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PubMed1975

Distribution of the femoral colony-forming cells in 226Ra-injected mice.

Distribution of damage caused by the retained 226-Ra to the femoral haemopoiesis has been studied in mice injected with 0.02 and/or 0.09 muCi of 226-Ra/g. The exocolonizing test and the 59-Fe uptake in recipient spleens have been used. Non-uniform radiation effect has been observed in the bone marrow cellularity as well as in the CFU counts within 10 weeks after nuclide injection. The lowest depression appears in the distal femoral ends. The changes are not so serious in the proximal parts and are only moderate in the shafts. The results have been discussed from several standpoints.

Animals↗

PubMed2005

Ultrafiltered pig leukocyte extract (UPLE, IMUNOR) potentiates hematopoiesis-stimulating effects of G-CSF in vitro and improves the outcome of treatment of hematopoietic radiation damage in mice with G-CSF.

Ultrafiltered pig leukocyte extract (UPLE, Imunor), a heterogeneous mixture of low molecular weight (<10 kD) substances released from disintegrated pig leukocytes was tested from the point of view of its hematopoiesis-modulating activities using experiments in vitro and in vivo. Attention was focused especially on evaluation of the contingent ability of UPLE to potentiate the hematopoiesis-stimulating effects of recobinant human granulocyte colony-stimulating factor (G-CSF). Experiments in vitro revealed the capability of sera from mice administered UPLE perorally (p.o.) to stimulate proliferation of progenitor cells for granulocytes and macrophages (GM-CFC) in cultures of normal bone marrow cells. In addition, UPLE, as well as sera from mice given UPLE, added to the cultures in combination with G-CSF enhanced the numbers of GM-CFC significantly over those induced by sera after administration of either of the preparations alone. In in vivo experiments, UPLE was found to increase the counts of GM-CFC per femur and femoral bone marrow cellularity in sublethally irradiated mice when administered p.o. after irradiation in combination with G-CSF in comparison with the effects of G-CSF alone. These results indicate the possibility of using UPLE, a commercially available preparation, for treatment of hematopoietic suppression of various etiology.

Animals↗

PubMed1996

Radioprotective effects of Rasayanas.

Oral administration of Rasayanas (indigenous preparations made up of herbal drugs) significantly increased total WBC count, bone marrow cellularity, natural killer cell and antibody dependent cellular cytotoxicity in gamma radiation (4 Gy) exposed mice. Also, Rasayanas reduced radiation induced lipid peroxidation in liver. The possible mechanisms of action of Rasayanas could be increased stem cell proliferation and its effect on free radical induced injury produced by radiation.

Animals↗

PubMed2002

Clinical and pathological criteria for the diagnosis of essential thrombocythemia, polycythemia vera, and idiopathic myelofibrosis (agnogenic myeloid metaplasia).

A set of clinical and pathological criteria for the diagnosis and staging of Philadelphia chromosome-negative myeloproliferative disorders (Ph(1-)-MPDs) is presented by including bone marrow histopathology as a significant tool to identify the early, manifest, and advanced stages of essential thrombocythemia (ET), polycythemia vera (PV), and idiopathic myelofibrosis/agnogenic myeloid metaplasia (IMF/AMM). This combined approach provides a pathognomonic clue to each of the different subtypes of Ph(1-)-MPDs and further enables recognition of the various steps in the evolution of the myeloproliferative process Increase and clustering of giant to large megakaryocytes with mature cytoplasm and multilobulated staghorn-like nuclei in a normal or only slightly increased cellular bone marrow represent major hallmarks of ET. Loose assemblies of small to giant pleiomorphic megakaryocytes containing deeply lobulated nuclei together with a proliferation of erythro- and granulopoiesis (panmyelosis) are the specific lesions of PV. The initial prefibrotic and the overt and more advanced myelofibrotic stages of IMF/AMM show a pronounced proliferation of an abnormal megakaryo- and granulopoiesis dominated by clustered atypical medium-sized to giant megakaryocytes with cloud-like, bulbous, and often hyperchromatic nuclei, which are not seen in allied subtypes of MPDs including chronic myeloid leukemia (Ph(1+)-CML) and myelodysplastic syndromes (MDS). The presented clinical and pathological criteria modify the Polycythemia Vera Study Group (PVSG) proposals for the Ph(1-)-MPDs by including bone marrow histopathology and are in keeping with features outlined in the new World Health Organization classification. The latter allows the differentiation of true ET from reactive thrombocytosis and from thrombocythemias as an eventually presenting finding in PV, IMF/AMM, MDS, and Ph(1+)-CML. Moreover, these diagnostic guidelines are able to separate latent and early PV from secondary erythrocytosis and to detect the prefibrotic and early stages of IMF/AMM. Myelofibrosis is not a feature of ET and is rarely observed in PV at time of diagnosis, but it becomes apparent during long-term follow-up and constitutes a prominent lesion during the course of IMF/ AMM. Life expectancy is almost normal in ET and is also not significantly altered during the first, but compromised during the second, decade of follow-up in PV. On the other hand, survival is substantially shortened in IMF/AMM, even for patients with thrombocythemia as a frequent finding of prefibrotic and early stage IMF/AMM.

