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Acute onset severe hypophosphataemia in transformed acute myeloid leukaemia: an unusual biochemical presentation
  1. Catelyn Cashion1,
  2. Paul Bonnitcha2,3,
  3. William Stevenson1,4
  1. 1Department of Haematology and Transfusion Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia
  2. 2Chemical Pathology Department, NSW Health Pathology, Royal Prince Albert Hospital, Camperdown, New South Wales, Australia
  3. 3Chemical Pathology Department, SydPath, St Vincent's Hospital Sydney, Darlinghurst, New South Wales, Australia
  4. 4Northern Blood Research Centre, Kolling Institute of Medical Research, St Leonards, New South Wales, Australia
  1. Correspondence to Dr Catelyn Cashion, Department of Haematology and Transfusion Medicine, Royal North Shore Hospital, St Leonards, NSW 2065, Australia; catelyn.cashion{at}health.nsw.gov.au

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Clinical presentation

A woman in her 60s had a 10-day history of a dry cough and thoracic back pain associated with a chest X-ray demonstrating an acute T9 compression fracture and a minor band of atelectasis in the right lower zone. She had been started on amoxicillin and tapentadol analgesia. Over the 24 hours prior to presentation, she had developed episodic visual changes and dizziness. On examination, there was mild confusion, normal oxygen saturations and a moderate sized left retinal haemorrhage The white cell count (WCC) at presentation was 351×109/L (reference interval 4.0–11.0) compared with a routine test performed 1 week prior to this presentation showing a WCC of 5.1×109/L indicating the highly proliferative nature of her disease at presentation.

This patient had dual diagnoses of high-risk myelodysplastic syndrome and smouldering myeloma, both identified 12 months prior. She had previously been treated with four cycles of azacitidine 75 mg/m2 followed by 4 cycles of lenalidomide 25 mg 21 days of a 28-day cycle, in combination with dexamethasone 40 mg weekly. Her other medical history included thyroid cancer treated with a thyroidectomy and radioactive iodine 35 years prior, glaucoma, atrial fibrillation, B12 deficiency and asthma.

Laboratory investigations

At the time of presentation, her haemoglobin was 68 g/L (RI: 115–165), platelet count was 102×109/L (RI: 150–450) and total WCC was 351×109/L with a differential of neutrophils 17.6×109/L (RI: 2.0–8.0), monocytes 115×109/L (RI: 0.2–1.0), lymphocytes 66.8×109/L (RI: 1.0–4.0) and blasts 147.5×109/L. The blood film was leucoerythroblastic with 52% monoblasts and promonocytes; there were dysplastic neutrophils and thrombocytopaenia (figures 1 and 2). Flow cytometry identified 2 populations of blasts: 8% CD34 positive and 78% CD33, CD64 and CD45 dim. Routine molecular markers were negative. Cytogenetic study of the peripheral blood showed a complex karyotype with evidence of clonal …

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Footnotes

  • Handling editor Patrick J Twomey.

  • Contributors PB and WS contributed to the identification of the case and CC and PB contributed to writing of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.