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Severe hypermagnesaemia related to laxative use in acute gastrointestinal graft-versus-host disease

Bone Marrow Transplantation volume 38, pages 71–72 (2006)Cite this article

Hypermagnesaemia is an unusual complication of allogeneic haemopoietic stem cell transplantation (HSCT). In one series of 311 patients undergoing allogeneic HSCT, severe hypermagnesaemia was reported in nine cases.1 Hypermagnesaemia is a well-recognised complication of laxative use, usually occurring in patients with renal dysfunction or small bowel hypomotility disorders. Magnesium in excess acts as a competitive calcium channel blocker, producing the clinical features of hypotension, autonomic dysfunction, cardiac conduction defects and neuromuscular junction blockade. To our knowledge, this complication has not been reported in the setting of acute gastrointestinal graft-versus-host disease (GVHD).

We report the case of a 43-year-old man, who developed life-threatening hypermagnesaemia associated with laxative use, following HLA-matched sibling non-myeloablative peripheral blood stem cell transplantation for M1 acute myeloid leukaemia (AML) in first complete remission (CR1). There was no significant past medical history. Remission induction was achieved using the ICE regimen (idarubicin 9 mg/m2 daily × 3, cytarabine 3 gm/m2 twice daily × 4, etoposide 75 mg/m2 daily × 7) but was complicated by multiorgan failure. Following two cycles of consolidation chemotherapy, he was enrolled in a trial of non-myeloablative HSCT for AML in CR1. He was conditioned with cyclophosphamide and fludarabine, and received 8.67 × 106/kg CD34+ cells harvested from his male sibling donor. Graft-versus-host disease prophylaxis consisted of cyclosporine A 3 mg/kg/day and methotrexate. On day +23 after HSCT, a maculopapular trunk rash consistent with stage II acute skin GVHD was noted. It resolved with oral prednisolone 100 mg daily. On day +28 after HSCT he developed diarrhoea. Stool microbiology was negative. From day +32, because of progressively worsening diarrhoea, he received intravenous methylprednisolone 500 mg daily for 3 days, followed by 180 mg daily. By day +34, the serum creatinine rose to 221 μmol/l from a normal baseline. On day +35 he received 2 Picolax (10 mg sodium picosulphate and 20 g magnesium carbonate), and 1 l of Colonlytely, a polyethylene glycol-based electrolyte solution, in preparation for colonoscopy. While ingesting these products, he developed a moderate hyporeflexic tetraparesis, accompanied by facial diplegia, fatiguable ptosis, a complex ophthalmoplegia, bulbar palsy, and tongue weakness. His serum magnesium at this time was 4.94 mmol/l, from 1.21 mmol/l that morning. Serum calcium and potassium were normal. On the same day, he developed oliguria secondary to intravascular hypovolaemia. His cyclosporine concentration was 433 μg/l and this drug was withheld. Features consistent with an ileus were noted, including cessation of previously profuse bowel movements. Some increase in strength was noted with calcium gluconate administration, and a saline diuresis was attempted. The following day, creatinine continued to rise and magnesium remained elevated at a concentration of 4.4 mmol/l. Haemodialysis was commenced with a post-dialysis magnesium of 1.97 mmol/l. Towards the end of the first dialysis, profuse bowel movements recommenced, and strength returned to pre-morbid concentrations. Nerve conduction studies were performed at this stage, showing an inconsistent increment at 2 Hz, and saddle-shaped increment at 20 and 30 Hz. There was no post-exercise facilitation. Dialysis was repeated the following day. On day +37, mycophenolate mofetil 500 mg intravenously twice daily was empirically commenced for ongoing diarrhoea. The diagnosis of GVHD was supported by biopsy findings from sigmoidoscopy. Severe diarrhoea persisted, despite subsequent reintroduction of cyclosporine, and daclizumab, etanercept, antithymocyte globulin and oral budesonide. Active therapy was withdrawn due to ongoing bloody diarrhoea, and the patient succumbed to GVHD.

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Authors and Affiliations

  1. Department of Haematology, Royal Adelaide Hospital, Adelaide, Australia

    D P Leong & P G Bardy

  2. Department of Neurology, Royal Adelaide Hospital, Adelaide, Australia

    T J Kleinig & T E Kimber

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  1. D P Leong
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  2. T J Kleinig
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Correspondence to P G Bardy.

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Leong, D., Kleinig, T., Kimber, T. et al. Severe hypermagnesaemia related to laxative use in acute gastrointestinal graft-versus-host disease. Bone Marrow Transplant 38, 71–72 (2006). https://doi.org/10.1038/sj.bmt.1705386

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