Bone Marrow↗

PubMed1984

Modification of the bone marrow toxicity of cis-diamminedichloroplatinum(II) in mice by diethyldithiocarbamate.

It has been shown that cis-platinum-induced nephrotoxicity in rats can be inhibited by diethyldithiocarbamate (DDC). We report here the bone marrow protective properties of DDC in hybrid (C57BL X BALB/c) mice exposed to single and fractionated doses of cis-platinum. Relatively nontoxic doses of DDC afford maximum protection, using that dose of cis-platinum that would result in the death of 50% of the mice within 9 days as an end point (dose-limiting gut toxicity in mice), when injected 0.5 to 2 hr following i.p. cis-platinum treatment. Survivals of colony-forming units in spleen, nucleated bone marrow cells, and peripheral white blood cell were used to assess the bone marrow protective properties of DDC following both single and fractionated doses of cis-platinum. A dose modification factor of 3.2 (based on colony-forming units in spleen survival) was obtained when DDC (1000 mg/kg) was injected into mice 0.5 hr after graded doses of cis-platinum. When fractionated doses of cis-platinum were used (6 mg/kg on Days 0, 10, 20, and 30), the survival of colony-forming units in spleen was markedly enhanced if the animals were rescued with DDC 0.5 hr following each cis-platinum dose. When bone marrow cellularity was measured immediately before and 2 days after each dose of cis-platinum, a similar pattern of depression and recovery was noted whether DDC was present or not; however, the depression was less marked in mice rescued with DDC. When peripheral white blood cell counts were monitored, the nadir and recovery were similar in the presence or absence of DDC; however, recovery occurred sooner in the animals that had received DDC. Our data support the ability of DDC to modify the bone marrow toxicity of cis-platinum in normal mice. Experiments are in progress in tumor-bearing animals exploring the differential protection afforded by DDC between bone marrow and tumor.

Animals↗

PubMed1984

Influence of feeding chlorocholine chloride and glyphosine on selected immune parameters in deer mice, Peromyscus maniculatus.

Exposure to the plant growth regulators, chlorocholine chloride (CCC) and glyphosine (GPS), resulted in significant immunomodulatory effects after feeding to deer mice (Peromyscus maniculatus) for 28 days. Cyclophosphamide (CP) and saline controls were included. Both CCC and GPS feeding levels were equivalent to 1, 10, 20, 40 and 80 mg/kg mouse/day. The parameters assessed were: spleen plaque forming cell (PFC) assays, hemolysin titers, white blood cell counts, bone marrow cellularity, hematocrits, plasma proteins, and spleen, liver, kidney, thymus and body weights. GPS significantly raised the ratio of liver/body wt, lymphocytes/g of spleen (at high doses only) and hemolysin titers (at low doses only). Lymphocyte viability was significantly reduced, while WBC counts and plasma protein levels were moderately lowered. CCC significantly reduced plasma proteins, PFCs/g of spleen, lymphocyte viability and hemolysin titers. It also affected thymus weights, WBC counts, lymphocytes/g of spleen and PFCs/10(6) lymphocytes. Most of the effects for both compounds followed a typical dose-response curve, but GPS gave a bimodal response in certain tests. The results demonstrate that CCC and GPS can act as immunomodulatory agents and show the feasibility of using deer mice for immunotoxicity studies of environmental contaminants and agricultural chemicals.

Animals↗

PubMed1977

Granulopoiesis : studies of bone marrow culture in chronic granulocytopenia and comparison with granulocyte kinetics.

