healthy and diabetic children.

Selenium status in Sudanese children with protein-calorie malnutrition.

In 68 Sudanese children with severe protein-energy malnutrition, age 1-4 years, the selenium status was investigated and the results were compared with those of healthy Sudanese and German children. The median selenium content in plasma of healthy Sudanese children (x = 59 micrograms/L) and with those of marasmus (x = 57 micrograms/L) were found to be in the same range. It was lower than in healthy German children (x = 82 micrograms/L). Patients with marasmic kwashiorkor exhibited still lower values (x = 42 micrograms/L. Within each group of malnourished children (marasmus, marasmic kwashiorkor, kwashiorkor) there were patients with low and with "normal" selenium values (taking the values of healthy German children as normal). Hair selenium values were not different between marasmic Sudanese children and healthy German children, probably due to reduced hair growth in malnourished children. Plasma glutathione peroxidase activity was reduced concomitantly with plasma selenium in the patients with protein-calorie malnutrition. There was a good correlation between plasma selenium and plasma glutathione peroxidase activity. A follow-up study showed that plasma selenium decreased during rehabilitation in those patients who had a "normal" value before treatment. This is probably due to the low selenium content of the two dietary formulae used, which contained 18 and 25 micrograms/L Se of formula,. It remains questionable whether the low selenium states and low selenium intake exhibit a healthy risk inhibiting further rehabilitation of the patients with severe protein-calorie malnutrition.

Acute selenium poisoning of a 2-year-old child.

After ingestion of an unknown amount of a gun blueing compound containing selenious acid (11 ml from the bottle fluid were missing, equivalent to 2.9 g Se) a 2-year-old girl suffered from continuous hyper-salivation, vomiting, diarrhoea, restlessness and muscle spasm. Blood pressure and pulse rate were increased. Symptomatic treatment was performed by parenteral fluid administration. The plasma Se concentration was increased to 20 times normal 5 h after ingestion. Erythrocyte Se exceeded plasma Se, 24 h after intoxication. Urinary Se excretion decreased parallel to the plasma Se concentration. Ten weeks later, the Se content of hair had risen to 10 times normal. The plasma glutathione peroxidase activity showed only a slight increase during the first 36 h, erythrocyte glutathione peroxidase, catalase and superoxide dismutase activities were not significantly altered. The child fully recovered.

Glutathione peroxidase and glutathione S-transferase activity of platelets.

A low Se intake in dietetically treated patients with phenylketonuria (PKU) or maple syrup urine disease (MSUD) leads to a marked reduction of the platelet glutathione peroxidase activity (GSHPx). The mean value amounted to 2.0 U/10(11) platelets with t-butyl hydroperoxidase (t-BOOH) (2.2 U/10(11) with H2O2) in patients and 5.8 U/10(11) with t-BOOH (5.4 U/10(11) with H2O2) in the control children. After Se supplementation with yeast rich in Se (dose: 135 micrograms Se/m2) the GSHPx activities rapidly increased. They reached a plateau after 2-3 weeks and remained there during the following 15-20 weeks of supplementation. After the cessation of supplementation there was a slow decrease, the values reached a low plateau after 24 weeks. In addition platelet glutathione S-transferase (GSHTf) was estimated with 1-chloro-2,4-dinitrobenzene. No significant difference between the values in healthy and dietetically treated patients in a low or normal Se state was observed. GSHTf did not exhibit peroxidase activity and did not show a compensatory increase when Se dependent GSHPx activity was low. The patients do not reveal clinical signs of disturbed platelet function. GSHPx may act in platelets via lipoxygenase on the prostaglandin pathway. The physiologic consequence of altered arachidonate metabolism, when GSHPx is deficient in platelets, remains to be elucidated.

Selenium supplementation: plasma glutathione peroxidase an indicator of selenium intake.

Plasma glutathione peroxidase activity is markedly reduced in dietetically treated patients with PKU or MSUD in comparison to health children of the same age. This is due to the low selenium content of their diet. During supplementation with yeast rich in selenium (200 micrograms selenium per day) for 3 months 2 healthy adults did not show any significant change of their plasma GSHPx activity. 5 dietetically treated patients with PKU or MSUD and a reduced selenium state showed a rapid increase of the plasma GSHPx activity after selenium supplementation were started with 120 micrograms Se/m2 x d. The values doubled within the first two days and reached a plateau after 1--3 weeks. The patients showed no clinical anomalities before or during the selenium supplementation besides the inherited defect of amino acid metabolism. Plasma GSHPx activity seems to be a good indicator of short-term changes of selenium intake in patients with reduced selenium state.