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  • 1
    Electronic Resource
    Electronic Resource
    Early institution of bromocriptine in Parkinson's disease inhibits the emergence of levodopa-associated motor side effects. Long-term results of the PRADO study (1996)
    Springer
    Journal of neural transmission 103 (1996), S. 699-715 
    Details
    ISSN: 1435-1463
    Keywords: Parkinson's disease ; bromocriptine ; L-DOPA ; levodopa ; motor fluctuations ; adverse effects ; early combination therapy ; long-term treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Long-term levodopa treatment in Parkinson's disease is typically associated with “motor side effects” consisting in dyskinesias and/or fluctuations in motility referred to as the on-off phenomena. The main objective of this prospective, randomized, multi-centre study was to determine to what extent the development of such complications could be prevented by partial substitution of levodopa monotherapy (L-DOPA/benserazide) by bromocriptine in patients with early symptoms of the disease. The basic trial population included 674 newly diagnosed Parkinsonian patients that were randomly allocated to monotherapy with levodopa or a combination therapy based upon a nearly 40% replacement of levodopa by bromocriptine. The two target regimens had to be consistently maintained for 42 months. Parkinsonian symptoms were assessed by means of the Webster rating scale, the Hoehn and Yahr scale, and the Zung Self-Rating Depression scale. Motor side effects and adverse events were recorded at each regular clinic visit. Neurological symptoms improved and stabilized in a similar manner during treatment with both regimens throughout the study period. Motor side effects were observed in more patients on levodopa alone than on combination therapy (28.8 vs 20%; p=0.008). According to Kaplan-Meier estimates the cumulative probability of experiencing motor side effects was 0.43 on monotherapy, compared to 0.28 on combination therapy, which was equal to a one third reduction of risk (p=0.025). In regard to motor side effects, the degree of substitution of levodopa proved relevant: patients with 〉50% substitution by bromocriptine exhibited half the risk observed in those with 〈30% (p=0.045). The overall burden of motor side effects, as reflected by a sum score based upon the relevance, the severity and the extent of motor dysfunction, was also significantly less on combination therapy (p=0.046). In conclusion, partial substitution of levodopa by bromocriptine (〉30%) as first-line treatment of Parkinson's disease proves active in the prophylaxis of levodopa associated motor side effects. Early combination therapy therefore extends the period of optimal disease control.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01271230
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  • 2
    Electronic Resource
    Electronic Resource
    Bromocriptine lessens the incidence of mortality in L-Dopa-treated parkinsonian patients: Prado-study discontinued (1992)
    Springer
    European journal of clinical pharmacology 43 (1992), S. 357-363 
    Details
    ISSN: 1432-1041
    Keywords: Parkinson's disease ; Bromocriptine ; L-Dopa/benserazide ; early combination therapy ; long-term ; therapy ; mortality ; cardioprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary L-Dopa supplemented by a peripheral decarboxylase inhibitor is considered the most potent therapeutic regimen prolonging active life in Parkinsonian patients. The long-term benefit of therapy is limited by adverse effects, such as dyskinesia and on-off phenomena, which can be mitigated by the concomitant administration of dopamine agonists, such as bromocriptine. In order to quantify the beneficial impact of early combination therapy, a controlled clinical trial (PRADO:PRA vi-del1 +DOpa) in patients with early Parkinson's disease was carried out, whereby L-Dopa monotherapy (in a fixed combination with benserazide (DoBe) was being compared with the same combination plus bromocriptine (DoBeBro). Patients were recruited and treated by 101 practising neurologists in the Federal Republic of Germany and in Hungary. 'Twenty seven clinical university centers cross-checked the patients at regular intervals. The trial started with 3 months of DoBe monotherapy (median dose of 375 mg L-Dopa for both randomized groups) followed by gradual substitution of DoBe by bromocriptine over 3 months in one of the groups (250 mg L-Dopa/10 mg bromocriptine). The target medication was maintained from study months 6 to 54. Parkinsonian symptoms were classified according to the Webster rating scale, the Hoehn and Yahr scale and the Zung Self-Rating Depression Scale. Adverse events and life status were checked at regular intervals. Special emphasis was given to motor performance tests. 