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Biomedical subjects

M van Gelder

Publications and source records attributed to M van Gelder.

11 recordsLinked to original sources
PubMed2006

[Kikuchi's histiocytic necrotising lymphadenitis: a benign disorder--not to be confused with malignant lymphoma].

A 26-year-old woman who later turned out to have the rarely seen histiocytic necrotising lymphadenitis of Kikuchi was twice diagnosed incorrectly with malignant T-cell lymphoma. She was treated with standard chemotherapy, whereas Kikuchi's disease has a self-limiting course. Fear for recurrent lymphoma greatly affected the patient's life until the proper diagnosis was ultimately made. This occurred after the patient herself had seen in her dossier that the diagnosis 'Kikuchi's histiocytic lymphadenitis' had been proposed by two pathologists of the consulted regional lymphoma board in the past, but had been rejected by the board after external consultation.

Adult↗
PubMed2006

Graft-versus-tumor effects on murine mammary carcinoma in a model of nonmyeloablative haploidentical stem cell transplantation.

Despite a slight decrease in mortality over the last decade, breast cancer still remains a leading cause of cancer-related death in women. Although anti-tumor effects have been observed after allogeneic stem cell transplantation (SCT), this treatment is not standard care owing to graft-versus-host disease (GVHD) and scarcity of suitable donors. With the aim of reducing treatment-related mortality and increasing donor availability in clinical situations, we developed a preclinical mouse model that combines nonmyeloablative conditioning with the use of haploidentical donor-recipient pairs. To mimic active disease, CB6F1 mice were inoculated with 5 x 10(4) 4T1 mammary carcinoma cells 10 days before transplantation. Keratinocyte growth factor (KGF) was used as GVHD prophylaxis. Syngeneic (CB6F1) SCT did not cure any of the mice and KGF treatment did not influence tumor development. After transplantation with haploidentical (B6CBAF1) bone marrow and splenocytes, however, tumor outgrowth was reduced and long-term disease-free survival (>3 months) was observed in 9/18 (50%) (P=0.0011) of the animals. We conclude that in a model of murine breast cancer, a graft-versus-tumor effect can be induced by a nonmyeloablative haploidentical SCT procedure.

Animals↗
PubMed2001

Recovery of erythropoiesis following allogeneic bone marrow transplantation for chronic lymphocytic leukaemia-associated pure red cell aplasia.

Pure red cell aplasia is a rare condition, that can be either idiopathic or associated with a lymphoproliferative disorder. The latter is considered to result from T cell-mediated suppression of haematopoiesis, and usually responds well to treatment with immunosuppressive medication. We describe a patient with B-CLL-associated pure red cell aplasia who did not respond to several courses of immunosuppressive treatment. Erythropoiesis was finally restored after allogeneic bone marrow transplantation.

Adult↗
PubMed1996

Treatment of relapsing experimental autoimmune encephalomyelitis with largely MHC-matched allogeneic bone marrow transplantation.

BUF rats suffering from severe relapsing experimental autoimmune encephalomyelitis (R-EAE), a model for multiple sclerosis, were treated with intensive cytoreductive therapy and grafting of allogeneic bone marrow (BM). BN.1B rats were used as EAE-resistant, largely MHC-matched donors, resembling human BMT from HLA-identical siblings. The treatment induces complete remission and low recurrence rates of R-EAE. Evidence is provided that the efficacy of the treatment depends on a high degree of lymphoablation: a minority of rats had host-type residual activated T lymphocytes in the CNS after treatment. Furthermore, complete replacement of host-type BM by donor-type hemopoietic cells is essential, as higher relapse rates were observed in animals with incomplete reconstitution by donor cells than in completely reconstituted rats. Overall, our results indicate that patients with severe MS might benefit from treatment with HLA-matched allogeneic BM.

Animals↗
PubMed1996

Both bone marrow- and non-bone marrow-associated factors determine susceptibility to experimental autoimmune encephalomyelitis of BUF and WAG rats.

To determine the feasibility of treatment with allogeneic bone marrow for experimental autoimmune encephalomyelitis, we investigated the susceptibility to experimental autoimmune encephalomyelitis of bone marrow chimeras using BUF, (WAG X BUF)F1 (high responder), and WAG (low responder) rats. In contrast to previous studies in which other rat strains were used, the response was largely determined by the genotype of the grafted bone marrow, but the influence of a non-bone marrow-associated factor was evident. The latter factor was identified as a low corticosterone response in BUF rats and a high corticosterone response in WAG rats. After adrenalectomy, a significant proportion of WAG rats developed clinical experimental autoimmune encephalomyelitis. The bone marrow-associated factor of resistance appeared to be the activity of cyclophosphamide-sensitive suppressor cells. The latter cells were found to interfere with the formation of inflammatory foci in the central nervous system, while corticosterone primarily prevents the clinical expression of lesions.

Animals↗
PubMed1996

Effective treatment of relapsing experimental autoimmune encephalomyelitis with pseudoautologous bone marrow transplantation.

