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  • 1
    Electronic Resource
    Electronic Resource
    Zur Beeinflussung der Purin- und Pyrimidinsynthese durch Allopurinol (1975)
    Springer
    Journal of molecular medicine 53 (1975), S. 255-260 
    Details
    ISSN: 1432-1440
    Keywords: Purine metabolism ; pyrimidine metabolism ; orotic acid ; allopurinol ; Purinstoffwechsel ; Pyrimidinstoffwechsel ; Orotsäure ; Allopurinol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Allopurinol führt durch Hemmung der Xanthinoxydase zu einem Abfall der Serumharnsäure und der renalen Harnsäureausscheidung bei gleichzeitigem Anstieg der Ausscheidung von Hypoxanthin und Xanthin im Urin. Der Anstieg der Oxypurinelimination ersetzt jedoch bei den meisten Patienten nicht die Abnahme der renalen Harnsäureausscheidung. Dies wird auf eine zusätzliche Hemmung der Purinsynthese de novo zurückgeführt. Eine unterschiedliche Beeinflussung der endogenen und exogenen Uratquote durch Allopurinol bietet eine alternative Erklärung des Purindefizites. Die Beeinflussung des Pyrimidinstoffwechsels beruht auf einer Hemmung des Enzyms Orotidyldecarboxylase durch die Ribonucleotide von Allopurinol, Xanthin und Oxipurinol. Sie geht mit einer vermehrten Ausscheidung von Orotsäure und Orotidin im Urin einher. Die zusätzliche Gabe von Ribonucleinsäure führt zu einer deutlichen Abnahme der durch Allopurinol hervorgerufenen Orotacidurie. Der Hemmung der Orotidyldecarboxylase folgt unter kontinuierlicher Allopurinolverabreichung ein Anstieg der Aktivität von Orotatphosphoribosyltransferase und Orotidyldecarboxylase, dessen Mechanismus noch nicht vollständig geklärt ist. Allopurinol wird rasch metabolisiert. Nur 3–10% werden unverändert im Urin ausgeschieden. Hauptmetabolit ist Oxipurinol. Ein kleiner Anteil wird zu den Ribonucleosiden und Ribonucleotiden1 von Allopurinol und Oxipurinol umgewandelt.
    Notes: Summary Allopurinol inhibits xanthinoxydase. This results in a decrease of the serum and urinary uric acid: Simultaneously the renal excretion of hypoxanthine and xanthine increases. In most patients, however, the decrease of urinary uric acid is not completely replaced by the increase of oxypurines. This is attributed to an additional inhibition of de novo purine biosynthesis. The different effect of allopurinol on the endogenous and exogenous urates offers an alternative approach to explain the “purine deficit”. The effect of allopurinol on the pyrimidine metabolism is due to an inhibition of orotidylic decarboxylase by the ribonucleotides of allopurinol, xanthine and oxipurinol. This inhibition is followed by an increase in the urinary excretion of orotidine and orotic acid. The additional administration of ribonucleic acid leads to a striking decrease of the allopurinol induced orotaciduria. The continuous administration of allopurinol also produces an increase in the activity of orotate phosphoribosyltransferase and orotidylic decarboxylase. At this time the mechanism of this increase in activity is not completely understood. Allopurinol is metabolized rapidly. Only 3–10% of an administered dose are excreted unchanged in the urine. Most of the allopurinol is oxidized to oxipurinol. A small portion is converted to the ribonucleosides and ribonuclcotides of allopurinol and oxipurinol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01469116
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  • 2
    Electronic Resource
    Electronic Resource
    Pseudohypoparathyroidism and hypocalcemic “myopathy” (1981)
    Springer
    Journal of molecular medicine 59 (1981), S. 1195-1199 
    Details
    ISSN: 1432-1440
    Keywords: Fallbericht ; Pseudohypoparathyreoidismus ; hypocalcämische Myopathie ; Case report ; Pseudohypoparathyroidism ; Hypocalcemic myopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A patient with the clinical features of pseudohypoparathyreoidism and elevated concentrations of serum CK and LDH, which normalized after successful therapy, is described. Clinical signs of myopathy did not exist. The bioptical material from the m. tibialis anterior was microscopically normal. The biochemical analysis revealed a reduced phosphorylase-a-activity with the total phosphorylase-activity (a and b) being within the normal range. The significance of these findings as well as possible pathogenetic mechanisms are discussed.
