Digital necrosis from dandelion tea

Extract

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Conflicts of interest: none declared.

Madam, Oxalate (C₂O₄²⁻) is a salt‐forming ion that combines with calcium to form the almost insoluble calcium oxalate.1 It is absorbed in the gastrointestinal tract and produced during liver metabolism of glycoxalate,2 but has no known function in humans. Oxalate excretion is primarily via the kidneys, undergoing glomerular filtration, tubular secretion and tubular reabsorption.3 Hyperoxaluria may occur as a primary genetic abnormality, or secondary to dietary, gastrointestinal or renal factors, and may have cutaneous manifestations. We report a patient with renal impairment who developed hyperoxalaemia causing peripheral gangrene due to the ingestion of large quantities of dandelion tea.

A 56‐year‐old man presented with black discoloration of his fingertips associated with severe pain and loss of function for 8 weeks (Fig. 1). He had type 2 diabetes and hypertension but took no medication relevant to the presenting symptoms. Three months previously he had been admitted to the intensive care unit with renal failure and had become intermittent haemodialyisis dependent. He had no relevant family history. He was an ex‐smoker, was unemployed and had no hobbies. He had been drinking 10–15 cups of dandelion tea daily for 6 months. Examination revealed digital ischaemia with necrosis of the distal phalanges of both thumbs and the lateral three digits of both hands. Both hands were cool, with reduced capillary refill time. No peripheral pulses were palpable in the limbs. Vasculitic and clotting screens were normal. Hyperoxalaemia had been recorded around the of onset of his hand symptoms (plasma oxalate 87 μmol L⁻¹; normal level < 10 μmol L⁻¹). As the patient was anuric, urinary oxalate could not be quantified. X‐rays of the patient's hands, and arterial Doppler measurements of his limbs, revealed heavily calcified vessels (Fig. 2a). Cardiac echo did not demonstrate thrombus. Skin biopsy from a finger revealed tissue necrosis. Renal biopsy, which had been undertaken just prior to his current presentation, showed deposition of oxalate crystals in the proximal tubules on a background of diabetic glomerulopathy (Fig. 2b). Liver biopsy excluded primary hyperoxaluria. Dandelion tea from the same source as the patient's, prepared in a similar way, produced a high oxalate level of 258 μmol L⁻¹. A diagnosis of secondary hyperoxalaemia due to high dietary oxalate with reduced renal clearance was made. The patient died 9 months after diagnosis.