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In their review, Arslan et al[1] did not describe the status of Helicobacter pylori(H. pylori) treatment with furazolidone and the resistance to this antibiotic. We have presented different surveys showing the resistance of H. pylori to furazolidone from Asia and South America. The resistance rates varied but were mostly low(< 5%). There are not enough data on its efficacy and resistance in the United States and Europe. H. pylori mutations occurring in the oor D gene, including A041 G, A122 G, C349A(G), A78 G, A112 G, A335 G, C156 T and C165 T, and in the por D gene, including G353 A, A356 G, C357 T, C347 T, C347 G and C346 A, have been indicated to be possibly related to the observed resistance. Additionally, to complete Arslan et al ’s statement regarding levofloxacin resistance, it should be noted that compound mutations of N87 A, A88 N and V65 I at codon Asn-87 were recently observed in the gyr A gene for the first time. However, the results on these topics are not sufficient, and more worldwide studies are suggested.
In their review, Arslan et al [1] did not describe the status of Helicobacter pylori (H. pylori) treatment with furazolidone and the resistance to this antibiotic. We have presented different surveys showing the resistance of H. pylori to furazolidone from Asia and South America. The resistance rates varied but were mostly low (<5%). There are not enough data on its efficacy and resistance in the United States and Europe. H. pylori mutations occurring in the oor D gene, including A041 G, A122 G, C349A (G), A78G, Al12G, A335G, C156T and C165T, and in the por D gene, including G353A, A356G, C357T, C347T, C347G and C346A, have been to complete the Arslan et al’s statement regarding levofloxacin resistance, it should be noted that the compound mutations of N87 A, A88 N and V65 I at codon Asn-87 were recently observed in the gyr A gene for the first time. However, the results on these topics are not sufficient, and more worldwide studies are suggested.