Metabolic disorders due to methanol poisoning

Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 1 Me abolic diso de s due o me hanol poisoning Tomas Saleka, Pe Humpolicekb,c, Pe Ponizilb,d Aim. The aim o his s udy is o compa e ma ke s o glome ula il a ion a e (GFR), es ima ed GFR (eGFR), and me a- bolic pa ame e s be ween admission and eco e y in 13 pa ien s o Tomas Ba a hospi al wi h me hanol poisoning du ing me hanol p oblems in he Czech Republic in 2012. The impac o me hanol concen a ion and age on me abolic pa ame e s we e disco e ed a he ime o admission o hospi al. Ma e ials and Me hods. The se um osmolali y, me hanol, e hanol, c ea inine, cys a in C, T oponin I, ALT, plasma pH and lac a e we e measu ed in hese 13 pa ien s. The eGFR om se um c ea inine (c ea nine eGFR) and om cys a in C (cys a in C eGFR) we e also de e mined. Resul s. Inc eased se um osmolali y and ma ke s o me abolic acidosis a e key indi ec labo a o y indings in pa ien s wi h me hanol poisoning. The e we e no signi ican changes in eGFR in ou pa ien s be ween admission and eco e y. Inc eased se um oponin I concen a ion was con i med as an indica o o myoca dial nec osis in ou pa ien s. Two pa ien s de eloped acu e kidney inju y (AKI) be o e admission. Conclusions. We ound s a is ically signi ican di e ences in se um osmolali y concen a ion, plasma pH and lac a e be ween admission and eco e y. We ound no changes in eGFR be ween admission and eco e y. One pa ien had ision p oblems due o damage o he occipi al lobes. Me hanol poisoning may cause inc ease in ma ke s o ca diac damage. Key wo ds: in oxica ion, osmolali y, me abolic acidosis, c ea inine, cys a in C Recei ed: May 10, 2013; Accep ed wi h e ision: Sep embe 19, 2013; A ailable online: Sep embe 27, 2013 h p://dx.doi.o g/10.5507/bp.2013.074 aDepa men o Clinical Biochemis y, Tomas Ba a Regional Hospi al in Zlin a.s., Zlin, Czech Republic bCen e o Polyme Sys ems, Polyme Cen e, Tomas Ba a Uni e si y in Zlín, Zlin cPolyme Cen e, Facul y o Technology, Tomas Ba a Uni e si y in Zlin, Zlin dDepa men o Physics and Ma e ials Enginee ing, Facul y o Technology, Tomas Ba a Uni e si y in Zlin, Zlin Co esponding au ho : Tomas Salek , e-mail: [email p o ec ed] INTRODUCTION Me hanol poisoning is a se ious medical, social and economical p oblem. Mass me hanol poisonings a e a e bu occu bo h in de eloped and de eloping coun ies1. Acciden al cases o me hanol poisoning a e epo ed2. Suicide a emp s using pu e me hanol a e also p esen ed in he li e a u e3. Almos all cases o acu e me hanol oxic- i y esul om acciden al inges ion4. Me hanol has ela- i ely low oxici y and i s me abolism is esponsible o he ans o ma ion o me hanol o i s oxic me aboli es, especially o mic acid5. An in e es ing ac is ha oxic and le hal doses o me hanol ha e no hi he o been de e - mined unequi ocally. 15 mL o 40% me hanol ha e caused dea h in some indi iduals, whe eas o he s ha e su i ed consuming as much as 500 mL o such solu ion. These di e ences a e p obably caused by he simul aneous e ha- nol consump ion, di e en ola e con en in he die o he ac i i y o me hanol me abolism sys ems6. Howe e , he minimal le hal dose o me hanol in humans has been assumed o be 1 g pe kg body weigh (b.w.) in pe sons no ha ing simul aneously consumed e hanol7. Typical ea u es o me hanol in oxica ions include me abolic acidosis, hype osmolali y, inc eased osmola gap, e inal damage wi h blindness, damage o pu amen and cauda e wi h neu ologic dys unc ion. Me abolic aci- dosis is caused by o mic acid, lac ic acid, and ke ones. Me hanol is oxidized by