Bone marrow damage

Moskalev et al. (1966a 1966b) reported that rats injected with high levels of 144Ce citrate died with acute bone marrow damage at relatively... 

Gy Hematopoietic syndrome characterized by bone marrow damage, anemia, lowered immune response, hemorrhage, and sometimes death 20... 

Bone marrow destruction May lead to death not as lethal as HD Severe discomfort to eyes Permanent corneal damage Harsh respiratory effects Damage to bone marrow Damage to digestive tract and endocrine systems... 

A reduction in total white blood cell counts to 60% of control values (p<0.05), but no changes in differential white cell counts or evidence of bone marrow damage, was found in rats intermittently exposed to 700 ppm 2-hexanone after 8 weeks during an 11-week study (Katz et al. 1980). These findings, although inconclusive, suggest that immunological effects may warrant some consideration in future assessments of the potential toxicity of inhalation exposure to 2-hexanone. 

Tice, R.R., Boucher, R., Luke, C.A. Shelby, M.D. (1987) Comparative cytogenetic analysis of bone marrow damage induced in male B6C3F1 mice by multiple exposures to gaseous 1,3-butadiene. Environ. Mutag., 9, 235-250... 

A major cause of morbidity and mortality in patients who receive cytotoxic treatment or radiotherapy for cancer is bacterial and fungal infections. Intensive chemotherapy is associated with fever and infection, and the development of neutropenia further increases this risk of infection. Consequently, maximum doses of some cytotoxic drugs are limited due to bone marrow toxicity. Higher doses of chemotherapy and radiation therapy have become possible due to a reduction in bone marrow damage with the availability of the CSFs for clinical use. 

Benzene affects the hematopoietic tissue in the bone marrow and also appears to be an immunosuppressant. There is a gradual decrease in white blood cells, red blood cells, and platelets, and any combination of these signs may be seen. Continued exposure to benzene results in severe bone marrow damage and aplastic anemia. Benzene exposure has also been associated with leukemia. 

NIDA s list of irreversible effects include hearing loss, limb spasms, brain damage, and bone marrow damage. Serious but potentially reversible effects include liver and kidney damage, and depletion of oxygen from the blood. 

Chromium is a mineral found naturally in foods. It is an essential nutrient. It helps control blood sugar, and this makes it important in diabetes and heart disease research. Studies on chromium as a fat burner haven t shown that it actually burns fat. In general, studies have come up with no evidence, or have had mixed results. Furthermore, too much of the mineral can be toxic. (This is highly unlikely from food alone, but quite possible with supplements.) Users can suffer kidney, liver, muscle, and bone marrow damage from taking in too much chromium. 

Benzene 80 Yes Yes bone marrow damage leukemia aplastic anemia depression... 

The oxidized metabolites of benzene, including reactive benzene oxide intermediate, are known to bind with DNA, RNA, and proteins. This can result in cell destruction, alteration of cell growth, and inhibition of enzymes involved in the processes of forming blood cells. This phenomenon is probably responsible for the bone marrow damage, aplastic anemia (lowered production of blood cells due to damage to bone marrow), and, in severe cases, leukemia associated with benzene exposure. 

The evaluation of micronuclei frequencies in peripheral blood polychromatic erythrocytes (PCE) and normochromatic erythrocytes (NCE) permits an assessment of both recently induced and chronically accumulated bone marrow damage. PCEs have a life span of about 24 hours and are good indicators of acute damage. NCEs have a life span of about 30 days and are good indicators of chronic damage. A... 

Luke CA, Tice RR, Drew RT. 1988a. The effect of exposure regimen and duration on benzene-induced bone-marrow damage in mice I. Sex comparison in DBA/2 mice. Mutat Res 203 251-271. 

Classification according to cause includes, for example, aplastic anaemia, which is due to bone marrow damage haemorrhagic anaemia due to blood loss haemolytic anaemia due to damage to red cell membranes iron deficiency anaemia due to lack of iron pernicious anaemia due to deficiency in B12 and so on. 

Anaemias are classified according to the size and haemoglobin content of erythrocytes or to the cause of the condition. In the latter classification bone marrow damage causes aplastic anaemia haemorrhagic and haemolytic anaemia are due to blood loss or damaged red cell membranes respectively, iron deficiency and pernicious anaemia are due to deficiency of iron and vitamin B12 respectively. 

