Marrow cell transplantation for infantile hypophosphatasia
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Published on: June 14, 2017
Michael P Whyte1, Joanne Kurtzberg, William H McAlister
1Center for Metabolic Bone Disease and Molecular Research, Shriners Hospitals for Children, St. Louis, Missouri 63131-3597, USA. mwhyte@shrinenet.org
Insights
Bone marrow cell transplantation offers hope for infantile hypophosphatasia, a rare metabolic bone disease. This study shows donor mesenchymal stem cells may ameliorate skeletal rickets, improving patient outcomes.
Area of Science:
- Biochemistry
- Genetics
- Pediatrics
Background:
- Hypophosphatasia is a severe inherited metabolic disorder caused by deficient tissue-nonspecific alkaline phosphatase (TNSALP) activity.
- The infantile form presents a grave prognosis, often leading to mortality within the first year of life.
Observation:
- A patient with infantile hypophosphatasia received T-cell-depleted, haplo-identical bone marrow transplantation.
- Initial engraftment was successful, showing clinical improvement and skeletal healing, but disease recurred due to partial host hematopoiesis return.
Findings:
- A subsequent boost of ex vivo expanded donor marrow cells enriched for stromal cells led to significant and prolonged clinical and radiographic improvement.
- Biochemical markers of hypophosphatasia remained unchanged, suggesting a mechanism beyond enzyme replacement.
Implications:
- Mesenchymal stem cell engraftment from donor marrow may be a key therapeutic mechanism for ameliorating skeletal disease in hypophosphatasia.
- This approach offers a potential strategy for managing severe, otherwise fatal, genetic bone disorders.
Abstract:
An 8-month-old girl who seemed certain to die from the infantile form of hypophosphatasia, an inborn error of metabolism characterized by deficient activity of the tissue-nonspecific isoenzyme of alkaline phosphatase (TNSALP), underwent the first trial of bone marrow cell transplantation for this heritable type of rickets. After cytoreduction, she was given T-cell-depleted, haplo-identical marrow from her healthy sister. Chimerism in peripheral blood and bone marrow became 100% donor. Three months later, she was clinically improved, with considerable healing of rickets and generalized skeletal remineralization. However, 6 months post-transplantation, worsening skeletal disease recurred, with partial return of host hematopoiesis. At the age of 21 months, without additional chemotherapy or immunosuppressive treatment, she received a boost of donor marrow cells expanded ex vivo to enrich for stromal cells. Significant, prolonged clinical and radiographic improvement followed soon after. Nevertheless, biochemical features of hypophosphatasia have remained unchanged to date. Skeletal biopsy specimens were not performed. Now, at 6 years of age, she is intelligent and ambulatory but remains small. Among several hypotheses for our patient's survival and progress, the most plausible seems to be the transient and long-term engraftment of sufficient numbers of donor marrow mesenchymal cells, forming functional osteoblasts and perhaps chondrocytes, to ameliorate her skeletal disease.
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