China
Africa
Explore chapters and articles related to this topic
Nucleic Acids as Therapeutic Targets and Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
When administered orally, busulfan causes significantly less nausea and vomiting than other DNA cross-linking agents and is therefore more acceptable to patients. Thus, when used to treat CML, it can keep patients almost symptom-free for long periods of time with relatively few side effects. However, frequent blood tests are necessary because myelosuppression may result in irreversible bone-marrow aplasia. Skin hyperpigmentation is also a common side effect during oral therapy, and progressive interstitial pulmonary fibrosis may occur more rarely. Other less frequent side effects include seizures, hepatic toxicity (i.e., veno-occlusive disease), and wasting syndrome. Levetiracetam has proved effective as prophylaxis for busulfan-induced seizures, and the anticonvulsant phenytoin is sometimes administered concurrently to prevent seizures, and benzodiazepines can be used to ameliorate busulfan-induced seizures when they are in progress. Finally, busulfan is a Group 1 carcinogen, and so should be avoided during conception, pregnancy and breast feeding.
The Development of Targeted Radiotherapy for the Treatment of the Small Round Cell Tumors of Childhood
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
Major toxicity was confined to bone marrow aplasia. In two patients receiving 50 mCi of 131I/UJ13A, a transient depression in lymphocytes or platelets was observed. Neither cytopenia was sufficient to require supportive therapy. Both patients receiving 55 mCi developed a profound marrow aplasia. In the first patient, this was irreversible and persisted until the patient died with progressive disease at 6 weeks. The second patient to receive 55 mCi also developed a pancytopenia which spontaneously reversed. No further escalation in dosage has been undertaken beyond this level. However, the availability of purged autologous marrow for transplantation renders continued dose escalation a possibility.
Critical Appraisal of Animal Models for Antibiotic Toxicity
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Patricia D. Williams, Girard H. Hottendorf
Chloramphenicol is the leading cause of drug-induced aplastic anemia in humans [1,21,58]. This anemia is the result of destruction of erythroid precursors in bone marrow. The bone marrow aplasia is irreversible and is associated with fatal pancytopenia. Although the incidence of this toxicity is low (1 in 30,000), the fatality rate approaches 100%. Though the mechanism of this toxicity is unknown, it has been suggested that it represents a form of hypersensitivity reaction.
Phenotypic variation in sickle cell disease: the role of beta globin haplotype, alpha thalassemia, and fetal hemoglobin in HbSS
Published in Expert Review of Hematology, 2022
Traditionally measured in peripheral blood as the percentage of HbF quantitated by alkali denaturation or HPLC is less informative than more direct measurements of the ‘F cells’ or ‘F reticulocytes’ [54] but these indices, although valuable research tools, are not usually available in the clinical setting. The uneven distribution among the red cell population also implies that red cells with low HbF levels are more likely to be destroyed, there being a direct relationship between HbF levels and irreversibly sickled cells [59]. This implies that blood, as sampled from peripheral veins, does not necessarily reflect the output from the bone marrow. In the aplastic crisis, where bone marrow aplasia occurs for 6–8 days, selective destruction of low HbF containing cells leads to a steep rise in overall HbF levels [60], and although this may be an extreme example, a similar effect could occur in other clinical complications. Analysis of the relevance of HbF levels to clinical complications should therefore be confined to HbF estimates during the steady state. Non-steady state conditions linked to increases in HbF include pregnancy [61], medroxy-progesterone acetate [62], and the use of hydroxyurea [63,64].
Is it time to reconsider prophylactic antimicrobial use for hematopoietic stem cell transplantation? a narrative review of antimicrobials in stem cell transplantation
Published in Expert Review of Anti-infective Therapy, 2021
Dilshad Jahan, Ed Peile, Md Arif Sheikh, Salequl Islam, Sharlene Parasnath, Paras Sharma, Katia Iskandar, Sameer Dhingra, Jaykaran Charan, Timothy Craig Hardcastle, Nandeeta Samad, Tajkera Sultana Chowdhury, Siddhartha Dutta, Mainul Haque
The first-ever sternal bone marrow transplant happened by intravenous injection to a sibling with aplastic anemia on December-13-1937. There was no adverse reaction observed. This patient received 43 transfusions in 52 days and 21.87 liters of blood and survived 53 days after hospital admission [17]. The bone marrow aplasia was reported to develop due to nuclear radiation exposure from the atomic bomb effects in the Second World War. Multiple reports in the 1950s documented that radiation-induced bone marrow aplasia was reversed in an animal model [18–21]. In 1957, the American Edward Donnall Thomas, described six cases of Allo-HSCT whereby patients received an intravenous infusion of marrow from a healthy donor. The diagnoses included chronic myelogenous leukemia, chronic lymphatic leukemia, multiple myeloma, massive cerebral hemorrhage, lung and chest metastases with an unidentified primary site, and carcinoma of the ovary with peritoneal metastases. The patient with chronic lymphatic leukemia and multiple myeloma had evidence of the growth of marrow. All six cases had demised within one hundred days. This study also reported HSCT failure in patients with no hematological diseases, no radiotherapy, chemotherapy, and a properly functioning immune system [22]. The concept of histocompatibility antigens had not been developed by this time. Thus no matching with the donor and recipient compatibility had been done for the patients in those studies [23].
A New Zealand White rabbit model of thrombocytopenia and coagulopathy following total body irradiation across the dose range to induce the hematopoietic-subsyndrome of acute radiation syndrome
Published in International Journal of Radiation Biology, 2021
Isabel L. Jackson, Ganga Gurung, Yannick Poirier, Mathangi Gopalakrishnan, Eric P. Cohen, Terez-Shea Donohue, Diana Newman, Zeljko Vujaskovic
The temporal sequence of bone marrow aplasia associated with prompt radiation exposure to humans at doses 2001). The early drop in the peripheral leukocyte count is followed by a progressive decline in platelet counts and development of a severe acute anemia during the second to third week post-exposure (Liebow et al. 1949). In the absence of spontaneous recovery associated with an increase in circulating leukocytes and platelets, death due to aplastic anemia, bacterial infections, and severe hemorrhage is common (Liebow et al. 1949). After the fourth week, multiorgan failure may occur, with stepwise development of injury to late responding normal tissues (e.g. pneumonitis, nephropathy) (Liebow et al. 1949).