Granulopoiesis was studied in 20 cases of chronic granulocytopenia (adults and children; acquired and congenital). Bone marrow colony growth in methylcellulose culture was compared with the turnover-rate of blood granulocytes labelled with 51Cr and with the bone marrow granulocyte labelling index (L.I.) after "in vitro" flash labelling with 3H-thymidine (3H-TDR). There was a positive correlation between colony forming cells (C.F.C.) content and turnover rate and between C.F.C. content and bone marrow cellularity but there was no statistically valid correlation between C.F.C. content and labelling index. In patients with acquired granulocytopenia the colony counts were increased in cases with autoimmune destruction of neutrophils and in one patient during granulocytic regeneration. The C.F.C. numbers were low in cases with neutropenia associated with granulocyte hypoplasia but the prognosis was better in those cases with the highest colony count. On the other hand, colony counts were variable and had no prognostic value in cases of neutropenia secondary to a bone marrow abnormality in maturation or mutiplication, either acquired or congenital, as revealed by turnover studies and autoradiographic data.

Adolescent↗

PubMed2000

Bone marrow pathology after bone marrow transplantation.

Trephine biopsy evaluation in patients who have undergone high dose chemotherapy with stem cell infusion performed by an experienced pathologist is important in evaluation of hematopoietical restitution, evaluation of complications such as graft rejection, infections, relapse or secondary neoplasms. In the first week after high dose chemotherapy or radiotherapy bone marrow aplasia is evident. In the case of accompanying myelofibrosis, fragmentation of reticular and collagen fibers is noticeable only following stem cell transplantation. The first precursors, which appear after the second or third week after transplantation are erythroid precursors found in small groups. Promyelocytes and myelocytes are observed between the second and fourth week, the ration off erythroid to myeloid populations at that time is 1:1. Megakaryocytes ate the last precursors to appear. Trephine biopsy evaluation is useful in diagnosis of graft rejection, especially in case of a discrepancy between the blood morphology examination and bone marrow cellularity. Granuloma formation is an unspecific finding, which requires diagnosis of infections. Residual disease can be recognized in histopathologic examination, or sooner, with immunophenotyping, cytogenetic examination using FISH or PCR. Secondary neoplasms to high dose radiotherapy or chemotherapy are usually lymphoproliferative processes connected with latent EBV infections, myelodysplastic syndromes and acute myeloblastic leukaemia.

Biopsy↗

PubMed1987

Different repopulation kinetics of erythroid (BFU-E), myeloid (CFU-GM) and T lymphocyte (TL-CFU) progenitor cells after autologous and allogeneic bone marrow transplantation.

Marrow recovery of erythroid (BFU-E), myeloid (CFU-GM) and T-lymphocyte (TL-CFU) progenitor cells was studied at various time intervals after autologous bone marrow transplantation in 10 patients with acute myeloid leukaemia in remission. These data were compared with those in 14 recipients of T-cell depleted allogeneic marrow grafts. The results indicate markedly different repopulation kinetics of BFU-E, CFU-GM and TL-CFU after autologous and allogeneic bone marrow transplantation. Following autografting reduced numbers of BFU-E and CFU-GM were always present at 2 months after transplantation. Between 2-6 and 6-24 months a gradual increase occurred, although reduced BFU-E and CFU-GM values were still noted in 50% of the cases in spite of normal bone marrow cellularity and restoration of peripheral blood counts. In contrast, in the allograft recipients normal BFU-E numbers appeared within 2 months after transplantation. In addition, CFU-GM values had become normal in 35% of the tests performed at 1-2 months and respectively in 66% and 100% at 2-6 and 6-24 months. The recovery pattern of TL-CFU differed from that of the other haemopoietic progenitor cells. TL-CFU showed a fast recovery, i.e. within 1 month after autologous bone marrow transplantation which was much more rapid than that of BFU-E and CFU-GM. After allografting, however, TL-CFU regenerated at a slower rate and reached normal levels between 2 and 6 months after transplantation. We suggest that the delayed restoration of myeloid and erythroid progenitor cells after autologous transplantation is related to a proliferative defect of the graft as a result of the preceding cytotoxic chemotherapy, the underlying malignant disease and/or cryopreservation. The slower recovery of the T lymphocyte precursors after allografting might be due to the immunological interactions between graft and host, the immuno-suppressive therapy and/or the in vitro T cell depletion of the graft.

Blood Cell Count↗

PubMed1997

Mitigating effects of interleukin 11 on consecutive courses of 5-fluorouracil-induced ulcerative mucositis in hamsters.

