Comment on Aluminum and zinc phosphide poisoning

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allegedly found in bed. Donna Seger. Department of Medicine and Emergency Medicine, TN Poison Center,. Vanderbilt University Medical Center, Nashville, TN ...
Clinical Toxicology vol. 47 no. 8 2009

838 3. Miller MJ, Gomez HF, Snider RJ, Stephens EL, Czop RM, Warren JS. Detection of loxosceles venom in lesional hair shafts and skin: application of a specific immunoassay to identify dermonecrotic arachnidism. Am J Emerg Med 2000; 18(5):626–628. 4. Wasserman GS, Stoecker WV, Alcara DC, Green JA. Systemic loxoscelism confirmed by bite-site skin surface ELISA. Mo Med 2009; 106(6 Nov/Dec):[in press]. 5. Vetter RS. Arachnids misidentified as brown recluse spiders by medical personnel and other authorities in North America. Toxicon 2009; 54:545–554.

Letters to the editor report is that the patient found a spider in bed with her. Now we can all be amused that the diagnosis in both cases was confirmed by the critter allegedly found in bed. Donna Seger Department of Medicine and Emergency Medicine, TN Poison Center, Vanderbilt University Medical Center, Nashville, TN, USA Kendra P. Parekh Department of Emergency Medicine, TN Poison Center, Vanderbilt University Medical Center, Nashville, TN, USA

1556-9519 1556-3650 LCLT Clinical Toxicology Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0

Author’s response to letter

References Clinical Toxicology Downloaded from www.informahealthcare.com by Dr Omid Mehrpour For personal use only.

To the Editor: We wish to thank the authors for their commentary pointing out areas of confusion (and amusement) in our report.1 Unfortunately, the requirement for a minimum number of words to display a picture sometimes results in omitting facts that support the diagnosis. As the authors note, there has been much discussion about the diagnosis of brown recluse spider bite made in nonendemic areas and even in areas in which the spider is not found at all.2 Tennessee is in the center of the primary North American area endemic for Loxosceles reclusa. In fact, according to etymologists, homes are found in Tennessee that are infested with dozens to hundreds of spiders at one time.3 We appreciate the authors’ description of typical loxoscelism. They note that there is no available diagnostic test. However, we do not agree that loxoscelism is a diagnosis of exclusion. The approach of “diagnosis by exclusion” requiring a great number of laboratory studies may be appropriate to nonendemic areas. Indeed, in an era of limited resources, we offer that such a cost-intensive approach is wasteful in areas where clinicians have frequent encounters (and experience) with brown recluse spider bite. If we test for every possible alternative explanation in disease processes for which there is not an analytic test with 100% specificity, we would be wasteful indeed. The art of medicine often demands that we exercise experience and judgment while forsaking the inclination to test, test, test. In our toxicology clinic, we see three to five patients a week with either cutaneous or systemic loxoscelism, which is only the tip of an iceberg. Ours is a subspecialty referral clinic, and many, many spider bites are cared for by primary care physicians because of their familiarity with the bite. The diagnosis is made without analytic studies to rule out viral, bacterial, mycoplasma, or richettsial illness. The authors report a case of a toddler with a blister, necrotic-target lesion, erythroderma, fever, GI distress, and hemolysis. Although extensive laboratory evaluation was obtained, the child did not return for follow-up titers. Because the grandmother subsequently stated that a tick had been found in bed, the diagnosis of tick-borne illness was made. The diagnosis was not confirmed analytically. The authors imply that their case is clinically similar to the one that we reported and therefore our patient’s rash may have been caused by a tick bite. But there are clinical differences. Our patient had the classic “red, white, and blue” lesion with a central area of ischemia and pallor (not just a necrotic lesion) that is typical of L. reclusa, not rickettsia. We agree that other clinical manifestations of tick and brown recluse spider envenomation may be similar. Ironically, what was removed from our Received 29 July 2009; accepted 29 July 2009. Address correspondence to Donna Seger, 501 Oxford House, Vanderbilt University Medical Center, Nashville, TN, USA. E-mail: [email protected]

1. Parekh K, Seger D. Systemic loxoscelism. Clin Toxicol 2009; 47:430–431. 2. Vetter RS. Arachnids misidentified as brown recluse spiders by medical personnel and other authorities in North America. Toxicon 2009; 54:545–547. 3. Vetter RS. The distribution of brown recluse spiders in the Southeastern Quadrant of the US in relation to loxoscelism diagnosis. SMJ 2009; 5:518–552. 1556-9519 1556-3650 LCLT Clinical Toxicology Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0