alcohol dehyd ogenase o o m- aldehyde, which is hen me abolized by o maldehyde dehyd ogenase o o mic acid. Fo ma e acid is an inhibi- o o mi ochond ial cy och ome c oxidase which causes his o oxic hypoxia8. This leads o educed adenosine iphospha e (ATP) p oduc ion. Neu o oxic e ec s o o mic acid o neu ons and glial cells was also demon- s a ed in neu al cul u es9. The op ic ne e is especially sensi i e o educed ATP p oduc ion. This is due o i s neu ons’ ha ing long axons and e y small diame e 10. B ain changes can be demons a ed by compu ed omog- aphy and magne ic esonance imaging11. Fo ma e is also oxic o e inal cells12. The e is a high le el o ee adical p oduc ion du ing acu e o mic acid poisoning in animal models13. Fo ma e is mainly esponsible o me abolic acidosis14. Di e en ial diagnosis o alcohol d inke s wi h high le els o se um osmolali y, inc eased osmola gap and me abolic acidosis also include isop opyl alcohol in- oxica ion15. De ini i e diagnosis o me hanol inges ion equi es de e mina ion o me hanol by gold s anda d es which is gas ch oma og aphy16. Acid base balance is e- quen ly discussed in pa ien s wi h me hanol in oxica ion. Ma ke s o GFR and ca diac damage a e no discussed in he li e a u e in such clinical si ua ions. Fo his eason we e alua ed hese ma ke s in his clinical se ing. Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 2 MATERIAL AND METHODS The s udy included 13 pa ien s wi h me hanol poi- soning a he Tomas Ba a hospi al in Zlin. The e we e 7 males and 6 emales. The age o pa ien s anged om 28 o 79 yea s, mean 53 yea s. All pa ien s su i ed. Two pa ien s wi h he lowes me hanol concen a ion we e ea ed only wi h e hanol. Ten pa ien s we e ea ed wi h bo h hemodialysis and e hanol. One pa ien o his com- bina ion ea men g oup also had omepizol. The onse o dialysis ea men anged om 15 min o 6 h a e admission. Se um osmolali y was measu ed by eezing poin dep ession. Se um me hanol was measu ed by gas ch oma og aphy. O he se um ma ke s we e measu ed by au oma ed Abbo A chi ec analyze . Se um e hanol was de e mined by enzyma ic pho ome y. Se um c ea inine was measu ed by a s anda dized pho ome ic enzyma ic me hod aceable o NIST SRM 967 e e ence ma e i- al17. C ea inine eGFR was es ima ed by he Lund Malmö equa ion18. Cys a in C was de e mined by a s anda dized immuno u bidime ic echnique aceable o ERM DA 471/IFCC e e ence ma e ial19. Cyss a in C eGFR was calcula ed by equa ion alida ed o his me hod and analyse . Se um oponin I concen a ion was pe o med using immunochemiluminiscen echnique. Se um alanin amino ans e ase was de e mined by enzyma ic me hod wi h py idoxal phospha e ac i a ion. Plasma pH was de- e mined by an elec ochemical me hod on a Radiome e acid-base analyze . We compa ed bo h c ea inine eGFR and cys a in C eGFR in 13 me hanol poisonings a admis- sion and a e eco e y. We also compa ed osmolali y, pH, ALT and lac a e be ween admission and eco e y. We looked a se um oponin I concen a ion which is a ma ke o ca diomyocy e nec osis. We used Risk, Inju y, Failu e, Loss, End-S age Renal Disease (RIFLE) c i e ia o he diagnosis o acu e kidney inju y20. U ine ou pu was measu ed o e ml/kg/hou in wel e pa ien s. The clinical and labo a o y s a us o one pa ien was so good ha u ine olume was no e alua ed. The s udy was ca - ied ou acco ding o he la es Decla a ion o Helsinki. I was app o ed by he E hic Commi ee o Tomas Ba a Hospi al. We we e allowed o collec and anonymously epo he e ospec i e da a o pa ien s. S a is ical e alua ion Impac o me hanol in oxica ion on me abolic ma k- e s was s