Clinical Toxicology vol. 47 no. 8 2009

838 Letters to the editor

3. Miller MJ, Gomez HF, Snider RJ, Stephens EL, Czop RM, Warren JS.Detection of loxosceles venom in lesional hair shafts and skin: applica-tion 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. Systemicloxoscelism 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 medicalpersonnel and other authorities in North America. Toxicon 2009;54:545–554.

LCLT1556-36501556-9519Clinical Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0Clinical Toxicology

Author’s response to letter

To the Editor:

We wish to thank the authors for their commentary pointing out areas ofconfusion (and amusement) in our report.1

Unfortunately, the requirement for a minimum number of words to dis-play a picture sometimes results in omitting facts that support the diagnosis.

As the authors note, there has been much discussion about thediagnosis of brown recluse spider bite made in nonendemic areasand even in areas in which the spider is not found at all.2 Tennesseeis in the center of the primary North American area endemic forLoxosceles reclusa. In fact, according to etymologists, homes arefound in Tennessee that are infested with dozens to hundreds of spi-ders at one time.3

We appreciate the authors’ description of typical loxoscelism. Theynote that there is no available diagnostic test. However, we do not agreethat loxoscelism is a diagnosis of exclusion. The approach of “diagnosisby exclusion” requiring a great number of laboratory studies may beappropriate to nonendemic areas. Indeed, in an era of limited resources,we offer that such a cost-intensive approach is wasteful in areas whereclinicians have frequent encounters (and experience) with brownrecluse spider bite. If we test for every possible alternative explanationin disease processes for which there is not an analytic test with 100%specificity, we would be wasteful indeed. The art of medicine oftendemands that we exercise experience and judgment while forsaking theinclination to test, test, test.

In our toxicology clinic, we see three to five patients a week witheither cutaneous or systemic loxoscelism, which is only the tip of aniceberg. Ours is a subspecialty referral clinic, and many, many spiderbites are cared for by primary care physicians because of their familiar-ity with the bite. The diagnosis is made without analytic studies to ruleout viral, bacterial, mycoplasma, or richettsial illness.

The authors report a case of a toddler with a blister, necrotic-targetlesion, erythroderma, fever, GI distress, and hemolysis. Althoughextensive laboratory evaluation was obtained, the child did not returnfor follow-up titers. Because the grandmother subsequently stated that atick had been found in bed, the diagnosis of tick-borne illness wasmade. The diagnosis was not confirmed analytically.

The authors imply that their case is clinically similar to the one thatwe reported and therefore our patient’s rash may have been caused by atick 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. Weagree that other clinical manifestations of tick and brown recluse spiderenvenomation may be similar. Ironically, what was removed from our

report is that the patient found a spider in bed with her. Now we can allbe amused that the diagnosis in both cases was confirmed by the critterallegedly found in bed.

Donna SegerDepartment of Medicine and Emergency Medicine, TN Poison Center,

Vanderbilt University Medical Center, Nashville, TN, USA

Kendra P. ParekhDepartment of Emergency Medicine, TN Poison Center,

Vanderbilt University Medical Center, Nashville, TN, USA

References

1. Parekh K, Seger D. Systemic loxoscelism. Clin Toxicol 2009;47:430–431.

2. Vetter RS. Arachnids misidentified as brown recluse spiders by medicalpersonnel and other authorities in North America. Toxicon 2009;54:545–547.

3. Vetter RS. The distribution of brown recluse spiders in the SoutheasternQuadrant of the US in relation to loxoscelism diagnosis. SMJ 2009;5:518–552.