Ulcerative mucositis is a painful, debilitating and dose-limiting toxicity of cancer chemotherapy. Current treatment is largely palliative and no adequate preventive treatment exists. Recently, we reported that recombinant human(rh) interleukin 11 (IL-11) favourably modified the course of mucositis following a single stomatotoxic regimen of 5-fluorouracil in hamsters. Although potentially beneficial, the clinically relevant issue of mucositis and myelosuppression during multicourse chemotherapy treatment was not addressed. The present study was undertaken to evaluate the effect of rhIL-11 on two consecutive courses of mucositis and myelosuppression in hamsters. Ulcerative mucositis was induced using a standardized protocol consisting of 5-fluorouracil (60 mg/kg) on days 1 and 2 followed by superficial irritation of the buccal mucosa on day 4. Animals treated with 100 microg of rhIL-11 for 12 consecutive days following each regimen of chemotherapy experienced a reduction in the incidence, severity, and duration of mucositis, a reduction in weight loss, and less morbidity and mortality relative to control animals. Bone marrow cellularity and function was not adversely affected by rhIL-11 treatment. The present study is consistent with the potential use of rhIL-11 treating patients at risk of developing ulcerative mucositis while undergoing intensive multicourse chemotherapy treatment.

Animals↗

PubMed1990

Pseudo-Chediak-Higashi anomaly in acute myeloid leukemia (M2) of childhood.

The frequency and clinical significance of the pseudo-Chediak-Higashi (PCH) anomaly were studied in 20 children with acute myeloid leukemia (AML) M2 in the FAB nomenclature. PCH granules were recognized as giant eosinophilic granules, measuring up to 5 microns, in the cytoplasm of leukemic cells on smears. At the electron microscope level, most PCH granules were round to oval and outlined by a limiting membrane, and contained homogeneous, granular, crystalloid, rod-like or myelin-like materials. The PCH anomaly was demonstrable in five (25.0%) of the 20 patients, which indicates that the anomaly is not rare in childhood AML M2. There were no differences between PCH anomaly-positive and PCH anomaly-negative groups with regard to hepatosplenomegaly, hemoglobin levels, white blood cell counts, bone marrow cellularity, t(8q-, 21q+) chromosome abnormalities or prognoses. Circulating leukemic cells were observed less frequently in the PCH anomaly-positive group than in the PCH anomaly-negative group (p less than 0.05); the leukemic cells were not demonstrable in three of the five patients in the former group, although they were detected in all 15 patients in the latter group. The existence of PCH granules and/or a defect of the cytoskeleton responsible for the PCH anomaly in leukemic cells may impede their movement from the bone marrow to the peripheral blood.

Adolescent↗

PubMed1986

Changes in granulocyte-monocyte colony-forming cells among leukocyte-interferon-treated chronic myelogenous leukemia patients.

Myeloid cytoreduction leading to hematologic remissions is frequently seen among patients with chronic phase Philadelphia-positive chronic myelogenous leukemia (CML Ph') treated with leukocyte interferon (IFN-alpha). In order extend our understanding of the events associated with interferon-induced myeloid cytoreductions, we have examined the changes in granulocyte-monocyte colony-forming cells (GM-CFC) in such CML Ph' patients. A total of 28 CML Ph' patients in hematologic remissions following IFN-alpha treatment had a median GM-CFC of 12 (range, 0-182)/1 X 10(5) bone marrow cells. This was significantly lower than the median GM-CFC of 104 (range, 44-815; p less than 0.01) in 22 untreated or minimally treated CML Ph' patients and the median of 72 (range, 30-204; p less than 0.05) in 18 normal controls. A gradual decline in the GM-CFC numbers from a median of 105 to a median of 1.8 was seen in six responding patients who were studied serially over a median period of 7.5 months. In these patients, we also observed a profound decline in the number of aspirated bone marrow nucleated cells and a decline in the bone marrow cellularity. The effect of treatment interruption for a median of 13 days was studied in five patients. In three of the patients who had received IFN-alpha for less than or equal to 6 months, treatment interruption resulted in rapid increase in the GM-CFC, while the GM-CFC did not change in the remaining two patients, who received IFN-alpha for one and two years. We conclude that treatment of CML patients with IFN-alpha resulted in a progressive decline of the bone marrow GM-CFC. The initially expanded pool of committed myeloid stem cells declines gradually, and at the time of hematologic remission the number of GM-CFC/10(5) nucleated bone marrow cells is lower than that of normal controls. In the early phases of IFN-alpha treatment, this inhibitory effect is rapidly reversible, but it seems to persist when the treatment is extended over more than one year.

Bone Marrow↗

PubMed2000

Effect of CYP2E1 induction by ethanol on the immunotoxicity and genotoxicity of extended low-level benzene exposure.

