Bone marrow hypocellularity

TCDD causes bone marrow hypocellularity, with specific decreases in the total number of hematopoietic stem cells (HSC) and lymphocyte precursors.42 16 Exposure to TCDD also diminishes mRNA levels of recombination activating gene-1 and terminal deoxy-nucleotidyl transferase in bone marrow cells.47 The best characterized effect of TCDD on bone marrow is the impaired maturation of B cells. A single dose of TCDD causes a transient, time- and dose-dependent, and developmental stage-specific impairment in B cell maturation, with mature B cells affected first, followed by depletion of B cell progenitors.45-46... 

Hemato 10 F 10 M (peripheral anemia bone 20 F marrow hypocellularity,... 

A 53 year old took methimazole 30 mg/day for 3 weeks and developed aplastic anemia associated with an increased peripheral blood lymphocyte count and a hypocellular bone marrow with plasmacytosis (44). 

Yamamoto A, Katayama Y, Tomiyama K, Hosoai H, Hirata F, Kimura F, Fujita K, Yasuda H. Methimazole-induced aplastic anemia caused by hypocellular bone marrow with plasmacytosis. Thyroid 2004 14(3) 231-5. 

Aplastic anemia, defined by the presence of pancytopenia and a hypocellular bone marrow in the absence of any abnormal blood cells, is a serious reaction that has been attributed to perphenazine in a single case (2). 

A 53-year-old woman developed leukoerythroblastosis with giant thrombocytes in the peripheral blood and was subsequently given amiodarone. The bone marrow became hypocellular with atypical megakaryocytes and several granulomata. 

Pancytopenia is a rare but potentially fatal complication, and numerous reports have been published. The characteristics and incidence of pancytopenia have been carefully re-evaluated from case reports and clinical trials published from 1980 to 1995 (38). Of 70 reported cases, 12 patients died (17%). Impaired renal function was the most important contributing factor (54%), particularly in fatal cases (10/12). Other important susceptibility factors included advanced age (over 65 years), hypoalbuminemia, concurrent infection, and/or concomitant multiple medications (particularly co-trimoxazole). The mean cumulative dosage was 675 (10-4800) mg, and the minimal cumulative methotrexate dose leading to fatal pancytopenia was 10 mg. This confirms that pancytopenia can occur at any time during treatment, even in the absence of known susceptibility factors. Bone marrow biopsy showed megaloblastosis and hypocellularity. Eosinophilia and increased mean corpuscular volume were rarely observed. In an overall review of five long-term prospective studies (511 patients), the calculated incidence of methotrexate-induced pancytopenia was 1.4%. Although severe myelo-suppression sometimes required folinic acid, there are as yet no data to determine whether prophylactic folate supplementation can reduce the incidence of pancytopenia. 

A 60-year-old man presented with fever, oral mucositis, pedal cellulitis, and bacteremia after a 6-week course of terbinafine 250 mg. He was taking concurrent yohimbine for impotence. Bone marrow examination showed a hypocellular marrow with myeloid maturation arrest. Treatment consisted of withdrawal of outpatient medications, broad-spectrum antibiotics, hydration. 

Rare cases of aplastic anemia have been reported (20). Some authors have suggested that the incidence of this complication may have been underestimated (21). The reaction is characterized by pancytopenia and the bone marrow shows profound hypocellularity, absence of precursor cells, and fatty replacement. Some studies have suggested a direct toxic effect of ticlopidine on bone... 

Figure 5. Photomicrograph demonstrating the histology using hematoxylin and eosin stains of the new bone. Note the trabeculated stmcture of the organized bone, and the presence of a hypocellular bone marrow.

Fig. 1. Most cellular bone marrow from PAPP-treated rats 3 days after SOO r. Contrast with hypocellularity of Fig. 2.

SM, as an alkylating agent, is particularly toxic to rapidly proliferating cells such as lymphoid and bone marrow cells. Leukocytosis is common within the first few days after exposure. White blood cell (WBC) coimts then begin to decrease starting from the third or fourth day after exposure and reach their minimum level at approximately the ninth day. This leukopenia is followed by a decrease in megakaryocytes and, finally, in the erythropoietic series (Willems, 1989 Tabaiestani et al., 1990 Balali-Mood et al., 1991). Bone marrow biopsies have shown hypocellular marrow and atrophy... 

Leukopenia has been the first manifestation to appear within the first days of postexposure. Thrombocytopenia and anemia followed later if the patients survived (WBCs of some patients dropped to less than 1,000 per cm ). Although most of these patients suffered skin bums, clinicians reported cases that had minor skin lesions and yet developed leukopenia. Bone marrow biopsies revealed hypocellular marrow and cellular atrophy involving all elements (Willems, 1989). Studies on the status of immimocompetent cells in the blood of patients exposed to HD showed that T cell... 

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