udied. These ma ke s we e ollowed: osmolali y, Lac a e and pH. To disco e he ela ionship be ween he le el o me hanol in oxica ion and hese ma ke s h ee s a is ical es s we e used, pai ed - es s o di e ences be ween he le els o indi idual ma ke s a he beginning and a he end o hospi aliza ion, co ela ions be ween indi idual ma ke s, age o pa ien s and me hanol le el (mmol/L) and linea eg ession wi h age and me hanol le el as ixed ac o s. RESULTS Key esul s o each pa ien a e summa ized in Table 1. We ound s a is ically signi ican di e ences in se um osmolali y concen a ion, plasma pH and lac a e be ween admission and eco e y. The esul s o pai ed wo-sample S uden 's - es a e shown in Table 2. A signi ican shi in osmola i y, lac a e and pH le el was ound. The di e - ences be ween he le el o osmolali y, pH and lac a e a he beginning and a he end o he apy we e signi ican a he P≤0.01; P≤0.01 and P≤0.05, espec i ely. Table 1. Sex, age, me hanol concen a ion and all s udie ma ke s a admission and discha ge o each pa ien . Sex Age Me hanol (mmol/L) Cys a in C (mg/L) C ea inine (µmol/L) Osmolali y (mmol/kg) Lac a e (mmol/L) pH U ine ou pu (mL/kg/h (1s day)) Dialysis adm. dis. adm. dis. adm. dis. adm. dis. adm. dis. M 69 5 0.95 0.98 68 72 294 288 7.39 7.42 2.27 No F 58 76 0.77 0.90 71 58 390 281 - - 7.11 7.47 1.72 YES F 63 55 1.12 0.92 79 56 373 288 0.9 1.4 7.09 7.41 4.67 YES M 42 12 0.66 0.63 73 75 303 - 1.5 7.30 7.40 1.56 YES F 35 33 1.27 1.25 77 55 348 290 8.3 7.08 7.42 0.57 YES M 48 62 1.68 0.62 167 44 374 280 7.6 6.82 7.50 2.76 YES M 79 10 1.55 0.94 80 61 310 282 4.4 0.9 7.33 7.49 2.3 YES F 58 38 0.80 0.72 84 58 378 286 5.1 1.8 7.09 7.46 5 YES M 42 63 0.70 0.70 68 80 409 - 1.4 -7.41 7.41 1.43 YES F 62 30 1.01 0.90 76 60 311 291 2.0 1.0 7.18 7.45 4.05 YES M 58 61 1.63 1.19 124 74 383 287 12.8 1.7 6.76 7.51 1.25 YES F 52 138 0.92 0.86 44 45 463 284 1.5 1.4 7.22 7.45 4.38 YES M 28 12 0.79 0.79 73 86 300 283 0.9 1.0 7.33 7.36 - No Mean ±SD 53.38 ±14.15 45.76 ±36.50 1.06 ±0.35 0.88 ±0.19 83.38 ±30.50 63.38 ±12.98 356.61 ±51.01 285.45 ±3.70 4.21 ±3.90 1.31 ±0.36 7.16 ±0.20 7.44 ±0.04 2.66 ±1.50 adm. is he ma ke le el a he admission ime; dis. is he ma ke le el a he eco e y ime = discha ge. Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 3 ha he inc ease in me hanol le el by 10 mmol/L will inc ease he osmolali y abou 13.0 ± 1.4 mmol/L. We ound inc eased oponin I abo e 99 h pe cen ile o heal hy popula ion in ou pa ien s (male 58 yea s old, emales 58, 35 and 58 yea s old). None o he pa ien s had clinical ea u es o acu e co ona y synd ome and elc- oca diog aphy showed no ischemic changes. The e was no di e ence in ei he c ea inine eGFR o cys a in C eGFR be ween admission and eco e y. Two pa ien s had AKI acco ding o RIFLE c i e ia. They me GFR c i e ia bu no u ine olume c i e ia (u ine ou pu below 0.5 mL/kg/h du ing hospi al s ay). AKI de eloped be o e admission o he hospi al. C ea inine and cys a in C dec eased and GFR inc eased in hese wo pa ien s du ing ea men . One pa ien - a 48 yea s old man - had ision p ob- lems. Magne ic esonance imaging o b ain e ealed ce- eb al whi e ma e swellings (semio al cen e ). Mos o he impai men s impac ed he co ona adia a cen e in he subco ical occipi al egions. The e was also haemo - hagicnec osis o basal ganglia, especially pu amen and he globus pallidus. DISCUSSION We compa ed me abolic pa ame e s and ma ke s o GFR be ween admission and discha ge. We ound in- c eased se um osmola i y and me abolic acidosis in he majo i y o pa ien s. I has been epea edly epo ed, ha se um osmolali y inc eases