    Notes: Zusammenfassung Es wird über einen Fall von Pseudohypoparathyreoidismus berichtet, bei dem gleichzeitig erhöhte CPK- und LDH-Konzentrationen im Serum festgestellt wurden, die sich nach Therapie normalisierten. Klinische Zeichen einer Myopathie bestanden nicht. Das Biopsiematerial vom m. tibialis anterior war mikroskopisch unauffällig. Biochemisch fand sich eine verminderte Phosphorylase-a-Aktivität bei normaler Gesamtphosphorylase-Aktivität (a und b). Die Bedeutung des Befundes und die möglichen pathogenetischen Mechanismen werden diskutiert.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721214
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  • 3
    Electronic Resource
    Electronic Resource
    Der Einfluß von Nahrungspurinen und -pyrimidinen auf die Pyrimidinsynthese des Menschen (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 1191-1197 
    Details
    ISSN: 1432-1440
    Keywords: Pyrimidine biosynthesis ; Dietary purines and pyrimidines ; Orotic acid ; Allopurinol ; Orotidine-5-phosphate-decarboxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Young healthy volunteers received a purine-free, isoenergetic formula diet over a period of 28 to 32 days. After a short time under formula diet alone 400 mg allopurinol were administered daily. After a further 10 days each volunteer received daily, in addition, either 4 g RNA, 4 g RNA-hydrolysate, 1 g guanosine-5-monophosphate (GMP), 1 or 3 g adenosine-5-monophosphate (AMP), uridine-5-monophosphate (UMP), cytidine-5-monophosphate (CMP) or adenosine, guanosine, uridine, cytidine, guanine, hypoxanthine, xanthine, cytosine and uracil. Finally the allopurinol was omitted. The renal excretion of total orotic acid (orotic acid and orotidine), uric acid and creatinine was determined daily; serum uric acid concentration and the enzyme activities of orotidine-5-phosphate-decarboxylase (ODCase) and hypoxanthine-guanine-phosphoribosyltransferase (HGPRTase) from erythrocytes were determined every other day. The results show that RNA, RNA-hydrolysate, purine- and pyrimidines and -nucleosides as well as hypoxanthine, and to a lesser extent adenine, diminish allopurinol-induced orotaciduria. This is compatible with an influence of dietary purines and pyrimidines on human pyrimidine biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01537430
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  • 4
    Electronic Resource
    Electronic Resource
    Buchbesprechungen (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 802-802 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711853
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  • 5
    Electronic Resource
    Electronic Resource
    Die Wirkung von Benzbromaronum auf die renale Harnsäureausscheidung Gesunder (1970)
    Springer
    Journal of molecular medicine 48 (1970), S. 426-432 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 1. Following a single oral dose of 100 mg Benzbromaronum in normal adults serum uric acid levels fall to 66,5% of the original value within 24 hours. 2. The serum uric acid begins to fall only after 3,25 hours. In the mean the urinary excretion of uric acid increases up to 34,86 mg during a period of 30 minutes. 4,75 hours after drug application the uric acid clearance reaches its highest point with an average value of 26,54 ml/min. Benzbromaronum does not influence the creatinine clearance. The lowest serum uric acid value occurs after 16 hours, after 20 hours a new increase begins. 3. The delayed effect of Benzbromaronum is also found with the same dose of Benziodaronum, but not with 1,5 g of Probenecid. The reason for this may be slow absorption, strong protein binding or the formation of a metabolite as the effective substance. 4. Under a daily intake of 100 mg Benzbromaronum the lowest level of serum uric acid is reached after 5–6 days. Corresponding to the fall in serum uric acid the urinary uric acid excretion rises. The day after the beginning of the drug application the increase of urinary uric acid excretion is higher then the calculated decrease of the pool.
