Osteoporotic fractures secondary to methotrexate therapy of acute leukemia in remission.
TL;DR: Four of 11 children with acute lymphoblastic leukemia on long‐term methotrexate therapy developed severe bone pain in their distal extremities andRadiologic examination revealed severe osteoporosis with associated fractures in 5 of these 11 children.
Abstract: Four of 11 children with acute lymphoblastic leukemia on long-term methotrexate therapy developed severe bone pain in their distal extremities. All were in good clinical and hematologic remission. Radiologic examination revealed severe osteoporosis with associated fractures in 5 of these 11 children. A trial of local radiotherapy was attempted in one patient with no response. Methotrexate therapy was stopped in 4 patients with marked improvement in their bone pain and osteoporotic lesions.
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TL;DR: The most prevalent mechanisms of osteoporosis caused by cancer treatment are discussed and therapeutic strategies for the prevention and treatment of therapy-induced bone loss are outlined.
Abstract: Many therapeutic regimens in cancer treatment carry the risk of causing or favoring the development of osteoporosis. Therapies in which hypogonadism may occur are most relevant in this respect. Prompt hormone replacement therapy is indicated in these patients. In patients in whom this is undesirable because of a hormone-dependent tumor, the risk of osteoporosis should be assessed by means of osteodensitometry, and prophylactic or therapeutic measures should be instituted if necessary. Early intervention improves outcome because osteoporosis therapy is most effective in preventing deterioration of bone mass. There remains much uncertainty in assessing the risk of combination chemotherapy with regard to the development of osteoporosis. Negative effects on the skeleton have, however, been demonstrated for individual drugs, such as methotrexate and ifosfamide. Negative effects of the tumor itself on bone metabolism may aggravate the degree of osteoporosis. Detailed data and long-term experience to assess the risk are urgently needed in this area and constitute an important research topic for the coming years and decades. This review discusses the most prevalent mechanisms of osteoporosis caused by cancer treatment and outlines therapeutic strategies for the prevention and treatment of therapy-induced bone loss.
354 citations
TL;DR: Children ages 10 to 20 years who receive intensive ALL therapy, including multiple, prolonged courses of corticosteroid, are at significant risk for developing osteonecrosis.
Abstract: PURPOSE: To determine the incidence, risk factors, and morbidity for osteonecrosis (ON) in children with acute lymphoblastic leukemia (ALL) treated with intensive chemotherapy including multiple, prolonged courses of corticosteroid. PATIENTS AND METHODS: The occurrence of symptomatic ON was investigated retrospectively in 1,409 children ages 1 to 20 years old receiving therapy for high-risk ALL on Children’s Cancer Group (CCG) protocol CCG-1882. RESULTS: ON was diagnosed in 111 patients (9.3% ± 0.9%, 3-year life-table incidence). The incidence was higher for older children (≥ 10 years: 14.2% ± 1.3% v < 10 years: 0.9% ± 0.4%; P < .0001), especially females 10 to 15 years old and males 16 to 20 years old (19.2% ± 2.3% and 20.7% ± 4.7%, respectively). In patients 10 to 20 years old, the incidence of ON was higher for females versus males (17.4% ± 2.1% v 11.7% ± 1.6%, respectively; P = .03) and for patients randomized to receive two 21-day dexamethasone courses versus one course (23.2% ± 4.8% v 16.4% ± 4.3%, ...
346 citations
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25 Feb 2012
TL;DR: Daunorubicin (Daunomycin, rubidomycin), Dimethyl triazeno imidazole carboxamide, Methyl-GAG, Mitomycin C, Streptozotocin, Prednisone and Prednisolone are investigated for the treatment of central giant cell granuloma.
Abstract: Mechlorethamine.- Cyclophosphamide.- Chlorambucil.- Melphalan.- Busulfan.- Methotrexate.- 6-Mercaptopurine.- 5-Fluorouracil.- Cytosine Arabinoside.- Hydroxyurea.- Actinomycin D.- Mithramycin.- Vinblastine.- Vincristine.- Procarbazine.- Prednisone and Prednisolone.- Investigational Agents.- 1,3-Bis(2-chloroethyl)-l-nitrosourea (BCNU).- Daunorubicin (Daunomycin, rubidomycin).- Dimethyl triazeno imidazole carboxamide.- Streptozotocin.- Dibromomannitol.- Methyl-GAG.- Mitomycin C.- Streptonigrin.- L-asparaginase.
