Prednisolone Pretreatment Research Articles

The adverse effect of prolonged prednisolone pretreatment in children with acute lymphoblastic leukemia.

Between 1971 and 1981, 699 children were diagnosed to have acute lymphoblastic leukemia (ALL) in Hungary. 34 of these children had received prednisolone therapy prior to the establishment of the diagnosis. The most frequent presumptive diagnoses that prompted steroid treatment were aplastic conditions and arthritic disorders. Leukemia was diagnosed when the presenting symptoms reappeared usually several weeks after the initiation of steroid therapy and often following withdrawal of the drug. Initial leukemic burden, as judged by leukocyte count and hepatosplenomegaly, was smaller in these patients than in other children with leukemia at the time of diagnosis. Although they entered remission at the same rate as the other patients, the length of continuous complete remission was significantly shorter in the prednisolone pretreated group. It appears that prolonged prednisolone therapy given before remission induction imparts a distinct unfavorable prognosis.

L‐Asparaginase and Prednisolone Pretreatment Followed by Rubidomycin and Cytosine Arabinoside for Induction of Remission in Adult Patients with Acute Myeloblastic Leukaemia

77 unselected adult patients with acute myeloblastic leukaemia (AML), including practically all AML patients from an area with 1.9 million inhabitants, were randomized for either (1) 5 days pretreatment with 1-asparaginase and prednisolone followed by a combination of rubidomycin and cytosine arabinoside (ARAP), or (2) treatment with a combination of rubidomycin, cytosine arabinoside and prednisolone without 1-asparaginase pretreatment (RAP). Complete remission was induced with ARAP in 12 patients (31%) and with RAP in 13 patients (34%). Thus pretreatment with 1-asparaginase did not improve the therapeutic response. The overall remission frequency was significantly higher below the age of 60; 50% compared to 13% above this age. Side-effects such as liver dysfunction, nausea and vomiting were more common in patients pretreated with 1-asparaginase. Sterilization of the gut did not improve the remission frequency with either regime.

Enhanced toxicity for mice of pactamycin with bacterial endotoxin.

Combinations of pactamycin and Salmonella typhosa 0901 endotoxin, administered simultaneously, killed more BALB/c mice than comparable doses of either agent alone The slopes of the dose-response curves for combinations of endotoxin and pactamycin were parallel to both that for endotoxin alone and the antitumor drug alone; therefore, no new mechanism of toxicity has been evoked by the combination. The synergistic toxicity of endotoxin and pactamycin was due to an in vivo interaction rather than a direct reaction between the two agents. Phenobarbital pretreatment protected the mice from toxicity of the antitumor agent alone but not from the lethal action of the combination. Pretreatment with endotoxin increased the resistance of the mice to both endotoxin alone and the combination. Third agents unable to protect mice from the synergistic toxicity of endotoxin and pactamycin were alpha[p-(fluoren-9-ylidenemethyl)-phenyl]-2-piperidine-ethanol, neomycin, phenylbutazone, polymyxin B, and tybamate. Prednisolone pretreatment alleviated the toxicity of the combination. For the restricted series of killed bacteria and bacterial products tested for capability to enhance the toxicity of pactamycin, only gram-negative bacterial cells were potent. These results indicated that pactamycin rendered the mice more susceptible to endotoxin and that endotoxin was the causal lethal agent.

Assay of corticotrophin. Prednisolone pretreatment instead of hypophysectomy in the adrenal ascorbic acid depletion test.

ABSTRACT The inhibitory effect of various corticosteroids and synthetic analogues on the stress-induced release of corticotrophin was measured in adult male rats by means of the adrenal ascorbic acid depletion test. All the compounds examined were active, dexamethasone and prednisolone being the most effective inhibitors. A single subcutaneous injection of a microcrystalline aqueous suspension of prednisolone (1.5 mg per rat), given about 2 hours before left-sided adrenalectomy, blocked completely the adrenal ascorbic acid depletion. Quantitative assays of a purified corticotrophin preparation were carried out with hypophysectomized and prednisolone-treated intact rats. The latter were less sensitive to corticotrophin, but the slopes of the calibration curves and the standard deviations appeared to be the same in both instances. It is concluded that it is feasible to replace the surgical hypophysectomy by prednisolone pretreatment in the ascorbic acid depletion test for corticotrophin.