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Biomedical subjects

S Lenhoff

Publications and source records attributed to S Lenhoff.

26 records · Page 2Linked to original sources
PubMed1997

No prevention of cytomegalovirus infection by anti-cytomegalovirus hyperimmune globulin in seronegative bone marrow transplant recipients. The Nordic BMT Group.

A randomized multicentre study was conducted to evaluate the effect of anti-CMV hyperimmune globulin in the prophylaxis of CMV infections in CMV seronegative allogeneic BMT patients who received a transplant from a seropositive donor or who had received blood products unscreened for CMV during the treatment before BMT. Twenty-eight patients were included in the study. Thirteen were randomized to receive and 15 not to receive intravenous CMV hyperimmune globulin. A dose of 0.4 g/kg of immunoglobulin was given on day -8 and 0.2 g/kg on days -1, +7, +14, +21, +28, +35, +42, +56 and +70 in relation to the day of transplantation. Among the 15 patients not given immunoglobulin CMV was isolated in three, and two of them developed clinical CMV disease. In addition, one more patient developed CMV antibodies without virus isolation. In five of the 13 patients given immunoglobulin the virus could be isolated, and four of them developed CMV disease. One additional patient showed seroconversion but no other findings of CMV infection. The incidence of acute and chronic GVHD was similar in the two arms. There was no significant difference in survival. In conclusion, the present results do not indicate a beneficial effect of CMV hyperimmune globulin infusions in the prophylaxis of CMV infection or disease in seronegative allogeneic bone marrow transplant recipients from a seropositive donor.

Adolescent↗
PubMed1996

Cytokine regulation of GM-CSF and G-CSF secretion by human umbilical cord vein endothelial cells (HUVEC).

The cytokine regulation of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF secretion by human umbilical cord vein endothelial cells (HUVEC) using quantitative immunoassays was studied. Unstimulated HUVEC produced no CSF. Interleukin 1 (IL-1), TNF and lipopolysaccharides (LPS) had stimulatory effects, with IL-1 being the most potent. GM-CSF and G-CSF secretion followed the same pattern, except that more GM-CSF was secreted. Exposure to stimuli for 30 min induced secretion, and detectable amounts in supernatants were found after 4 h incubation. CSF secretion was strictly regulated by the presence of a stimulus in a concentration dependent manner, and there were no signs of any endogenous downregulatory mechanism. No other cytokine tested had any stimulatory effect of its own. However, addition of IL-3 to stimulated HUVEC enhanced both GM-CSF and G-CSF secretion in a dose-dependent manner. In addition, TNF, and to a lesser degree LPS, enhanced IL-1-induced secretion. The only cytokine with a prominent downregulatory effect was IFN-gamma. IL-4 and IL-10, which downregulate CSF secretion by monocytes, had only minor effects.

Cells, Cultured↗
PubMed1996

Effects of immunosuppressive drugs and antibiotics on GM-CSF and G-CSF secretion in vitro by monocytes, T lymphocytes and endothelial cells.

We studied the effects of eight antibiotics, cyclosporin and corticosteroids on the in vitro secretion of GM-CSF and G-CSF by monocytes. T lymphocytes and endothelial cells. The aim was to evaluate a possible mechanism for these drugs in the delay of haemopoietic recovery after high-dose chemotherapy or bone marrow transplantation. Corticosteroids were prominent inhibitors of GM-CSF secretion by monocytes and T lymphocytes, but not by endothelial cells. In contrast, G-CSF secretion by monocytes was unchanged whereas that of endothelial cells was enhanced in the presence of corticosteroids. Cyclosporin efficiently down-regulated GM-CSF secretion by T lymphocytes and had also a minor effect on CSF secretion by endothelial cells, whereas monocyte secretion was unaffected. Stimulated T lymphocytes derived from patients under treatment with cyclosporin had impaired capacity to secrete GM-CSF compared to controls. Among the antibiotics, cephalosporins inhibited GM-CSF secretion by T lymphocytes, and GM- and G-CSF secretion by endothelial cells. Ciprofloxacin and sulphmethoxazole had minor effects on GM-CSF secretion by T lymphocytes and endothelial cells. No antibiotic significantly influenced GM-CSF secretion by monocytes.

Adrenal Cortex Hormones↗
PubMed1996

Transplantation with allogenic bone marrow from a donor with systemic lupus erythematosus (SLE): successful outcome in the recipient and induction of an SLE flare in the donor.

OBJECTIVE: To investigate the transfer of autoimmunity by allogenic bone marrow transplantation. METHODS: Bone marrow transplantation was performed in a 43 years old man with acute myeloid leukaemia (AML) in remission. The donor was his HLA identical brother who had a mild systemic lupus erythematosus (SLE). Autoantibodies, including antinuclear, anti-C1q, and anticardiolipin antibodies, were measured before and after transplantation. RESULTS: Transient mild graft versus host disease (GvHD) developed in the recipient in the weeks following transplantation. The donor had persistently high concentrations of anti-C1q antibodies to the collagenous region of the complement component C1q. Three months after transplantation the recipient developed antiC1q antibodies that persisted for two months. No other autoantibodies and no SLE-like manifestations appeared. Chronic GVHD started five months posttransplant and responded to intensified immunosuppressive treatment. Three years post-transplant the patient was in unmaintained remission. Within a few weeks after bone marrow donation the donor's disease was exacerbated with development of severe pulmonary alveolitis which required treatment with cyclophosphamide. CONCLUSIONS: When bone marrow transplantation was performed in a patient with AML with bone marrow from an HLA identical brother who had SLE, no evidence of transfer of disease was obtained. However, the recipient temporarily produced anti-C1q antibodies which was a characteristic feature of the donor's SLE and was probably produced by the transplant. The flare of the donor's SLE might be related to the bone marrow tap.