LCLT1556-36501556-9519Clinical Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0Clinical Toxicology

Comment on Aluminum and zinc phosphide poisoning

To the Editor:

We read with interest the recent review article on aluminum and zincphosphide poisoning.1 As this is a common poisoning in Iran and wehave a significant number of published articles involving poisoningwith these compounds, we have a concern with respect to the review ofthe topic. The author states that hyperglycemia in this poisoning israre, and as such articles discussing glucose changes in these poisoningcases were limited. However, we have published a good number ofpapers that describe hyperglycemia in aluminum and zinc phosphidepoisoning.2–6 Aluminum phosphide poisoning has been postulated tostimulate cortisol, glucagon, and adrenaline secretion or inhibit insulinsynthesis1 that may cause hyperglycemia. In addition, Chugh et al.7

reported findings of 50 cases that showed a significant rise in plasmacortisol (>1048 nmol/L) in 40% of cases. Aluminum phosphide poi-soning has also been reported to be associated with acute pancreatitis andhyperglycemia in some cases,8 suggesting that the effect of aluminumphosphide on the pancreas may have a role in causing hyperglycemia inthis setting.

We would like to bring your attention and the attention of the readersto additional more recent published data regarding the prevalence ofhyperglycemia and its potential as a prognostic factor in aluminumphosphide poisoning4.

Omid MehrpourDepartment of Forensic Medicine and Clinical Toxicology,

Faculty of Medicine, Birjand University of Medical Sciences,Birjand, Islamic Republic of Iran

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: donna.seger@vanderbilt.edu

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: omehrpour@razi.tums.ac.ir

Clin

ical

Tox

icol

ogy

Dow

nloa

ded

from

info

rmah

ealth

care

.com

by

McG

ill U

nive

rsity

on

05/2

4/13

For

pers

onal

use

onl

y.

Clinical Toxicology vol. 47 no. 8 2009

Letters to the editor 839

Dan KeylerDepartment 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 MedicalSciences, Tehran, Islamic Republic of Iran

References

1. Proudfoot AT. Aluminum and zinc phosphide poisoning. J Toxicol ClinToxicol 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: possiblebenefit 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 phos-phide poisoning as a potential prognostic factor. Hum Exp Toxicol2008; 27:591.

5. Shadnia S, Mehrpour O, Abdollahi M. Unintentional poisoning by phos-phine 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 JMed 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 alumi-num phosphide poisoning. Hum Exp Toxicol 2007; 26:979–981.

LCLT1556-36501556-9519Clinical Toxicology, Vol. 1, No. 1, August 2009: pp. 0–0Clinical Toxicology

Author’s response to letter

To the Editor:

I am grateful to Dr. Mehrpour and his colleagues for drawing attentionto hyperglycemia as a complication of acute aluminium phosphidepoisoning. At the time of writing the review, hyperglycemia had notattained, in my estimation at least, the importance it now has as a resultof their work on it as a possible prognostic indicator. Given the volumi-nous literature on this poisoning it was impracticable for the review tocatalog every publication on it. The reason their most recent publica-tions were not included is that the review was submitted to the Journalearly in 2008 and the references were not updated thereafter.

The actions of aluminium phosphide on glucose homeostasis are clearlycomplex and some of the references Dr. Mehrpour’s letter lists (2, 3, and6) were referred to in the review. References 4 and 5 were published afterthe review was completed. It was hoped that quoting the paper by Profes-sor Chugh and his colleagues1 and that of Arora2 would obviate the need toreference too many earlier studies on effects on blood glucose concentra-tions and the pathological changes in the adrenal glands.

I thank Dr. Mehrpour for his comments.

Alex ProudfootNational Poisons Information Service (Birmingham Unit),

City Hospital, Birmingham, UK

References

1. Chugh SN, Kishore K, Aggarwal N, Attri S. Hypoglycaemia in acute alu-minium phosphide poisoning. J Assoc Physicians India 2000; 48:855–856.

2. Arora B, Punia RS, Kalra R, Chugh SN, Arora DR. Histopathologicalchanges in aluminium phosphide poisoning. J Indian Med Assoc 1995;93:380–381.

Clin

ical

Tox

icol

ogy

Dow

nloa

ded

from

info

rmah

ealth

care

.com

by

McG

ill U

nive

rsity

on

05/2

4/13

For

pers

onal

use

onl

y.