Comment on Aluminum and zinc phosphide poisoning To the Editor: We read with interest the recent review article on aluminum and zinc phosphide poisoning.1 As this is a common poisoning in Iran and we have a significant number of published articles involving poisoning with these compounds, we have a concern with respect to the review of the topic. The author states that hyperglycemia in this poisoning is rare, and as such articles discussing glucose changes in these poisoning cases were limited. However, we have published a good number of papers that describe hyperglycemia in aluminum and zinc phosphide poisoning.2–6 Aluminum phosphide poisoning has been postulated to stimulate cortisol, glucagon, and adrenaline secretion or inhibit insulin synthesis1 that may cause hyperglycemia. In addition, Chugh et al.7 reported findings of 50 cases that showed a significant rise in plasma cortisol (>1048 nmol/L) in 40% of cases. Aluminum phosphide poisoning has also been reported to be associated with acute pancreatitis and hyperglycemia in some cases,8 suggesting that the effect of aluminum phosphide on the pancreas may have a role in causing hyperglycemia in this setting. We would like to bring your attention and the attention of the readers to additional more recent published data regarding the prevalence of hyperglycemia and its potential as a prognostic factor in aluminum phosphide poisoning4. Omid Mehrpour Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Islamic Republic of Iran

Received 25 June 2009; accepted 23 July 2009. Address correspondence to Dr. Omid Mehrpour, Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Birjand University of Medical Sciences, Ghafari Avenue, Birjand, Islamic Republic of Iran. E-mail: [email protected]

Clinical Toxicology vol. 47 no. 8 2009

Letters to the editor Dan Keyler Department of Medicine, Division of Clinical Pharmacology, Hennepin County Medical Center, Minneapolis, MN, USA Shahin Shadnia Loghman Hakim Hospital Poison Center, Faculty of Medicine and Toxicological Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Islamic Republic of Iran

Clinical Toxicology Downloaded from www.informahealthcare.com by Dr Omid Mehrpour For personal use only.

References 1. Proudfoot AT. Aluminum and zinc phosphide poisoning. J Toxicol Clin Toxicol 2009; 47:89–100. 2. Abder-Rahman H. Effect of aluminum phosphide on blood glucose level. Vet Hum Toxicol 1999; 41:31–32. 3. Shadnia S, Rahimi M, Pajoumand A, Rasouli MH, Abdollahi M. Successful treatment of acute aluminum phosphide poisoning: possible benefit of coconut oil. Hum Exp Toxicol 2005; 24:215–218. 4. Mehrpour O, Alfred S, Shadnia S, Keyler DE, Soltaninejad K, Chalaki N, Sedaghat M. Hyperglycemia in acute aluminum phosphide poisoning as a potential prognostic factor. Hum Exp Toxicol 2008; 27:591. 5. Shadnia S, Mehrpour O, Abdollahi M. Unintentional poisoning by phosphine released from aluminum phosphide. Hum Exp Toxicol 2008; 27:87. 6. Sarma PS, Narula J. Acute pancreatitis due to zinc phosphide ingestion. Postgrad Med J 1996; 72:237–238. 7. Chugh SN, Ram S, Mehta LK, Arora BB, Saini AS, Malhtra KC. Adrenocortical involvement in aluminum phosphide poisoning. Indian J Med Res 1989; 90:289–294. 8. Verma SK, Ahmad S, Shirazi N, Barthwal SP, Khurana D, Chugh M, Gambhir HS. Acute pancreatitis: a lesser-known complication of aluminum phosphide poisoning. Hum Exp Toxicol 2007; 26:979–981. 1556-9519 1556-3650 LCLT Clinical Toxicology Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0

839 Author’s response to letter To the Editor: I am grateful to Dr. Mehrpour and his colleagues for drawing attention to hyperglycemia as a complication of acute aluminium phosphide poisoning. At the time of writing the review, hyperglycemia had not attained, in my estimation at least, the importance it now has as a result of their work on it as a possible prognostic indicator. Given the voluminous literature on this poisoning it was impracticable for the review to catalog every publication on it. The reason their most recent publications were not included is that the review was submitted to the Journal early in 2008 and the references were not updated thereafter. The actions of aluminium phosphide on glucose homeostasis are clearly complex and some of the references Dr. Mehrpour’s letter lists (2, 3, and 6) were referred to in the review. References 4 and 5 were published after the review was completed. It was hoped that quoting the paper by Professor Chugh and his colleagues1 and that of Arora2 would obviate the need to reference too many earlier studies on effects on blood glucose concentrations and the pathological changes in the adrenal glands. I thank Dr. Mehrpour for his comments. Alex Proudfoot National Poisons Information Service (Birmingham Unit), City Hospital, Birmingham, UK

References 1. Chugh SN, Kishore K, Aggarwal N, Attri S. Hypoglycaemia in acute aluminium phosphide poisoning. J Assoc Physicians India 2000; 48:855–856. 2. Arora B, Punia RS, Kalra R, Chugh SN, Arora DR. Histopathological changes in aluminium phosphide poisoning. J Indian Med Assoc 1995; 93:380–381.