Primary hyperoxaluria is characterized by severe urolithiasis, nephrocalcinosis, and early renal failure. As treatment options are scarce, we aimed for a new therapeutic tool using colonic degradation of endogenous oxalate by Oxalobactor formigenes. Oxalobacter was orally administered for 4 weeks as frozen paste (IxOC-2) or as enteric-coated capsules (IxOC-3). Nine patients (five with normal renal function, one after liver-kidney transplantation, and three with renal failure) completed the IxOC-2 study. Seven patients (six with normal renal function and one after liver-kidney transplantation) completed the IxOC-3 study. Urinary oxalate or plasma oxalate in renal failure was determined at baseline, weekly during treatment and for a 2-week follow-up. The patients who showed >20% reduction both at the end of weeks 3 and 4 were considered as responders. Under IxOC-2, three out of five patients with normal renal function showed a 22-48% reduction of urinary oxalate. In addition, two renal failure patients experienced a significant reduction in plasma oxalate and amelioration of clinical symptoms. Under IxOC-3 treatment, four out of six patients with normal renal function responded with a reduction of urinary oxalate ranging from 38.5 to 92%. Although all subjects under IxOC-2 and 4 patients under IxOC-3 showed detectable levels of O. formigenes in stool during treatment, fecal recovery dropped directly at follow up, indicating only transient gastrointestinal-tract colonization. The preliminary data indicate that O. formigenes is safe, leads to a significant reduction of either urinary or plasma oxalate, and is a potential new treatment option for primary hyperoxaluria.

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bradycardia, where nitroglycerine may not be suitable [1]. Although coronary artery spasm is diagnosed by angiography using provocative drugs like Acetylcholine and Ergonovine, an exercise test following hyperventilation is an equivalent non-invasive test to diagnose this condition [2]. Thus, a negative provocative stress test ruled out the possibility of vasospastic angina in this patient. The Naranjo probability score confirmed an adverse drug reaction (Score 6) [3]. There is no previous association of iron sucrose with coronary vasospasm. In the Fenton and Haber-Weiss reaction, free metal ions like iron facilitate the production of toxic hydroxyl radicals from superoxide radicals [4], which can inhibit the synthesis of prostacyclin, influencing vessel tone [5]. This is a probable explanation for coronary spasm precipitated by the drug in our patient. The use of iron sucrose has addressed issues of anaphylaxis and infection to a large extent. Recommendation for higher doses and its good tolerability reduces the visits for iron treatment. However, it rarely poses potential hazards, the possibility of coronary artery spasm being one such complication. Conflict of interest statement. None declared.