Potential additive effects of ethanol consumption, a common life-style factor, and low-level benzene exposure, a ubiquitous environmental pollutant, were investigated. Ethanol is a potent inducer of the cytochrome P-450 2E1 (CYP2E1) enzyme, which bioactivates benzene to metabolites with known genotoxicity and immunotoxicity. A liquid diet containing 4.1% ethanol was used to induce hepatic CYP2E1 activity by 4-fold in female CD-1 mice. Groups of ethanol-treated or pair-fed control mice were exposed to benzene or filtered air in inhalation chambers for 7 h/d, 5 d/wk for 6 or 11 wk. The initial experiment focused on immunotoxicity endpoints based on literature reports that ethanol enhances high-dose benzene effects on spleen, thymus, and bone marrow cellularity and on peripheral red blood cell (RBC) and white blood cell (WBC) counts. No statistically significant alterations were found in spleen lymphocyte cellularity, subtype profile, or function (mitogen-induced proliferation, cytokine production, or natural killer cell lytic activity) after 6 wk of ethanol diet, 0.44 ppm benzene exposure, or both. This observed absence of immunomodulation by ethanol alone, a potential confounding factor, further validates our previously established murine model of sustained CYP2E1 induction by dietary ethanol. Subsequent experiments involved a 10-fold higher benzene level for a longer time of 11 wk and focused on genotoxic endpoints in known target tissues. Bone marrow and spleen cells were evaluated for DNA-protein cross-links, a sensitive transient index of genetic damage, and spleen lymphocytes were monitored for hprt-mutant frequency, a biomarker of cumulative genetic insult. No treatment-associated changes in either genotoxic endpoint were detected in animals exposed to 4.4 ppm benzene for 6 or 11 wk with or without coexposure to ethanol. Thus, our observations suggest an absence of genetic toxicity in CD-1 mice exposed to environmentally relevant levels of benzene with or without CYP2E1 induction.

Animals↗

PubMed1991

Effects of recombinant transforming growth factor-beta 1 on hematologic recovery after treatment of mice with 5-fluorouracil.

Transforming growth factor beta 1 (TGF-beta 1) has been shown to inhibit bone marrow colony formation after in vitro treatment as well as after in vivo administration to normal mice. These data suggest that TGF-beta might either protect, or further depress, progenitor cell levels in mice exposed to a cell cycle-active drug such as 5-fluorouracil (5FU). rTGF-beta 1 was administered repeatedly by either the i.v. or i.p. routes to mice during the hyperproliferative state of the bone marrow that occurs 7 to 9 days after the i.v. administration of 150 mg/kg 5FU. The formation of both multilineage and the more differentiated (CFU-c) colonies was inhibited by 20 to 40%/culture, and 66 to 93%/mouse. When multiple doses of rTGF-beta 1 were administered systemically immediately before the injection of 5FU, the resulting rebound in the number of CFU-c and multilineage colonies containing granulocyte, erythroid, megakaryocyte, and macrophage lineage colonies per culture was markedly inhibited by 30 to 77%, whereas the total number of CFU per mouse was inhibited up to 93%. This effect was maximal when rTGF-beta 1 was administered at daily doses of greater than or equal to 5 micrograms/mouse for at least 3 days. This inhibition of the recovery of the bone marrow from 5FU treatment induced by rTGF-beta 1 was a delayed transient response because by day 16 the progenitor cell numbers and bone marrow cellularity were identical to the 5FU-treated marrow controls.

Animals↗

PubMed2001

Hematopoietic failure after hemorrhagic shock is mediated partially through mesenteric lymph.