wi h me hanol poisoning21 and ha me hanol in oxica ion causes high anion gap me a- bolic acidosis22. The acidosis seen in ea ly clinical cou se is caused di ec ly by o mic acid p oduc ion. Lac a e is p oduced la e as o mic acid in e e es wi h in acellula espi a ion and p omo es anae obic me abolism5. These indings a e seen in common clinical p ac ice. Di e en ial diagnosis o alcohol in oxica ion includes e hanol, e hyl- englycol and isop opyl alcohol in oxica ion15. Table 2. A e age di e ences in ma ke le els a he beginning and a he end o he apy. Cys a in C (mg/L) C ea inine (µmol/L) Osmolali y (mmol/kg) Lac a e (mmol/L) pH ALT eGFR Cys a in C eGFR C ea inine 0.18 ± 0.09 20.00 ±9.88 71.27 ±15.56** 3.24 ±1.20* -0.28 ±0.06** 0.77 ±0.71 -0.26 ±0.14 -0.23 ± 0.13 (A e age change ± s anda d e o o he mean). The s a is ical di e ences by pai ed - es ( alue). ALT is alanine amino ans e ase; eGFR is es ima ed glome ula il a ion a e. * P≤0.05, ** P≤0.01. Table 3. Co ela ion be ween he indi idual ma ke s and age o me hanol le el. Osmolali y (mmol/kg) Lac a e (mmol/L) pH age -0.43 -0.35 0.06 me 0.95** 0.01 -0.27 age is he Pea son co ela ion coe icien be ween age and ma ke me is he Pea son co ela ion coe icien be ween me hanol le el and ma ke . ** P≤0.01 by es ing o he signi icance o he co ela ion coe icien . Table 4. Mul iple co ela ion be ween he indi idual ma ke s and combina ion o age wi h me hanol. Osmolali y (mmol/kg) Lac a e (mmol/L) pH me /age 0.97** 0.36 0.27 me /age is he mul iple co ela ion coe icien be ween age an me ha- nol le el as independen a iables and ma ke as dependen a iable. **P≤0.01 by es ing o he signi icance o he mup iple co ela ion coe icien . Table 5. Pa ial co ela ion be ween he indi idual ma ke s and age o me hanol wi h emo ed e ec o second a iable. Osmolali y Lac a e pH Rpa cage -0.622 -0.361 -0.010 Rpa cme 0.964* -0.083 -0.267 Rpa cage is pa ial co ela ion be ween ma ke and age (e ec o me hanol le el is emo ed). Rpa cme is pa ial co ela ion be ween ma ke and me hanol le el (e ec o age is emo ed). * P≤0.05 by es ing o he signi icance o he pa ial co ela ion coe icien . The signi ican e ec on he osmolali y was subse- quen ly con i med by he co ela ion be ween osmolali y and me hanol le el (Table 3, P≤0.01). The co ela ion be ween osmolali y and me hanol le el was con i med by he mul iple co ela ion (Table 4). The co ela ion coe icien be ween osmolali y and age me hanol was 0.97 which, compa ed o he co ela- ion o me hanol only (Table 2; 0.95), showed a nonsig- ni ican inc ease. The small impac o age was con i med by pa ial co ela ion coe icien (Table 5) which con- i med he ela ions be ween he osmolali y and me ha- nol (P≤0.01; =0.96) bu no be ween age and me hanol. Mo eo e , based on he linea eg ession we can s a e Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 4 We ound no s a is ically signi ican changes in eGFR. The small numbe o pa ien s may also con ibu e o his esul . Fu he , we a e no able o accu a ely de e mine small GFR changes in pa ien s on dialysis ea men . Two pa ien s ull illed he GFR c i e ia o AKI. We a e unable o conclude ha me hanol in oxica ion caused his s a e. Dehyd a ion could also ha e played a pa in he de elop- men o AKI. Neph o oxic d ugs, sepsis and mul io gan dys unc ion p obably did no cause AKI in ou pa ien s. Acu e enal ailu e de eloped in some s udies in pa ien s wi h me hanol poisoning23. The limi a ion o ou s udy is ha we did no measu e me hanol and o mic acid in u ine. This could be use ul o be e unde s and he kine - ics o me hanol and o ma e elimina ion24. Fo