Oxalobacter formigenes lowers oxalate in childen with oxalosis
A German pilot study found that Oxalobacter formigenes bacteria may be a viable treatment option for primary hyperoxaluria type 1.
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Bernd Hoppe, MD, of Children’s Hospital Cologne, and his colleagues studied the use of O. formigenes in 16 patients. The bacteria—which naturally colonize the colon of vertebrates and use oxalic acid as its sole source of energy—were administered orally for four weeks either as a frozen paste (nine patients) or as enteric-coated capsules (seven patients).
The nine patients who took the bacteria as a frozen paste (the IxOC-2 group) consisted of five
with normal renal function, three with renal failure, and one who had undergone liver-kidney transplantation; the seven patients who took the enteric-coated capsules (the IxOC-3 group) consisted of six with normal renal function and one who had undergone liver-kidney transplantation. Patients were considered responders if they showed a greater than 20% reduction in urinary oxalate (or plasma oxalate in the renal failure cases) at the end of weeks 3 and 4.
In the IxOC-2 group, three of the five patients with normal renal function experienced a 22%-48% reduction in urinary oxalate. The two patients with renal failure experienced a significant reduction in plasma oxalate and amelioration of clinical symptoms. In the IxOC-3 group, four of the six patients with normal renal function had a reduction of urinary oxalate ranging from 38.5%-92%.
The researchers observed decreased plasma oxalate levels in 10 of the 13 patients in both groups
with normal or stable kidney function, resulting in a significant decrease in mean plasma oxalate in both groups.
All patients in the IxOC-2 group and four in the IxOC-3 group had detectable levels of O. formigenes in stool during treatment, but “fecal recovery of the bacteria dropped directly at follow-up, indicating only transient gastrointestinal-tract colonization,” the investigators
wrote in Kidney International (2006; 70:1305-1311).
“We were able to show that oral O. formigenes administration is safe, that it transiently colonizes the intestinal tract, and that it exerts its metabolic activity to enhance the non-urinary removal of endogenous oxalate through enteric elimination, thus supporting previous data in animal trials.”
Noting that treatment options for patients with primary hyperoxaluria are limited, the investigators concluded that “new therapeutic regimens are clearly needed. The data obtained in this study let us speculate that O. formigenes might be a very promising new kind of treatment for this mostly devastating disease.”
Primary hyperoxaluria type 1 is an inherited disease caused by a shortage of the hepatic enzyme
alanine:glyoxylate aminotransferase, which prevents oxalate buildup. Pyridoxine is the only available therapy for decreasing urinary oxalate in patients with this disease.
In a commentary accompanying the new study, Dawn Milliner, MD, of the Mayo Clinic in Rochester, Minn., pointed out that pyridoxine benefits only about 30%-50% of patients with primary hyperoxaluria type 1. The only other modality for decreasing urine oxalate excretion is liver transplantation. The new study “opens a much needed new chapter in treatment of primary hyperoxaluria,” she wrote.
“If the results are confirmed, Oxalobacter should be useful in all types of primary hyperoxaluria and may be fruitful for study in enteric and other forms of hyperoxaluria as well.”