OBJECTIVE: To determine whether hemorrhagic shock-induced bone marrow failure is mediated by the gut through the production of toxic mesenteric lymph and whether shock-induced bone marrow failure could be prevented by division of the mesenteric lymphatics. DESIGN: Prospective, controlled study. SETTING: University surgical research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Rats were divided into five groups: unmanipulated controls (n = 12), hemorrhagic shock with laparotomy (n = 8), hemorrhagic shock with mesenteric lymph duct ligation (n = 10), sham shock with laparotomy (n = 6), and sham shock with mesenteric lymph duct ligation (n = 7). At either 3 or 6 hrs after resuscitation, bone marrow was obtained for determination of early (cobblestone forming cells) and late (granulocyte-macrophage colony forming unit and erythroid burst forming unit) hematopoietic progenitor cell growth. Parallel cultures were plated with plasma (1% and 2% v/v) from all groups to determine the effect of lymphatic ligation on hematopoiesis. MEASUREMENTS AND MAIN RESULTS: Bone marrow cellularity, cobblestone forming cells, granulocyte-macrophage colony forming unit, and erythroid burst forming unit growth in rats subjected to hemorrhagic with lymph duct ligation were similar to those observed in sham-treated animals and significantly greater than in rats subjected to shock and laparotomy without lymphatic duct ligation. Plasma from rats subjected to shock without lymph ligation was inhibitory to hematopoietic progenitor cell growth. In contrast, this shock-induced inhibition was not observed with plasma obtained from shocked rats that underwent mesenteric lymph ligation. CONCLUSIONS: Hemorrhagic shock suppresses bone marrow hematopoiesis as measured by a decrease in early and late progenitor cell growth. This suppression appears mediated through mesenteric lymph as the effect is abrogated by mesenteric lymph duct ligation. These data clearly demonstrate a link between the gut and bone marrow failure after hemorrhagic shock

Animals↗

PubMed1990

The effect of dextran sulphate on CFU-S and nucleic acids in blood and haemopoietic tissues in irradiated mice.

The effect of synthetic polyanion dextran sulphate on the development and recovery of radiation-induced haemopoietic damage in mice was investigated. Dextran sulphate (mol. wt. 500,000 D) in the dose of 40 mg.kg-1 of body weight was injected i.p. 3 days before single total body irradiation with a dose of 7.8 Gy gamma-rays. The animals were examined from hour 6 to day 26 after irradiation, i.e. from hour 78 to day 29 after DS-treatment. In irradiated mice DS-pretreatment showed some positive effect on the CFU-S number in bone marrow (less in spleen and blood), bone marrow cellularity, attenuated the radiation-induced changes of erythrocytes (number, MCV) and of RNA concentration in blood. The changes of other parameters (spleen cellularity, liver CFU-S, leukocyte count and DNA concentration in blood) were the same as in unprotected animals. In conclusion, we can say that DS-pretreatment had a beneficial effect on the recovery of radiation-induced damage of erythropoiesis but not on granulopoiesis or lymphopoiesis.

Animals↗

PubMed2006

Magnetic resonance investigation of bone marrow following priming and stem cell mobilization.

PURPOSE: To evaluate application of MRI and magnetic resonance spectroscopy (MRS) to monitor bone marrow cellularity during pretransplant priming with chemotherapy and hematopoietic growth factor (HGF) administration. MATERIALS AND METHODS: A total of 10 lymphoma and myeloma patients, in remission following induction therapy and considered eligible for high-dose therapy and autologous stem cell transplantation, were included in the study. MR investigation was scheduled four times: at study entry, and one, two, and four weeks following priming. Priming with cyclophosphamide and recombinant human granulocyte colony-stimulating factor (rhG-CSF) started the day after study entry. MR parameters studied in a region of interest were as follows: bone marrow intensity on short-time inversion-recovery (STIR) turbo spin-echo (TSE; thus STIRTSE) and on T1-weighted TSE (T1TSE) images, T2 value for fat component, T2 value for water component, water/fat ratio (W/F), T1 value for fat component, and T1 value for water component. RESULTS: The results did not support the hypothesis that hematopoietic expansion quantitated and monitored by MR correlates to the level of mobilized progenitor cells. CONCLUSION: The results indicate that release of stem cells is a more complex phenomenon than hematopoietic expansion and reduction of fat tissue in bone marrow.

Aged↗

PubMed1996

Prevention of transmission of hepatitis C virus in bone marrow transplantation by treating the donor with alpha-interferon.

Transmission of hepatitis C virus (HCV) in the setting of allogeneic bone marrow transplantation can occur through an infected marrow donor. Prevention of transmission may reduce the risks of peritransplant complications. We describe a 43-year-old patient with chronic myelogenous leukemia whose HLA-identical donor was found to be HCV antibody positive and HCV RNA positive by polymerase chain reaction (PCR). The patient was HCV antibody negative and HCV RNA negative by PCR of the serum. For 6 months before bone marrow transplantation, the donor was treated with alpha-interferon at a standard dose. After 3 months, HCV RNA was no longer detectable by PCR. Interferon was discontinued 1 week before harvest. Bone marrow cellularity was normal. Engraftment was prompt. The recipient's serum remained negative for HCV RNA at 1, 3, 5, and 10 months after transplantation. Hepatitis C transmission from a viremic donor to an HCV-seronegative recipient may be preventable by treating the donor with alpha-interferon.

Adult↗