Vi amin C equi emen in pa ien s wi h acu e pneumonia du ing ea men wi h an ibio ics
[in Russian]
Mochalkin NI.
V ach Delo. 1975 Sep;(9):88-92. Russian. No abs ac a ailable.
PubMed:
h p s ://www.ncbi.nlm.nih.go /pubmed/1210310
English ansla ion o his pape was a anged by Ha i Hemilä in 2015
[email p o ec ed]
h ps://www.m .helsinki. i/home/hemila
The scanned Russian ex is a he end o his documen .
The ansla ion o his Russian pape was a anged because he ial was included in
he Coch ane e iew (2013) on i amin C and pneumonia:
h ps://doi.o g/10.1002/14651858.CD005532.pub3
h ps://hdl.handle.ne /10138/225862
Me a-analyses ha e indica ed ha i amin C may ha e in luence on pneumonia in ce ain con ex s:
h ps://doi.o g/10.1097/00006454-199709000-00003
h ps://doi.o g/10.7205/MILMED.169.11.920
h ps://doi.o g/10.1177/014107680710001109
h ps://www.ncbi.nlm.nih.go /pmc/a icles/PMC2099400
h ps://doi.o g/10.3390/nu9040339
h p s ://www.ncbi.nlm.nih.go /pmc/a icles/pmc5409678
h ps://www.m .helsinki. i/home/hemila/Vi C_pneumonia.h m
Ce ain analyses on i amin C and pneumonia ha e been shown o be lawed:
h ps://doi.o g/10.1039/d0 o02189j
h ps://doi.o g/10.1038/s41430-022-01091-9
h ps://doi.o g/10.3389/ med.2020.595988
Commen s:
The da a in his pape had been published p e iously in 1970 by Mochalkin.
See compa ison o he da a a he end o his PDF- ile, and see he 1970 pape :
h ps://doi.o g/10.5281/zenodo.7097483
Thus, his pape does no seem o ha e new da a compa ed wi h he 1970 pape .
1
SUMMARY by he au ho , copied om he Russian ex (see h ough he link abo e)
VITAMIN C BALANCE IN PATIENTS WITH ACUTE PNEUMONIA DURING
ANTIBIOTICOTHERAPY
(English i le used by Mochalkin in he summa y o he pape )
SUMMARY
N.I. Mochalkin (Odessa)
Two g oups (se en y each) o pa ien s wi h acu e pneumonia ea ed in a hospi al a e analysed. The
i s ecei ed cou se eamen wi h penicillin, s ep omycin, oxy e acyclin. The second ecei ed he
same an ibio ics in associa ion wi h asco bic acid (AA).
I was ound ha pa ien s o he i s g oups showed a apidly ad ancing educ ion o he
AA con en in he blood plasma and a educed u ina y exc e ion o AA. The AA de ici was
especially p onounced in he e acyclin ea ed pa ien s; in he s ep omycin ea ed pa ien s his
de ici was smalle and in he penicillin ea ed pa ien s s ill smalle .
Resul s indica e ha an ibio ico he apy in combina ion wi h asco bic acid enhanced he
eco e y o pa ien s wi h acu e pneumonia.
2
UDC 616.24-002.1-085.33:612.015.3
VITAMIN C BALANCE IN PATIENTS WITH ACUTE PNEUMONIA DURING
ANTIBIOTICOTHERAPY
D . N.I. Mochalkin (Odessa)
In e es in esea ch in o acu e pneumonias is undiminished wi h many s udies dedica ed o ques ions
o ae iology, pa hogenesis, clinical p og ession, p e en ion and ea men o acu e pneumonias. The
le el o in e es is due o he lack o any educ ion in occu ence o he illness o all segmen s o
he popula ion and o he inc easing endency o he illness o be p o ac ed and p og ess in o a
ch onic o m, leading o pa ien disabili y and equen ly o un imely dea h (L.I. Fogelson, 1963;
A.J. Tsigelnik, 1964; N.S. Molchano , 1964, 1966; S.M. Ga alo , 1968; V.P. Sil es o , 1974).
An ibio ics can educe i amin con en in he body and inhibi he body's immunobiological
esponsi eness, which in u n signi ican ly educes he e icacy o he apy and inc eases he
likelihood ha side e ec s will occu .
