Letter to the Editor: “Reply to “Comment on ‘Cytochrome-C Oxidase Inhibition in 26 Aluminum Phosphide Poisoned Patients’””

To the Editor:

We are thankful to Dr. Amores et al. for their comments. We could not estimate blood phosphine concentrations because of technical difficulties; the major difficulty being a lack of analytic grade phospine for a standard. How blood phosphine concentrations could have correlated with either cytochrome-c oxidase activity or clinical phospine toxicity is difficult to assess, as phosphine progressively combines with oxyhemoglobin to form methemoglobin and hemichrome species with the products being dependent on time and concentration. Further, their interaction leads to formation of phosphates and phosphites (1,2).

In 23 of 26 patients the dose ingested was known. In 15 survivors, the mean ± SD dose was 4.03 ± 1.66 gm (range 1.5–10 gm) and in 8 non-survivors it was 4.71 ± 2.36 gm (range 1.5–9 gm). In three patients (one survivor and 2 non-survivors), the exact dose was not known. All these patients were northwest Indian Punjabis, as our Institute is a tertiary care center and acts as referral center for north and northwest India. In 16 patients, the blood sample was drawn within 12 hours and the assay completed within the next 24 hours. In the remaining 10 patients, the time interval between ingestion and blood sample was between 12–24 hours with assays being completed within the following 24 hours. None of them was on any known medication and they all received standard supportive care. We agree that in the present study it is difficult to draw any conclusions about the role of cytochrome-c oxidase activity inhibition in platelets in setting of aluminum phosphide poisoning. However, we have tried to provide a possible mechanism, which needs to be confirmed.