In a 73-year-old patient who developed granulocytopenia while taking clozapine, G-CSF and leukocyte counts were reliable indicators of the evolution of the condition, showing an abortive form of toxic bone-marrow damage with subsequent recovery (139). 

Mustard gas is also a radiomimetic (Sidell eta/., 1997). It destroys precursor cells in the bone marrow leading to leukopenia, thrombocytopenia, pancytopenia, and anemia (Borak and Sidell, 1992 Dacre and Goldman, 1996). Infection can be seen secondary to bone marrow damage (Sidell et al, 1997). Bone marrow aplasia and death can be seen in severe cases. 

Adverse effects include gastrointestinal upset which tends to be mild. Optic and peripheral neuritis occur with prolonged use (which should be avoided) but are uncommon. The systemic use of chloramphenicol is dominated by the fact that it can cause rare (between 1 18 000-100 000 courses) though serious bone marrow damage. This is of two types ... 

Nitrogen mustards, as anticancer alkylating agents, were first tested on experimental lymphoma in mice and the results were sufficiently encouraging to warrant a therapeutic trial in man. The response of fhe first patient was as dramatic as that of the first mouse, following 10 days treatment. But severe bone marrow damage occurred and, disappointingly, as the bone marrow recovered so did the tumour in addition, with further courses, the tumour rapidly became resistant. 

Bone marrow Leucopenia and thrombopenia may be a result of bone-marrow damage caused by copper deposits, although this can also be due to splenomegaly. 

In 20-25% of cases, side effects are observed, depending mainly on the dose (hypersensitivity reactions, aphthous lesions, arthralgia, nausea, fever). All in all, treatment of Wilson s disease with penicillamine is considered to be successful and safe. If jrenicill-amine is not well tolerated or if serious side effects are observed (e.g. kidney or bone-marrow damage, polyneuropathy, pemphigus), treatment must be discontinued. Penicillamine usually causes pyridoxin deficiency, so that substitution (25—40 mg/day) is recommended, particularly as chronic liver damage also leads to vitamin Bg deficiency. If necessary, electrolytes and trace elements also have to be substituted. 

The first death resulting from bone marrow aplasia induced by chloramphenicol eye-drops was described in 1955 (17). Chloramphenicol causes two types of bone marrow damage (18). 

In a small fraction of patients who survive the chronic type of bone marrow damage, myeloblastic leukemia develops (41,42). In most instances this complication has appeared within a few months of the diagnosis of aplasia and was considered to be a sequel of chloramphenicol treatment. Sometimes the delay was shorter. The majority were either children or adults aged 50-70 years. 

Chloroquine inhibits myelopoiesis in vitro at therapeutic concentrations and higher. In a special test procedure, a short-lasting anti-aggregating effect could be seen with chloroquine concentrations of 3.2-32 pg/ml (SEDA-16, 303). These effects have clinical consequences. Chloroquine and related aminoquinolines have reportedly caused blood dyscrasias at antimalarial doses. Leukopenia, agranulocytosis, and the occasional case of thrombocytopenia have been reported (SEDA-13, 804) (22). There is some evidence that myelosuppression is dose-dependent. This is in line with the hypothesis that 4-aminoquinoline therapy merely accentuates the cyto-penia linked to other forms of bone marrow damage (SEDA-11, 584) (SEDA-16, 302). 

Ludin H. Blut- und Knochenmarkschadigungen durch Medikamente. [Blood and bone marrow damage caused by drugs.] Schweiz Med Wochenschr 1965 95(31) 1027-32. 

Toxicity. Serious medication-related adverse effects associated with actual or potential damage to tissues, organs, or the entire body system. Toxicity may be directly related to critically elevated blood levels of a drug and may be acute (as in tricyclic antidepressant overdose) or chronic (as in prolonged, moderately elevated lithium level). A drug may also produce "toxic effects" at therapeutic doses (such as phenothiazine s potential for inducing bone marrow damage, which in turn causes decreased production of white blood cells). 

Death may occur between the fifth and tenth day postexposure because of pulmonary insufficiency complicated by a compromised immune response from mustard-induced bone marrow damage. 

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