ma e is especially oxic o ne e cells and he op- ic ne e. These cells need la ge amoun s o ene gy. The inhibi ion o cy och ome c oxidase leads o low le els o ATP and cell dys unc ion. The g ea sensi i i y o he op ic ne e o o ma e is well clinically documen ed in la ge epidemic p oblems in Cuba and in animal models10. Ou pa ien s we e assessed by an oph halmologis . One pa ien had ision p oblems. Magne ic esonance imag- ing o he b ain e ealed ce eb al whi e ma e swellings (semio al cen e ). Mos o he impai men s impac ed he co ona adia a cen e in he subco ical occipi al egions. The e was also he hemo agic nec osis o he basal gan- glia, especially he pu amen and globus pallidus. Simila indings ha e been desc ibed in he li e a u e11. Today, ca diac oponins a e he gold s anda d o he diagnosis o myoca dial nec osis25. We ound no ca diac oponins in pa ien s wi h me hanol poisoning in he da abase o PubMed. Fou o ou pa ien s had ele a ed se um le els o oponin I. In summa y, ou esul s con i m well-known da a on acid base and osmola i y diso de s in pa ien s wi h me ha- nol poisoning. One new inding was ele a ion o oponin I in some pa ien s. The majo limi a ion o ou s udy is he small numbe o pa ien s and he ac ha we do no measu e se um o u ine o mic acid. CONCLUSIONS We ound s a is ically signi ican di e ences in se um osmolali y concen a ion, plasma pH and lac a e be ween admission and eco e y. We ound no changes in eGFR be ween admission and eco e y. We ound inc eased se um oponin I concen a ion as an indica o o myo- ca dial nec osis in ou pa ien s. One pa ien had ision p oblems due o damage o occipi al lobes. This should be aken in o accoun in ea ing hese pa ien s. 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Clinical Chemis y and Labo a o y Medicine: CCLM/FESCC 2010;48:1619-21. doi:10.1515/CCLM.2010.318 20. Eknoyan G, Lamei e N, Ecka d KU, Kasiske BL, Kidney Disease: Imp o ing Global Ou comes (KDIGO) Acu e Kidney Inju y Wo k Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 5 G oup. KDIGO Clinical P ac ice Guideline o Acu e Kidney Inju y. Kidney in e na ional Supplemen s 2012;2:1-138. 21. Mea he all R, K ahn J. Excess Se um Osmolali y Gap a e Inges ion o Me hanol. Clinical Chemis y 1990;36:2004-7. 22. Lim S. Me abolic Acidosis. Ac a Medica Indonesiana 2007;39:145-50. 23. Ve hels D, Moulin P, Hau oid V, Wi ebole X, Jadoul M, Han son P. Acu e Renal Inju y Following Me hanol Poisoning: Analysis o a Case Se ies. In e na ional Jou nal o Toxicology 2004;23:267-73. doi:10.1080/10915810490506795 24. Ho da KE, Mundal H, U dal P, McMa in K, Jacobsen D. Ex emely Slow Fo ma e Elimina ion in Se e e Me hanol Poisoning: a Fa al Case Repo . Clinical Toxicology (Philadelphia, Pa.), 2007;45:516-21. doi:10.1080/15563650701354150 25. Thygesen K, Alpe JS, Ja e AS, Simoons ML, Chai man BR, Whi e HD. Join ESC/ACCF/AHA/WHF Task Fo ce o he Uni e sal De ini ion o Myoca dial. Thi d Uni e sal De ini ion o Myoca dial In a c ion. Eu opean Hea Jou nal 2012;33:2551-67. doi:10.1093/eu hea j/ ehs184 LETTER TO THE EDITOR: METABOLIC DISORDERS DUE TO METHANOL INTOXICATION Hossein Sanaei-Zadeh Co espondence: D Hossein Sanaei-Zadeh, Medical School, Shi az Uni e si y o Medical Sciences, Eme gency Room/Di ision o Medical Toxicology, Haz a Ali-Asgha (p) Hospi al, Meshkin am S ee , 7143918796 Shi az, I an, e-mail: h-sanaiezadeh@ ums.ac.i Dea Edi o , I ead wi h in e es he s udy pe o med by Salek e al. ecen ly published on-line in you jou nal1. In e es ingly, he au ho s ha e been ying o e alua e changes in some me abolic pa ame e s in me hanol-poisoned