[Excretion of the urinary enzymes alanine aminopeptidase and beta-glucuronidase in cystostatic perfusion therapy]. / Ausscheidung der Harnenzyme Alaninaminopeptidase (AAP) und beta-glucuronidase (BGC) bei zytostatischer Perfusionstherapie.

Following cytostatic perfusion therapy in patients with malignant melanoma of the lower extremity despite a separation of the regional circulation from the systemic circulation a rhythmically phase-like increased excretion of urinary enzymes and protein developes. The changes in the behaviour of the excretion of enzymes registered under tumour therapy without a simultaneous reaction of usual functional parameters emphasize the importance of the urinary enzymes as early phase parameters. In this study the urinary enzymes were used for the judgement of the systemic effect of the cytostatic perfusion therapy.

[Renal enzyme excretion in tumors and tumor therapy]. / Renale Enzymausscheidung bei Tumoren und Tumortherapie.

None of the hitherto investigated enzymes of the urine can be used as marker for the proof of tumours. Hopeful starts in this respect are to be seen in an increased beta-glucuronidase excretion and in a decreased gamma-glutamyl transpeptidase excretion as well as in an increased LDH5/LDH1 ratio. The lysozyme excretion with the urine gives important references to the differential diagnosis, the assessment of the prognosis and therapy of acute leucoses. An importance obtained enzyme determinations in the urine for the clarification of pathobiochemical processes of the alteration of the kidney by neoplasms, tumour-lysis-syndromes, cytostatics, tumour radiation and operations of tumours. Courses of enzyme excretion during tumour therapy which as a rule show a rhythmic hyperenzymuria allow conclusion to the moment of the flow the catabolic products of the tumour at the kidney and to the different reaction of the tubular epithelium to these substances.

Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs.

Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.