Adult↗
PubMed1994

A randomized trial comparing busulfan with total body irradiation as conditioning in allogeneic marrow transplant recipients with leukemia: a report from the Nordic Bone Marrow Transplantation Group.

Between October 1988 and December 1992, 167 patients with leukemia receiving marrow transplants from HLA-identical donors and conditioned with cyclophosphamide (120 mg/kg) were randomized to additional treatment with either busulfan (16 mg/kg, n = 88) or total body irradiation (TBI; n = 79). The busulfan-treated patients had an increased cumulative incidence of veno-occlusive disease of the liver, ie, 12% compared with 1% in the TBI group (P = .009). Furthermore, hemorrhagic cystitis occurred in 24% of the busulfan patients versus 8% in the TBI patients (P = .003). In patients with advanced disease beyond first remission or first chronic phase, transplantation-related mortality was 62% among the busulfan-treated patients compared with 12% among the TBI recipients (P = .002). These differences between the two groups were statistically significant in multivariate analysis. Seizures were seen in 6% of the busulfan-treated patients and were absent in the TBI group (P = .03). Grade II-IV of acute graft-versus-host disease (GVHD) was similar in the two groups, but grade III-IV and chronic disease was more common in the busulfan-treated group (P = .04). Death associated with GVHD occurred in 17% of the busulfan-treated group and 2% of the TBI group (P = .003). Patients treated with busulfan had a 3-year actuarial survival of 62%, which was worse than the 76% among those treated with TBI (P < .03). In multivariate analysis, poor survival was associated with advanced disease (P < .0001), no posttransplant septicemia (P = .0006), grade II-IV GVHD (P = .006), and busulfan treatment (P < .02). The incidence of relapse did not differ between the two groups. Relapse-free survival was also similar in the two treatment groups on analysis of data from all patients, children, patients with early disease, and those with acute myeloid leukemia, acute lymphoblastic leukemia, and chronic myeloid leukemia. However, in adults (P = .05) and patients with advanced disease (P = .005), leukemia-free survival was significantly better in those treated with TBI. We conclude that patients treated with busulfan have more early toxicity and an increased transplant-related mortality in patients with advanced disease. TBI is therefore the treatment of choice, especially in adults and patients with advanced disease. However, busulfan is an acceptable alternative for patients with early disease and for those in whom TBI is not feasible.

Adolescent↗
PubMed1991

Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in serum in bone marrow transplanted patients.

Colony-stimulating factors (CSF) are being increasingly used to accelerate hematopoietic recovery after bone marrow transplantation. To study the endogenous serum levels of CSF in bone marrow transplanted patients we have used immunoassays measuring granulocyte-macrophage colony-stimulating factor (GM-CSF) with a sensitivity of 0.10 ng/ml and granulocyte colony-stimulating factor (G-CSF) with a sensitivity of 0.05 ng/ml. Serum samples, taken from the conditioning treatment until engraftment, were analysed in 13 patients receiving allogeneic transplants and in eight patients receiving autologous transplants. Ten patients had acute myeloid leukemia, seven acute lymphoblastic leukemia, one acute undifferentiated leukemia, two non-Hodgkin's lymphoma and one multiple myeloma. Samples were taken 1-2 times before transplantation and 1-2 times per week after transplantation (median of 46 days in allotransplant recipients and 32 days in autotransplant recipients); 17% of the allogeneic transplanted patients and 35% of the autologous transplanted patients had detectable levels of G-CSF. In both types of transplantation the G-CSF concentrations were low: median 0.06 (range 0.05-0.14) and 0.08 (range 0.05-0.40) ng/ml respectively. GM-CSF was detected only in one analysed sample in all patients. There was no evidence of increased CSF levels related to engraftment or documented infections.

Acute Disease↗
PubMedDate not supplied

NRAS mutations are rare in acute myeloid leukaemias with t(8;21) or inv(16).

Using PCR and direct sequence methodology, 19 haematologic malignancies with trisomy 8, 18 with t(8;21)(q22;q22) and 8 with inv(16)(p13q22) were screened for NRAS mutations. Of the 45 samples analyzed, 4 (9%) had a mutation; both wild-type and mutated alleles were observed in these 4 cases. Three of the mutations (involving codons 12 and 13) were found in the trisomy 8 group and 1 (codon 61) among the inv(16) samples. No specific clinical similarities were found in the 3 patients with +8 and NRAS mutation. By analyzing two sequential samples from the patient with inv(16) and NRAS mutation, it was shown that the mutation had occurred after the inversion. Since no NRAS mutations were detected among the t(8;21) samples and only 1 was found in the inv(16) group, we conclude that acute myeloid leukaemias with t(8;21) or inv(16) generally arise and progress without the involvement of NRAS mutations.

Acute Disease↗