pa ien s ha ha e been comple ely ob ious om he e y i s begin- ning. In o he wo ds, hey compa ed se um osmolali y concen a ions, plasma pH, and lac a e be ween admis- sion and eco e y o 13 me hanol-poisoned pa ien s and ound s a is ically signi ican di e ences in his compa i- son. Howe e , he eason o his compa ison was no discussed in he a icle. I is well known ha me hanol is ini ially me abolized o o maldehyde and hen o o mic acid2. Fo mic acid causes a me abolic acidosis and di- ec ly inhibi s mi ochond ial cy och ome oxidase leading o cellula hypoxia and inc ease in he lac a e concen a- ions, u he exace ba ing he acidosis3. Apa om his, I had some conce ns ega ding he managemen o hei pa- ien s and he in luences o he ea men on he s udied pa ame e s, as well. Excep desc ip ion abou one pa ien who had p esen ed wi h ision p oblem, he au ho s did no men ion any hing abou hei pa ien s’ symp oms and signs, hyd a ion o hei pa ien s, and adminis a ion o sodium bica bona e o hem. They managed wo pa ien s only wi h e hanol because hey had he lowes me hanol concen a ion in hei se ies. I should be poin ed ou ha he managemen p io i ies in me hanol poisoning depend upon he ci cums ance o p esen a ion and no me hanol concen a ion, pe se. Fo ins ance, i he pa ien s ha e any o he pH<7.25-7.30, isual sign and symp oms, enal ailu e, signi ican elec oly e dis u bances un esponsi e o con en ional he apy, se um me hanol concen a ion abo e 50 mg/dL, o de e io a ion in i al signs despi e in ensi e suppo i e ca e, hemodialysis should be pe - o med2. Fu he mo e, i is no clea why one o he pa ien s was concomi an ly ea ed wi h e hanol, omepi- zole, and hemodialysis. O no e, omepizole is ecom- mended as a i s -line ea men o me hanol-poisoned pa ien s who p esen wi hou oph halmologic impai men o se e e acidosis2,4. In his case, omepizole may ob ia e he need o hemodialysis2,4. Also, bo h omepizole and e hanol al e he me abolism o each o he . The e o e, co-adminis a ion o e hanol and omepizole has no been ecommended2. The au ho s showed ha he e we e no signi ican changes in es ima ed glome ula il a ion a e (eGFR) be ween admission and eco e y in hei pa ien s. Did hey pay a en ion o he in luence o hyd a ion o he pa ien s (i any) a hospi al admission on hei eGFR ha migh happen be o e aking blood samples? I so, was hei sample size (only 13 pa ien s) s a is ically su icien o eaching such a conclusion? I wonde i hey conside ed he e ec s o hemodialysis and he adminis a ion o e hanol and sodium bica bona e on pH, se um osmolali y, o co ela ion be ween osmo- lali y and me hanol le el. In Table 1, I no ed ha he e we e missing da a abou osmolali y concen a ions and lac a e le els a he eco e y ime o wo and six pa ien s, espec i ely. Could hese missing da a in e e e wi h he accu a e s a is ical analysis and calcula ion o he pa ial co ela ion coe icien be ween osmolali y and me hanol le el, and lac a e and me hanol le el? Mo eo e , i is no clea wha logic ela ionship exis s be ween me hanol poisoning and se um alanine amino- ans e ase o which he au ho s ha e compa ed his pa- ame e be ween admission and eco e y o he pa ien s. In addi ion, ou pa ien s had inc eased oponin I abo e 99 h pe cen ile o heal hy popula ion. I should be men ioned ha hese pa ien s had no clinical ea u es o acu e co ona y synd ome and hei elec oca diog aphs we e no mal. Does i eally show ca diac damage in hese pa ien s? Finally, he au ho s had wo pa ien s wi h acu e kidney inju y (AKI) ha was de eloped be o e admission o he hospi al and hey could no ind any explana ion o ha excep dehyd a ion. Could myoglobinu ia ha e a ole in he de elopmen o AKI in hei pa ien s2? REFERENCES 1. Salek T, Humpolicek P, Ponizil P. Me abolic diso de s due o me hanol poisoning. Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub 2013 Sep 27. doi:10.5507/bp.2013.074. 2. Ba celoux DG, Bond GR, K enzelok EP, Coope H, Vale JA; Ame ican Academy o Clinical Toxicology Ad Hoc Commi ee on he T ea men Guidelines o Me hanol Poisoning. Ame ican Academy o Clinical Toxicology p ac ice guidelines on he ea men o me hanol poi- soning. J Toxicol Clin Toxicol 2002;40:415-46. Biomed Pap Med Fac Uni Palacky Olomouc Czech Repub. 2013; 157:XX. 6 3. Jacobsen D, McMa in KE. Me hanol and e hylene glycol poisonings. Mechanism o oxici y, clinical cou se, diagnosis and ea men . Med Toxicol 1986;1:309-34. 4. The College o Eme gency Medicine. CME An ido e Guidelines 2008. Accessed 25 June 2012. h p://www.colleme gencymed.ac.uk/Shop- Floo /Clinical%20Guidelines/Clinical%20Guidelines/de aul .asp (ac- cessed May 2013). REPLY TO THE LETTER TO EDITOR Tomas Saleka, Pe Humpolicekb,c, Pe Ponizilb,d aDepa men o Clinical Biochemis y, Tomas Ba a Regional Hospi al in Zlin a.s., Zlin, Czech Republic bCen e o Polyme Sys ems, Polyme Cen e, Tomas Ba a Uni e si y in Zlín, Zlin cPolyme Cen e, Facul y o Technology, Tomas Ba a Uni e si y in Zlin, Zlin dDepa men o Physics and Ma e ials Enginee ing, Facul y o Technology, Tomas Ba a Uni e si y in Zlin, Zlin Co esponding au ho : Tomas Salek , e-mail: [email p o ec ed] Dea P o esso Sanaei-Zadeh, Thank you o you le e o commen on he a icle “Me abolic diso de s due o me hanol in oxica ion”. I is di icul o ollow he logic o he i s pa o you commen s. Changes ob ious om he ou se , has no meaning. The au ho s men ioned high le els o se um osmola i y and me abolic acidosis on page 1 along wi h easons o measu ing GFR and ma ke s o ca diac dam- age. Na u ally, ea men esul ed in imp o ed acid base dysbalance. The au ho s ha e also p o ided addi ional de- ails o answe you ques ions as ollows: all pa ien s we e examined physically. This included hyd a ion/dehyd a ion assessmen and all pa ien s wi h a pH unde 7.1 ecei ed Sodium Bica bona e. Two only had clinical signs o de- hyd a ion bu no AKI acco ding o RIFLE c i e ia. Fou pa ien s we e unconscious. This p esen ed p oblems o us. Some o hese had omi ing while he o he s we e ad- mi ed on suspicion o alcohol in oxica ion. All had oph- halmological and neu ological examina ion.T ea men wi h e hanol was ollowed by omepizol in one pa ien . T ea men was closely moni o ed and end o he apy was de e mined acco ding o se um me hanol concen a ion. Missing da a in Table 1: The e we e a la ge numbe o blood samples be ween he i s and las sampling o each pa ien . Some pa ien s had physiological esul s a ew hou s a e ea men . Fo his eason, he physician did no o de all he es s a he end o he hospi al s ay. Rela ion be ween me hanol poisoning and ALT. Nea ly all d ugs and oxins can inc ease li e es esul s like ALT. T oponin. Ca diac oponin I and T a e ca dio speci ic. They a e no eleased om any o he o gan. The e we e 2 pa ien s wi h acu e kidney inju y. These had no clinical signs o dehyd a ion. Myoglobinu ia as a cause o AKI. The i s pa ien wi h AKI had an alanineamino ans e - ase (AST) le el o 0:51 uka /L and nega i e u ine s ip es o blood. Clinically signi ican myoglobinu ia was unlikely. You a e igh , a sample size o 13 is e y small o s a is ical conclusions. Un o una ely, me hanol poison- ing canno be c ea ed o sa is y medical publica ions. We hope ha some o you ques ions ha e been answe ed.