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  • Bisphosphonate  (1)
  • I-131-p-iodo-phenylpentadecanoic acid  (1)
  • Prevention  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Cancer-associated hypercalcemia ; Bisphosphonate ; Pamidronate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After a 48-hour rehydration period 28 of 31 patients with cancer-associated hypercalcemia (serum calcium ≥2.8 mmol/1) were treated intravenously with the bisphosphonate pamidronate. In three patients fluid repletion with 0.9% saline solution had already normalized serum calcium levels. Pamidronate was given in a single infusion on day 0, the dose of pamidronate adapted to the severity of hypercalcemia. If the serum calcium concentration was ≥2.8 mmol/1 on day 3, application of pamidronate was repeated. In all patients normocalcemia was restored; mean serum calcium decreased from 3.2±0.35 on day 0 to 2.15±0.32 on day 12. Hypercalcemia recurred in 11 patients, seven of these underwent pamidronate treatment according to the same therapeutical regimen. Normal calcium levels were attained in five cases. Side effects were of minor gravity:brief hyperthermia occurred in four patients and transient, asymptomatic hypocalcemia was noticed in nine cases.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 106 (1983), S. 143-147 
    ISSN: 1432-1335
    Keywords: Doxorubicin ; Acute cardiac toxicity ; Prevention
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In two groups of female patients with metastatic breast cancer who had all been pretreated with doxorubicin (350 mg/m2), acute cardiac effects following i.v. doxorubicin bolus injection (60 mg/m2) were recorded on the basis of systolic time intervals (STI). In six patients who received doxorubicin only the ratio between the heart-beat-corrected preejection period and left ventricular ejection time (PEPI:LVETI) as well as the PEP index were found to be significantly increased with a peak at 6 h following drug infusion (P〈0.001). Another six patients received an identical chemotherapeutic regimen and, in addition, a combination of tocopherol (200 mg i.m. 6 h before treatment) and nifedipine (60 mg p.o. daily from 2 days before doxorubicin infusion). In the pretreatment group, the PEPI: LVETI ration and PEP index remained unchanged during the posttreatment period. Pharmacokinetic analysis of drug concentrations in the plasma revealed a significantly accelerated distribution and elimination of doxorubicin after combined tocopherol and nifedipine pretreatment, although no statistically significant differences could be found in calculated drug levels in the peripheral compartment between both treatment groups. Our results indicate that acute cardiac reactions reflected by changes in STI values can be prevented by combined tocopherol and nifedipine pretreatment.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European journal of nuclear medicine 12 (1986), S. S32 
    ISSN: 1619-7089
    Keywords: I-131-p-iodo-phenylpentadecanoic acid ; Doxorubicin ; Cardiotoxicity ; Myocardial fatty acid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was designed to evaluate if doxorubicin (D) can impair myocardial fatty acid utilization. To this end we studied the myocardial utilization of 131I-pIPPA in untreated (Co, n=6) and D (20 mg/kg intraperitoneal) treated rats. D was given 24 h (24 D, n=6) and 48 hours (48 D, n=6) before tracer administration. One min after i.v. 131I-pIPPA (50 μCi) injection, the hearts were rapidly removed, frozen in liquid nitrogen, weighed, and counted. Following lipid extraction of homogenized heart extracts 131 I radioactivity distribution was analyzed by thin-layer chromatography (TLC). In additional rat experiments, high energy phosphates (12 rats/group) and carnitine (20 rats/group) were determined enzymatically in heart extracts. The mean pIPPA uptake in rat heart (%dose/g) was 2.49 in Co, 1.74 in 24 D, and 2.36 in 48 D rats. Usually five peaks were separated by TLC, that with a mean Rf value of 0.92 corresponding to 131I-pIPPA, the remaining four representing catabolites of pIPPA metabolism. The mean relative amount of unmetabolized 131I-pIPPA as compared to the sum of 131I-pIPPA catabolites was less in Co than in 24 D or 48 D rats (P〈0.05) ( $$\bar x$$ : 46.5% vs 72.4% vs 59.4%, respectively). The mean carnitine content of heart extracts was higher in Co (0.55 μM/g) than in D treated rats (24 D, 0.42 μM/g; 48 D, 0.46 μM/g) P〈0.05). The total amount of higher energy phosphates was not different between the groups. However the mean ATP/AMP ratio was higher in Co (35.9) than in 24 D (22.3) or 48 D (27.1) rats (P〈0.05). We conclude that D therapy is accompanied by a partial reversible impairment in myocardial pIPPA utilization, possibly mediated by carnitine deficiency. Thus, 131I-pIPPA might be useful in patients on D therapy to evaluate eventual D-induced effects on myocardial fatty acid utilization.
    Type of Medium: Electronic Resource
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