This s udy in es iga ed he me abolism o asco bic acid and he clinical indica o s o acu e
pneumonia in 140 pa ien s di ided in o wo g oups, he i s g oup ea ed wi h an ibio ics
exclusi ely and he second g oup ea ed wi h he same an ibio ics in conjunc ion wi h asco bic
acid. All pa ien s we e male, aged 20 o 61.
The pa ien s we e di ided in o wo equal g oups. In he i s g oup (70 pa ien s), pa ien s
we e p esc ibed an ibio ics in a e age he apeu ic doses, bu wi hou asco bic acid (25 we e gi en
penicillin, 15 we e gi en s ep omycin, 15 we e gi en penicillin and s ep omycin, and 15 we e
gi en e acycline).
The second g oup (70 pa ien s) ecei ed he same an ibio ics in he same dosage as he i s
g oup o pa ien s, bu 39 o hem we e addi ionally gi en asco bic acid o ally a a a e o 50 mg pe
100,000 IU o an ibio ics, i.e. a minimum dose o asco bic acid*, and 31 pa ien s ecei ed asco bic
acid a a a e o 100 mg pe 100,000 IU o an ibio ics, i.e. he op imum dose o asco bic acid (N.I.
Mochalkin).
* The minimum and op imum doses o asco bic acid o p e en de iciency o asco bic acid in he body du ing
an ibio ico he apy we e de e mined expe imen ally on animals and es ed unde clinical condi ions.
3
The an ibio ics and he i amins we e p esc ibed du ing he i s en days. The daily dose o
penicillin was 6 million IU, he daily dose o s ep omycin was 0.5–1.0 million IU in amuscula ly,
and he daily dose o e acycline (oxy e acycline) was 0.6 million IU o ally.
E icacy o he apy in bo h g oups was measu ed on he basis o he ime o eco e y,
empe a u e, ESR, whi e blood cell coun in pe iphe al blood, pe iod o he disappea ance o mois
ale, he ime o he pneumonic loci de ec ed by X- ay o dispe se and he du a ion o he apy.
The ini ial le el o asco bic acid was measu ed be o e moni o ing he changes in he
asco bic acid con en in he blood plasma (in mg%) and in he u ina y exc e ion o asco bic acid (in
mg/hou ). An ibio ics we e hen p esc ibed; he concen a ion o asco bic acid was measu ed in he
plasma (using a me hod adap ed om Fa me and Ab ) and in he u ine (using a me hod de eloped
by Zheleznyako a) on days 5, 10, 15, 20 and 30.
The pa ien s we e discha ged om he hospi al only a e all he es s indica ed no mal
le els. Clinical labo a o y es s we e hen pe o med a in e als o a pe iod o one mon h on he
subjec s as ou pa ien s.
The i amin C balance was moni o ed du ing bo h he inpa ien and ou pa ien phases o
obse a ion. Table 1 shows he sa u a ion o asco bic acid in he body du ing he pe iod ha
pa ien s we e obse ed (mean alues in absolu e numbe s, compa a i e alues in %)
As he da a show (Table 1), he balance o asco bic acid in he pa ien s signi ican ly changes
du ing an ibio ico he apy.
Fo example, he asco bic acid con en in he plasma in he i s g oup o pa ien s ell o
57.53% by day 5 and o 56.16% by day 10 o he apy. The mg/hou u ina y exc e ion o asco bic
acid ell co espondingly o 76.47% and 61.76%.
Once pa ien s had ceased o ake an ibio ics and consequen ly he in lamma o y p ocess in
he lungs ceased, he impai ed me abolism o asco bic acid slowly eco e ed. Howe e , i had only
eached 93.15% o he backg ound le el by day 30.
The pic u e was e y di e en o pa ien s in g oup II. Rega dless o signi ican C i amin
in ake, by day 5 he asco bic acid con en in he plasma had allen o 88.73%, a e which he e was
apid compensa ion o he subsequen asco bic acid de iciency, and by day 15 asco bic acid had
eco e ed o ini ial le els. By day 30, he concen a ion o asco bic acid in he plasma had eached
105.6% o he ini ial alue.
The u ina y exc e ion o asco bic acid la gely e lec ed he changes in he blood.
The esul s o he e icacy o he wo me hods o ea ing he acu e pneumonias a e
p esen ed in Table 2 (da a in %).