329 citations
TL;DR: The role of Folic Acid Deficiency and Vitamin B1 Metabolism in Nonanemic Epileptic Patients, and Predisposing Factors, are discussed.
Abstract: Introduction .............................................................. Definition ................................................................. Predisposing Factors .......................................................... Classification .............................................................. TheNervousSystem ........................................................ Thecerebellum ......................................................... PeripheralNeuropathy .................................................... Subacute or Chronic Encephalopathy ........................................ Other Mental Symptoms .................................................... ....... ........................................... Folic Acid Deficiency ..................................................... MegaloblasticAnemia ..................................................... Folic Acid and Vitamin B1 Metabolism in Nonanemic Epileptic Patients ................................................ ClinicalImplicatio ns ...................................................... Neonatal Coagulation Defects .............................................. TheSkeletalSystem ........................................................ Metabolic Bone Disease and Vitamin D Deficiency ConnectiveTissue ........................................................... GumHypertrophy ....................................................... Facial Skin Changes .............. : .......................................
269 citations
Cites background from "Osteoporotic fractures secondary to..."
...(6) It has also been suggested that the antifolate effects of the antiepileptic drugs may contribute to the problem (Reynolds, 1972b), especially as methotrexate, a well-known folate antagonist, may cause osteoporosis (Ragab et al., 1970)....
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257 citations
References
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TL;DR: The occurrence of what the author interpreted as an "acceleration phenomenon" in the leukemic process as seen in the marrow and viscera of children with acute leukemia treated by the injection of folic acid conjugates1 and pteroyltriglutamic acid (teropterin) — and an experience gained from studies on folic .
Abstract: IT IS the purpose of this paper to record the results of clinical and hematologic studies on 5 children with acute leukemia treated by the intramuscular injection of a synthetic compound, 4-aminopteroylglutamic acid (aminopterin). This substance is an antagonist to folic acid regarding the growth of Streptococcus faecalis R. The occurrence of what he interpreted as an "acceleration phenomenon" in the leukemic process as seen in the marrow and viscera of children with acute leukemia treated by the injection of folic acid conjugates1 — pteroyltriglutamic acid (teropterin) and pteroyldiglutamic acid (diopterin) — and an experience gained from studies on folic . . .
1,543 citations
TL;DR: The results obtained allowed us to assess the importance of knowing the carrier and removal status of canine coronavirus, as a source of infection for other animals, not necessarily belonging to the same breeds.
Abstract: Excerpt Over the past few years, several attempts have been made to identify the sources of human serum alkaline phosphatase (or phosphatases) by immunological (1), electrophoretic (2-4), or chemic...
172 citations
154 citations
TL;DR: It is shown that rats in which growth is arrested by PGA-deficiency, and which due to aminopterin are refractory to PGA, grow remarkably when given concentrates of the citrovorum factor, which is a biologically active derivative of PGA.
Abstract: SummaryRat liver slices form from synthetic folic acid (PGA) a factor (CF) utilized for growth by Leuconostoc citrovorum; this conversion is inhibited by aminopterin. In rats given PGA, a similar inhibition of the synthesis of CF is shown by a marked decrease in the urinary excretion of CF following the administration of aminopterin. The antagonist not only prevents the metabolic alteration of PGA but also competes with the product (CF) derived from PGA. The lethal action in rats of aminopterin, 25 μg daily, is not prevented by PGA, but the daily administration of 250,000 units of CF completely counteracts the toxic effects of the antagonist. That CF is a biologically active derivative of PGA is shown by the fact that rats in which growth is arrested by PGA-deficiency, and which due to aminopterin are refractory to PGA, grow remarkably when given concentrates of the citrovorum factor.
118 citations
TL;DR: Investigation of fourteen patients treated with folio aeid antagonists of psoriasis provides evidence of their effectiveness and comments on some of their side efFects.
Abstract: T H E use of folio aeid antagonists in tbe treatment of psoriasis was introduced by CJubner and August (1951) and tbe work of Rees and bis associates (1955, 19.')9) established that tbis treatment was efFeetive and relatively safe. This paper is a report of tbe investigation of fourteen patients treated witb folic aeid antagonists which provides furtber evidence of tbeir effectiveness and comments on some of their side efFects,
96 citations