587 patients (302 in the DoBe group and 285 in the DoBeBro group) were available for intention-to-treat analysis. Both groups were homogeneous at baseline in all observed parameters. DoBe and DoBeBro proved equi-effective in terms of antiparkinsonian activity after the substitution phase (P II) had been completed. In September 1991, after a median observation period on target medication of 38.4 months in the DoBe group and 40.1 months in the DoBeBro group, 18 versus 8 deaths had been registered. The Logrank test as well as analysis using the Cox model, both adjusted for age and sex, showedP-values of 0.018 and 0.021, respectively. The mortality risk associated with L-Dopa therapy was reduced by more than 50 % by its combination with bromocriptine. The study was terminated due to this difference in mortality. The causes of death were classified by the treating physicians and consultants. At the time of study termination 152 patients in the DoBe group and 121 in the DoBeBro group had already discontinued study medication. Of those further 26 patients had died by the date of the final evaluation, 15 on DoBe and 11 on DoBeBro. The results imply that combination therapy with bromocriptine should be preferred over L-Dopa monotherapy from the very beginning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02220609
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  • 3
    Electronic Resource
    Electronic Resource
    Erhöhtes Serum-Myoglobin bei Niereninsuffizienz (1981)
    Springer
    Journal of molecular medicine 59 (1981), S. 247-248 
    Details
    ISSN: 1432-1440
    Keywords: Myoglobin ; Renal failure ; Myocardial infarction ; Myoglobin ; Niereninsuffizienz ; Myokardinfarkt
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 44 Patienten mit chronischer Niereninsuffizienz unterschiedlicher Äthiologie wurde das immunreaktive Serum-Myoglobin bestimmt und mit den Werten von Probanden mit normaler Nierenfunktion verglichen. Es fand sich — unabhängig von der Grunderkrankung — eine hoch signifikante lineare Korrelation zwischen dem Serum-Myoglobin und der Serum-Kreatinin-Konzentration. Bei Patienten mit Serum-Kreatinin-Werten über 550 µMol/1 (6,2 mg-%) lagen die Serum-Myoglobin Konzentrationen fast regelmäßig im pathologischen Bereich. Dies gilt auch für chronische Dialysepatienten. Die Befunde zeigen, daß bei Patienten mit höhergradiger, chronischer Niereninsuffizienz das Serum-Myoglobin nur mit Einschränkung zur Infarktdiagnostik geeignet ist.
    Notes: Summary In 44 patients with chronic renal failure of varied etiology serum immunoreactive myoglobin was measured and compared to values obtained in patients with normal renal function. Irrespective of the underlying disease a highly significant linear correlation was found between serum immunoreactive myoglobin and serum creatinine concentration. In patients with serum creatinine concentrations above 550 µmol/1 (6.2 mg%) serum myoglobin was as a rule elevated above the range found in the controls with normal renal function. This was also true in dialysis patients. These result demonstrate that serum myoglobin may only be used with restrictions in the diagnosis of myocardial infarction in patients suffering from advanced chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476583
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Radioimmunologische Bestimmung von Human-Myoglobin in der Diagnostik des akuten Myokardinfarkts (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 225-235 
    Details
    ISSN: 1432-1440
    Keywords: Angina pectoris ; Diagnostic criteria ; Myocardial infarction ; Serum myoglobin ; Radioimmunoassay ; Angina pectoris ; Diagnostik ; Myokardinfarkt ; Radioimmunoassay ; Serum-Myoglobin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Ein Radioimmunoassay zur Bestimmung von Serum-Myoglobin (SMb) wird vorgestellt. Bei 50 gesunden Probanden beträgt der Meßwertbereich 0–90 ng/ml. Serielle Bestimmungen an 10 Patienten mit akutem Myokardinfarkt beziehungsweise Angina pectoris (AP) zeigen, daß SMb bei Myokardinfarkt vor CK und CK-MB pathologische Werte erreicht (im Mittel 250±95 ng/ml bei stationärer Aufnahme 3,3±1,4 h nach AP-Beginn). Die gleichzeitig bestimmte NAC-aktivierte CK liegt zu diesem Zeitpunkt noch im Normbereich und erreicht pathologische Werte erst 6,2±1,9 h nach Schmerzbeginn. Der Peak des Serum-Myoglobins liegt mit 506±194 ng/ml 8,8±2,8 h, der der CK mit 905±475 mU/ml 20,0±7,8 h nach Anginabeginn. CK-MB und CK unterscheiden sich im zeitlichen Verlauf nur unwesentlich. Ein Patient mit ausgeprägter AP hat bei sonst unauffälligem Enzymmuster pathologisch erhöhte SMb-Werte. Methodische und klinische Ergebnisse werden diskutiert.
    Notes: Summary A radioimmunoassay was developed to determine serum myoglobin (SMb). 50 healthy persons showed values between 0 and 90 ng/ml. Serial tests of 10 patients following acute myocardial infarction or during angina pectoris (AP) indicated that SMb reached pathological values before CK and CK-MB (average 250±95 ng/ml at the time of hospitalisation which corresponds to 3.3±1.4 h after beginning of angina pectoris). At hospitalisation the simultaneously determined CK was within normal limits and reached pathological values only 6.2±1.9 h after the onset of angina. Maximum of SMb was 506±194 ng/ml occurring 8.8±2.8 h after the beginning of AP, maximum of CK was 905±475 mU/ml occurring 20.0±7.8 h after AP. CK-MB and CK differed only slightly in their time course. One patient with severe AP had pathologically increased SMb values whilst all other enzymes were completely normal. Methodical and clinical results are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477491
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