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.
CONFLICT OF INTEREST STATEMENT
Au ho ’s con lic o in e es disclosu e: None decla ed.
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Imp o ing Global Ou comes (KDIGO) Acu e Kidney Inju y Wo k
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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.
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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
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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.