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Biomedical subjects

J L Steegman

Publications and source records attributed to J L Steegman.

10 recordsLinked to original sources
PubMed2000

Transfer of autoimmune hypothyroidism following bone marrow transplantation from a donor with Graves' disease.

We describe the transfer of a different autoimmune thyroid disorder by bone marrow transplantation. The donor had euthyroid Graves' disease after treatment with antithyroid drugs and stable oxopthalmos, with persistent thyroid autoantibodies. One year after bone marrow transplant, the recipient developed atrophic autoimmune hypothyroidism. Six months later the donor developed transient subclinical hypothyroidism followed by clinical hyperthyroidism. In both recipient and donor the presence of thyrotropin (TSH)-binding inhibitory immunoglobulins was documented. Although TSH receptor antibodies usually act as a TSH agonist causing thyrotoxicosis, they can also can act as a TSH antagonist causing primary hypothyroidism. This case may be an example of how the same antibody can act as an agonist in the donor and an antagonist in the bone marrow recipient, causing two different autoimmune disorders: primary hypothyroidism in the recipient and Graves' disease in the donor.

Adult↗
PubMed1995

Busulfan and melphalan as conditioning regimen for autologous peripheral blood stem cell transplantation in multiple myeloma.

Twenty-four patients with multiple myeloma (MM), three (12.5%) in complete remission (CR) and 21 (87.5%) in partial remission (PR) were treated with high-dose chemotherapy (HDCT) (busulfan 12 mg/kg+melphalan 140 mg/m2) as preparative regimen for autologous peripheral blood stem cell (PBSC) transplantation. These cells were previously collected by leukapheresis after mobilization by high-dose cyclophosphamide (HD Cy)+rhGM-CSF (18 patients) or rhG-CSF alone (six patients). Considering 23 evaluable patients following HDCT, the CR rate was 58% (14 patients) and the PR rate was 38% (nine patients). One transplant-related death occurred following this regimen (4%). With a median follow-up of 20 months (range 4-34) after transplantation, 21 patients are alive (87%). Disease progression after transplantation was observed in four patients. Overall and relapse-free actuarial survival at 24 months was 91% and 74%, respectively. 12 patients (50%) remain in CR 15 months (4-34) post transplant. The major toxicity was mucositis. Busulfan+melphalan is a safe and feasible conditioning regimen for APBSCT in MM with acceptable toxicity and a high objective response rate, which may result in prolonged survival.

Adult↗
PubMed1992

Ph-positive chronic myeloid leukemia with t(8;21)(q22;q22) in blastic crisis.

A patient diagnosed with chronic myeloid leukemia was studied periodically during his illness. The result showed the presence of a Philadelphia (Ph) chromosome by a 9;22 translocation as a single abnormality to the time of blastic crisis. At that time, the chromosome studies showed a clonal evolution. Furthermore, a second derivated line was added to the Ph line. This new anomaly consisted of a 8;21 translocation, considered as specific of M2 type acute nonlymphoblastic leukemia of French-American-British classification.

Adult↗
PubMed1987

Study of different factor VII deficiency variants in nine families from Spain.

Twenty-three patients with congenital factor VII (FVII) deficiency, belonging to 9 kindreds were studied. Immunological variants were classified according to the relationship between FVII coagulant activity (FVIIC) and the level of FVII antigen (FVIIAg), considering 3 previously described groups: VII-, VII+ and VIIR. Activation variants were determined by the reactivity pattern with three different thromboplastins. One patient was classified as VII-, 16 as VII+, and 6 as VIIR. Three patients belonging to the same kindred showed a Padua 2 FVII deficiency, and 1 patient showed a Padua 1 variant. There was no correlation between antigenic or activation variants and severity of bleeding tendency. Classical autosomal recessive mode of inheritance was observed in VII- and VII+ families. Nevertheless, a possible autosomal dominant trait was observed in VII+ kindreds.

Adult↗
PubMed1982

Translocation (11;14) in B-cell lymphoproliferative disorders.

A number of chromosomes other than chromosome No. 8 participate in formation of the 14q+ marker in lymphoproliferative disorders. Among them is chromosome No. 11 which appears to be important because its break points are constant; it is also possibly significant because of its participation in cytogenetic alterations in B-cell disorders.

Chromosome Banding↗