    Notes: Zusammenfassung 1. Die einmalige orale Gabe von 100 mg Benzbromaronum führt innerhalb von 24 Std zu einer Senkung des Serumharnsäurespiegels auf durchschnittlich 66,5% des Ausgangswertes. 2. Die Serumharnsäure beginnt nach 3,25 Std abzufallen. Die Harnsäureausscheidung steigt im Mittel bis auf 34,86 mg pro Sammelperiode an. Die Harnsäureclearance erreicht 4,75 Std nach Arzneimittelgabe mit durchschnittlich 26,54 ml/min den höchsten Wert. Die Kreatininclearance wird von Benzbromaronum nicht beeinflußt. Der tiefste Serumharnsäurewert wird nach 16 Std erreicht, nach 20 Std beginnt ein Wiederanstieg. 3. Der langsame Wirkungseintritt nach Benzbromaronum findet sich auch nach Benziodaronum in gleicher Dosis, nicht aber nach 1,5 g Probenecid. Langsame Resorption, starke Eiweißbindung oder Notwendigkeit der Umwandlung in eine wirksame Form werden als Ursache hierfür zur Diskussion gestellt. 4. Unter einer Dauermedikation von täglich 100 mg Benzbromaronum wird nach 5–6 Tagen eine maximale Verminderung der Serumharnsäurekonzentration erreicht. Dem Serumharnsäureabfall entspricht ein Anstieg der renalen Harnsäureausscheidung. Dabei ist die Harnsäuremehrausscheidung im Urin am Tag nach Arzneimittelgabe größer als die errechnete Poolabnahme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01487010
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  • 6
    Electronic Resource
    Electronic Resource
    Eigenschaften der Hypoxanthinguaninphosphoribosyltransferase (HGPRTase) bei einem Gichtpatienten mit verminderter Aktivität dieses Enzyms (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 63-68 
    Details
    ISSN: 1432-1440
    Keywords: Gout ; Hypoxanthineguanine-phosphoribosyltransferase ; Partial deficiency ; Physicochemical properties ; Gicht ; Hypoxanthinguaninphos-phoribosyltransferase ; Verminderte Aktivität ; Physikochemische Eigenschaften
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei einem Gichtpatienten mit verminderter Aktivität der HGPRTase wurde dieses Enzym aus Erythrozyten und Fibroblasten näher untersucht. Die HGPRTase des Patienten weist im Vergleich zu den Kontrollen unterschiedliche kinetische und physikalische Eigenschaften auf. Der apparente Km-Wert des ungereinigten Erythrozytenenzyms des Patienten ist für die Substrate Hypoxanthin und Guanin höher, für PRPP niedriger als bei Normalpersonen. Das Erythrozytenenzym des Patienten ist bei +4°C und +80°C stabiler, das Enzym aus Fibroblasten bei +57°C dagegen labiler als die Kontrollen. Ein Hemmstoff der HGPRTase beim Patienten konnte nicht gefunden werden. Purinnukleoside und-nukleotide hemmen die Aktivität der HGPRTase aus Erythrozyten bei dem Patienten und Normalpersonen unterschiedlich. Die Saccharosegradientenultrazentrifugation von Hämolysat führt sowohl beim Patienten als auch bei den Kontrollen zum Auftreten eines einzigen Peaks von HGPRTase-Aktivität mit identischer Sedimentationskonstanten. Die bei unserem Gichtpatienten erhobenen Befunde sind mit einer Strukturgenmutation vereinbar.
    Notes: Summary Some physicochemical properties of HGPRTase were studied in hemolysates and fibroblasts of a gout patient with partial deficiency of this enzyme. In comparison to normal HGPRTase the mutant enzyme from erythrocytes was found to have an elevated apparent Km-value for hypoxanthine and guanine and a lower Km-value for PRPP. The patient's enzyme from erythrocytes is more stable at +4°C and +80°C, the enzyme from fibroblasts more labile than that of controls. The inhibition of the mutant enzyme by some purine nucleosides and-nucleotides differed from that found in controls. No evidence was shown for an inhibitor of the patient's HGPRTase from erythrocytes. Ultracentrifugation of hemolysate in a saccharose gradient revealed no difference in the sedimentation coefficient.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01491336
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  • 7
    Electronic Resource
    Electronic Resource
    Über die Senkung des Harnsäurespiegels im Plasma durch Benzbromaronum (1968)
    Springer
    Journal of molecular medicine 46 (1968), S. 1318-1319 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Benzbromaronum decreases plasma uric acid by increasing uric acid clearance and urinary excretion of uric acid. Following a single oral dose of 100 mg uric acid levels fall to 50–70% of the original value; as a rule this effect lasts for two days.