4
Ou esea ch he e o e indica es ha p esc ibing a cou se o he apeu ic doses o an ibio ics
esul ed in a dec ease in he asco bic acid con en in he blood and educed u ina y exc e ion o
asco bic acid in pa ien s su e ing om acu e pneumonia. I should also be no ed ha pa ien s who
did no ecei e su icien i amins ook signi ican ly longe o eco e in e ms o he clinical
labo a o y indica o s ha we e in es iga ed. An ibio ico he apy in combina ion wi h asco bic acid
enhanced he eco e y o pa ien s wi h acu e pneumonia.
The e a e cu en ly se e al di e en iews ega ding he mechanism o he ad e se e ec o
an ibio ics on i amin me abolism. The e a e sugges ions ha an ibio ics may accele a e he
des uc ion o i amins in o gans and issues o con ibu e o apid exc e ion o i amins om he
body o inc ease he body's need o i amins. I may also be he case ha hypo i aminosis is a
esul o a change in he con en o he gu ha is by an ibio ics. Finally, i is also sugges ed ha
an ibio ics ha e a di ec an i i amin e ec .
The di e ence in he esul s o he apy in his homogeneous g oup o pa ien s, in ou iew,
is explained by he s a e o asco bic acid me abolism in pa ien s wi h acu e pneumonia. Analysis o
ou da a and he li e a u e da a does no lea e any doub ha , in he case o acu e pneumonia, he
in ensi y o edox p ocesses inc eases and he body's need o asco bic acid also inc eases.
Supplemen al asco bic acid con ibu es o an inc ease in he gene al immunobiological
esponsi eness o he body, educing he du a ion o he apy and imp o ing he ou comes o acu e
pneumonias.
The e o e, when ea ing acu e pneumonias wi h an ibio ics (penicillin, s ep omycin, and
oxy e acycline), we would expec o obse e asco bic acid de iciency in he pa ien . Pa ien s
ea ed wi h an ibio ics wi hou supplemen al asco bic acid eco e signi ican ly mo e slowly.
To p e en i amin C de iciency and u he complica ions, an ibio ico he apy o acu e
pneumonias mus be combined wi h simul aneous p esc ip ion o asco bic acid.
A minimum dose would be 1 mg o asco bic acid pe 2000 IU o an ibio ics. An op imal
dose would be 1 mg o asco bic acid pe 1000 IU o an ibio ics.
5
Li e a u e
—Aliso P.A., Veselo skya T.A. and Kuzne so a A.P. VMZ [ВМЖ], 1960, 4, p. 55
—B emene S.M. e al. An ib. [Антиб.], 1964, IX, 7, p. 661
—Vlaso V.K. Klin. med. [Клин. мед.], 1958, 36, 12, p. 72
—G omashe skaya L.L. An ib. [Антиб.], 1960, 3, p. 110
—Zheleznyako a I.S. Gigiena i sani a iya [Гигиена и санитария], 1951, 12, p. 41
—Kachu ina N.A. An ib. [Антиб.], 1964, IX, 5, p. 426
—Molchano N.S., S a skaya V.V. Klinika i lechenie os yh pne monij [Клиника и лечение
острых пневмоний], Lening ad, 1971
—Mosk iche a L.I. Klin. med. [Клин. мед.], 1961, 39, 3, p. 38
—Mochalkin N.I. Doc o al Thesis (in Russian), Lening ad, 1971.
—No iko a V.A. in: Ma e ialy VI nauchn. sessii VNIIV MZ USSR [Материалы VI научн.