Several human and experimental autoimmune diseases, including the current model for multiple sclerosis (MS), ie relapsing experimental autoimmune encephalomyelitis (R-EAE), have been reported to respond with complete remission to lympho- and myeloablation and rescue with transplantation of bone marrow (BMT) from healthy donors. Since treatment with autologous BM was as effective in our arthritis model as treatment with allogeneic BM from healthy rats, and in view of the much lower risk of autologous BMT in clinical practice, we have investigated treatment of R-EAE with pseudo-autologous (PSA) BM. PSABM is harvested from animals in the same active stage of R-EAE as the syngeneic recipients which are to be treated. Our results show that PSABM is as effective as syngeneic BM, except for a higher incidence of artificially induced relapses. We also demonstrated that lymphocytes present in the autologous BM graft may contribute to the occurrence of relapses post-transplantation. The implications of our results for a possible clinical application in the treatment of MS patients are discussed. If such treatment is envisaged, the use of T cell-depleted autografts seems mandatory, particularly as human BM contains 10 times more lymphocytes than rat BM.

Animals↗
PubMed1995

Treatment of relapsing experimental autoimmune encephalomyelitis in rats with allogeneic bone marrow transplantation from a resistant strain.

We previously showed that relapsing experimental autoimmune encephalomyelitis (R-EAE) in BUF rats, a model for multiple sclerosis, responds favorably to treatment with TBI and syngeneic BMT. Relapses of paresis occurred less frequently than in untreated controls, but were not completely prevented. Therefore, we investigated the effect of allogeneic BMT from the resistant WAG rat strain. BUF rats were treated with either high-dose TBI or CY and Bu followed by allogeneic BMT. This treatment induced complete remission, and reduced both the spontaneous and induced relapse rate more efficaciously than syngeneic BMT. Evidence is provided that a subclinical GVHR contributes to the prevention of spontaneous relapses. The almost complete absence of induced relapses likely results from the repopulation by the resistant immune system of the donor, which proved to be functional by responding to immunization with type II collagen. It is thus unlikely that a BMT-related immunodepression contributed to the lower incidence of induced relapses. We propose that allogeneic BMT should be considered for the treatment of severe progressive MS with a poor prognosis.

Animals↗
PubMed1993

Preserved organic anion transport in mutant TR- rats with a hepatobiliary secretion defect.

The in vivo biliary secretion of a number of organic anions in mutant TR- rats was studied. The secretion of bilirubin glucuronide (BG), the glutathione conjugate of bromosulfophthalein, dibromosulfophthalein, and indocyanine green was reduced to 2, 15, 50, and 75% of normal, respectively. Surprisingly, the secretion of bilirubin ditaurate (BDT) was entirely normal under these conditions. In isolated TR- rat liver perfusion experiments (recirculating setup), the hepatobiliary secretion of BG and BDT was reduced to 1 and 50% of normal, respectively. There was considerable residual concentrative transport of BDT under these conditions (bile-to-perfusate concentration ratio of 190 +/- 60; normal, 730 +/- 480), whereas for BG the concentration step was completely abolished (bile-to-perfusate concentration ratio of 1.3 +/- 1.0; normal, 60 +/- 40). In a single-pass isolated TR- rat liver perfusion study, BDT secretion after bolus administration (1 mumol) was abnormal; the peak secretion was retarded to 20 min after injection (normal 7.5 min), and the secretion rate was decreased to 19% of normal. BDT, as an organic dianion, is a substrate for the "canalicular multispecific organic anion transporter" (cMOAT), a carrier protein that is defective in TR- rats. Its considerable residual secretion in certain experimental conditions suggests the preservation of a low-affinity pathway for secretion of some cMOAT substrates in TR- rats.

Animals↗
PubMed1993

Treatment of experimental allergic encephalomyelitis in rats with total body irradiation and syngeneic BMT.

Experimental allergic encephalomyelitis (EAE) was induced in Buffalo rats by immunization with syngeneic spinal cord homogenate in complete adjuvant. EAE, an autoimmune disease of the central nervous system (CNS), is regarded as a model for multiple sclerosis. When severe paresis had developed, rats were treated with high-dose total body irradiation (TBI) and transplanted with syngeneic BM from healthy donors. Nine Gy TBI followed by syngeneic BMT greatly accelerated recovery of paresis compared with untreated controls. In 6-33% of the treated animals a relapse of EAE was observed shortly after treatment. Reimmunization 20 days after treatment, resulted in a relapse in 12-44% of the rats. Employing the maximally tolerated dose of TBI (10 Gy) did not significantly alter the incidence of spontaneous or induced relapses. Furthermore, it was shown that irradiation of the CNS only was not sufficient for the induction of complete regression of paresis. The origin of the cells responsible for these relapses is discussed, as is the importance of reimmunization in evaluating the effect of treatment of experimental autoimmune disease.

Animals↗