    Notes: Zusammenfassung Benzbromaronum senkt die Plasmaharnsäure durch eine Steigerung der Harnsäureclearance und Harnsäureausscheidung im Harn. Nach einer einmaligen oralen Dosis von 100 mg tritt eine Abnahme des Harnsäurespiegels auf 50–70% des Ausgangswertes auf, die in der Regel 2 Tage anhält.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01747129
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  • 8
    Electronic Resource
    Electronic Resource
    Gout and uric acid nephropathy: Some new aspects in diagnosis and treatment (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 1233-1239 
    Details
    ISSN: 1432-1440
    Keywords: Hyperuricaemia ; Gout ; Nephropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been recognized that primary disorders of uric acid metabolism result from impaired renal excretion or increased endogenous production of uric acid. It has also been found that these two mechanisms do not comprise two distinct syndromes, but may each constitute a group of syndromes. Contrary to earlier as well as currently published reports we conclude from our clinical and experimental experience that the fraction of so-called over-producers is less than 1% of all patients with primary hyperuricaemia and gout. A procedure for the diagnosis of uric acid overproduction is suggested. The manifestation of hyperuricaemia and gout mainly depends on renal uric acid clearance and is greatly influenced by dietary habits in most of the patients. An impaired renal uric acid excretion results in an increased intestinal excretion; this partly compensates for the defect. Normalization of serum uric acid should be achieved by dietary regimens with or without additional drug treatment, but not by drug treatment alone. With drug treatment xanthine oxidase inhibitors are preferable to uricosurics; no other xanthine oxidase inhibitor besides Allopurinol has been in clinical trial, however. Due to the enhancement of uric acid clearance with uricosurics, there are groups of patients who should not be treated with these drugs. Fixed combinations of Allopurinol and uricosurics should not be used. Drugs which have uricosuric as well as other pharmacologic properties are under investigation. So far they have not reached general clinical application.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01540471
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  • 9
    Electronic Resource
    Electronic Resource
    A study of dose-response relationships of allpurinol in the presence of low or high purine turnover (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 153-159 
    Details
    ISSN: 1432-1440
    Keywords: Allopurinol ; Uric acid ; Oxypurines ; Orotic acid ; Dietary purines ; Overproduction ; Purine deficit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of allopurinol (125–500 mg/m2 body surface) were studied in normal subjects during periods of 18 days both during a purine-free, isoenergetic liquid formula diet and additional intake of ribonucleic acid, 4 g/day. Plasma uric acid and renal excretion of uric acid, oxypurines (hypoxanthine plus xanthine) and orotic acid were measured and total purine excretion calculated. Effects of allopurinol were evaluated by comparison of the results obtained in the steady state during diet alone (average of days 7–10) with those during allopurinol administration (days 16–18). During the purine-free diet, plasma uric acid was lowered more than urinary uric acid by allopurinol on doses of 250–500 mg/m2 (44%–54% of control values on 500 mg/m2), demonstrating an increase in renal clearance. At the same dose, the uric acid lowering effect of allopurinol was more pronounced with than without purine loads (plasma 41%, urine 32% of control on 500 mg/m2 during purine intake), while renal uric acid clearance was decreased. The more pronounced reduction of uric acid excretion during purine administration was balanced to the greater part by a more pronounced increased in oxypurine excretion. Total purine excretion was reduced by about 20% during the purine-free diet irrespective of dose. The size of this purine deficit was doubled, but was also independent of dose during addition of purines. Orotic acid excretion increased with dose during allopurinol treatment and was reduced by addition of purines. With respect to uric acid lowering effects, these results are in accordance with findings in patients overproducing uric acid endogenously and suggest that the uric acid lowering effect of allopurinol is enhanced with increasing concentrations of purine bases, presumably due to the tight binding of oxipurinol to xanthine oxidase. The small uricosuric effect of allopurinol seen during ingestion of the purine-free diet possibly is attributable to drug-induced orotic aciduria. The increase in size during purine intake of the purine deficit may result from reduced absorption of dietary purines during allopurinol treatment. Apparently, maximum effects of allopurinol on endogenous synthesis and/or absorption of purines from the gut are exerted by low doses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01727784
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  • 10
    Electronic Resource
    Electronic Resource
    Differentialindikation Urikosurika und Allopurinol (1989)
    Springer
    Journal of molecular medicine 67 (1989), S. 313-315 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01892902
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