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Postheparin-diamine oxidase (histaminase) in anaphylaxis.

The level of plasma postheparin-diamine oxidase was determined in two patients three days after an anaphylactic shock and was controlled four weeks, and also six months later. A decrease of the enzyme levels to about 10% of a control group was found and a slow enzyme increase to about 40% observed six months later. It seems probable that in anaphylaxis a depletion of the enzyme in liver and small intestine occurs as could be shown in animals after heparin load.

[Possible clinical importance of the activation of diamine oxidase (histaminase) in heparin treatment of renal diseases (author's transl)]. / Mögliche klinische Bedeutung der Aktivierung der Diaminooxidase (Histaminase) bei der Heparinbehandlung renaler Erkrankungen.

Heparin up until now has been in renal diseases for its anticlotting effect. An additional property of heparin is the activation of the diamine oxidase (histaminase). Whether a possible clinical importance of the diamine oxidase activation in heparin treatment of renal diseases exists or not remains unknown and is discussed.

Serum ribonuclease activity in patients during parenteral nutrition, chronic hemodialysis and acute pancreatitis.

Animal experiments have shown that malnutrition and protein deficiency states, respectively are associated with elevated tissue ribonuclease (RNase, E.C. 3.1.4.22) activities. The causal intracellular alterations are unknown. Assuming that increased tissue RNase activities are reflected by serum levels, a study was made of the serum RNase activities in 10 healthy controls eating a normal diet (group I), 7 patients on long-term parenteral nutrition (group II), 13 chronic hemodialysis patients (group III), and 9 patients with acute pancreatitis (group IV). In group I the serum RNase activity corresponded to 195.3 + or -58.8 U/ml. A significant (p less than 0.005) elevation was noted in groups II (314.6 +/- 95.3 U/ml) and III (374.1 +/- 102.1 U/ml), no difference being detected in group IV (295.1 +/- 191.9 U/ml).

Combined decrease of postheparin-diamine oxidase (histaminase) and postheparin-lipoproteinlipase in inflammatory diseases.

Diamine oxidase (DAO, histaminase), according to Schayer, is an essential enzyme in histamine metabolism. It metabolises also a variety of diamines such as putrescine and cadaverine and is generally accepted to be identical with histaminase. Lipoproteinlipase (LL) is assumed to play an essential role in lipid metabolism. In vertebrates, parenterally applied heparin causes a marked dose-dependent rise of the plasma level of both enzymes mainly due to the release from the enzyme containing organs. The plasmatic level changes of DAO and LL after heparin application (200 U/kg b.wt., i.v.) have been studied in 30 patients suffering from 20 different, predominantly inflammatory diseases. In all cases the release of postheparin diamine oxidase (PHD) and of post-heparin lipoproteinlipase (PHLA) was found to be markedly decreased. There existed a highly significant correlation between the degree of the release of both enzymes (r=0.843, p less than 0.0005). In all patients normal levels of plasma insulin were detected. No correlation was found between PHLA and plasma triglycerides levels. Decrease of PHD respectively PHLA was a more sensitive biochemical parameter than were changes of serum glutamic pyruvic transaminase in acute hepatitis and of C reactive protein (CRP) in chronic inflammatory kidney diseases. This finding is most likely a general phenomenon in inflammatory diseases. Besides hormonal regulation inflammation-dependent effects on PHLA have to be discussed.

Serum level changes of endogenous and postheparin diamine oxidase (histaminase) in clinical and experimental hepatitis.

In patients suffering from acute viral hepatitis (n = 12) an about 50 per cent decrease of serum diamine oxidase (DAO, histaminase, E.C.N. 1.4.3.6) was detected as compared to a healthy control group (n = 24). Normally, the intravenous injection of heparin is promptly followed by a marked rise of plasma DAO. In viral hepatitis, however, after application of heparin (200 IU/kg b.w., i.v.) the enzyme release from the visceral organs into the plasma was markedly decreased. There was an inverse correlation between the serum glutamic pyruvic transaminase (SGPT) and the postheparin enzyme. Normalization of SGPT occurred before the normalization of post-heparin diamine oxidase (PHD). In galactosamine "hepatitis" of rats (800 mg Gal-N/kg b.w., i.p.), in contrary to human viral hepatitis plasma DAO increased about 5-fold after heparin application. This increased PHD in plasma of Gal-N rats was correlated to enhanced animal's endogenous plasma DAO activity (r=0.685, p less then 0.0005, n = 54). The cause of these enzyme activity changes and its possible pathophysiological meaning are still unknown. It is concluded from these experiments that in Gal-N "hepatitis" of rats plasmatic DAO level changes are mediated by endogenous heparin, released from disrupted mast cells. Increased basal DAO levels correspond to the enhanced release after heparin application, both possibly induced by less stable binding of the enzyme to the cells of the small intestine in inflammation. Both, decreased endogenous and post-heparin DAO levels in human hepatitis would correspond to a depletion of the enzyme containing organs.

Diamine oxidase (histaminase) in chronic renal disease and its inhibition in vitro by methylguanidine.

The activity of plasma diamine oxidase (pyridoxal containing amine oxidase, histaminase, DAO), E. C. N. 1. 4. 3. 6., was found to be normal in 14 patients with chronic renal disease of different origins. However, after administration of heparin (200 IU/kg body weight, i.v.), the release of the enzyme into the plasma of the patients was markedly decreased when compared to that found in a group of 8 healthy volunteers. In patients with chronic renal failure the plasma concentration of pyridoxalphosphate, the coenzyme of DAO, was found to be significantly decreased. Furthermore methylguanidine, which is thought to be an important uremic toxin, was shown to be a potent non-competitive inhibitor of DAO in vitro (Ki5 X 10(5) M). The organ concentrations of methylguanidine are thought to correspond with the Ki value detected, as distribution studies using the tritiated toxin revealed organ accumulation up to five times the plasma level. Therefore, the decrease of DAO release after heparin stimulation in patients with chronic renal failure may be explained, in part, by inhibition of the enzyme as well as by a decreased coenzyme level. The results suggest that disturbed histamine metabolism may be involved in the production of some of the clinical symptoms commonly associated with chronic renal failure.

[Vitamin B6-deficiency and -substitution in chronic uremia (author's transl)]. / Vitamin B6-Mangel und- Substitution bei chronischer Urämie.

In patients with chronic renal failure on potatoe-egg-diet (0.4 g protein/kg body weight) an alimentary vitamin B6-deficiency occurs, which can be overcome by 20 mg vitamin B6/day. Chronic hemodialysis causes a vitamin B6 loss which amounts to a quantity similar to the daily urinary excretion in normal persons. No hints for an inhibition of the synthesis of pyridoxal phosphate could be found.