сессии ВНИИВ МЗ СССР], 1967, p. 144
—Se gee N.V. in: Os ye pne monii [Острые пневмонии], Moscow 1961, p. 120
6
Table 1
G oup No. o
pa ien s
Asco bic acid con en in blood plasma by days U ina y exc e ion o asco bic acid by days
Ini ial 5 h
day
10 h
day
15 h
day
20 h
day
30 h
day Ini ial 5 h
day
10 h
day
15 h
day
20 h
day
30 h
day
I 70 0.73
100%
0.42
57.53
0.41
56.16
0.57
78.08
0.62
84.93
0.68
93.15
0.68
100%
0.52
76.47
0.42
61.76
0.42
61.76
0.45
66.18
0.65
95.59
II 70 0.71
100%
0.63
88.73
0.67
94.37
0.71
100.0
0.73
102.82
0.75
105.63
0.65
100%
0.61
93.85
0.60
92.31
0.63
96.92
0.64
98.46
0.67
103.8
G oup No. o
pa ien s
T ea men
me hod
Body
empe a u e
no malised by
10 h day
Indica o s no malised by 16 h day o ea men A e age
ea men
du a ion
Mean±SE
(days)
Mois ales
disappea ed
ESR
(e y h ocy e
sedimen a ion
a e)
Leukocy osis Lung x- ay
pa e n
P±mp
I 70 An ibio ics 77,14±5,02 68,57±5,55 58,57±5,89 81,43±4,65 67,14±5,61 23,7±0,38
II 70 An ibio ics
+ asco bic
acid
97,14±1,99 98,57±1,44 97,14±1,44 98,57±1,42 88,57±3,80 17,4±0,66
7
Commen s by Ha i Hemilä in 2015
The ables below compa e he igu es o Table 2 (1975) abo e wi h da a published p e iously by
Mochalkin (1970)
h ps://doi.o g/10.5281/zenodo.7097483
The uppe se o h ee g oups I, II, III a e he da a published by Mochalkin (1970) ea lie .
Those da a we e epo ed as he numbe o pneumonia pa ien s who we e cu ed by 16 h day.
The second se below combines da a o g oups II and III o Mochalkin (1970).
Then he numbe o pa icipan s in g oups I and II+III is ans o med o pe cen ages, which a e
iden ical wi h hose epo ed in Table 2 o Mochalkin (1975), see abo e.
Thus, he Table 2 o Mochalkin (1975) epo s he same da a as Mochalkin (1970), bu g oups II
and III a e combined and epo ed in pe cen ages. In Table 2 abo e, he g oup II is hus he
combina ion o g oups II and III o Mochalkin (1970).
8
The da a o g oups I, II, and III we e epo ed by Mochalkin in 1970
Compa ison II s III is included in Coch ane e iew on i amin C and pneumonia by Hemilä and Louhiala
Du a ion
Tempe a u e No maliza ion by 16 h day o eco e y
G oups No. o no maliza ion We a le ESR Leucocy es Lung (days)
in 1970 pa icip Vi C (g) by 10 h day gone X- ay Mean
I 70 0 54 48 41 57 47 23,7
II 39 0.25-0.8 37 38 36 38 33 19,1
III 31 0.50-1.6 31 31 31 31 29 15,1
G oups
II and III
combined ie 37 + 31 = 68
I 70 0 54 48 41 57 47 23,7
II + III 70 0.25-1.6 68 69 67 69 62 17,33
T ans o ma ion
o in ege s o % o
pa icipan s ie 68/70 = 97.14%
I 70 0 77,14% 68,57% 58,57% 81,43% 67,14%
II + III 70 0.25-1.6 97,14% 98,57% 95,71% 98,57% 88,57%
The igu es ma ked by bold a e iden ical wi h he igu es epo ed by
Mochalkin (1975)
Thus, he 1975 pape epo s abou he same s udy as he 1970 pape
УДК 616.24-002.1-085.33:612.015.3
С-ВИТАМИННАЯ ОБЕСПЕЧЕННОСТЬ БОЛЬНЫХ ОСТРОЙ ПНЕВМОНИЕЙ ПРИ
ЛЕЧЕНИИ АНТИБИОТИКАМИ
Канд. мед. наук Н. И. МОЧАЛКИН (Одесса)
Интерес к изучению острых пневмоний не только не угасает, а наоборот,
вопросам этиологии, патогенеза, клинического течения, профилактики и лечения этого
страдания посвящено большое число исследований, что связано с отсутствием
снижения заболеваемости среди всех слоев населения и с нарастающей тенденцией к
затяжному их течению, а также перехода в хроническую форму, приводящую к ранней
инвалидности больного и нередко к преждевременной смерти (Л. И. Фогельсон, 1963;
А. Я. Цигельник, 1964; Н. С. Молчанов, 1964, 1966; С. М. Гавалов, 1968; В. П.
Сильвестров, 1974).
Применение антибиотиков может привести к снижению содержания витаминов в
организме и к угнетению иммунобиологической реактивности организма, что, в свою
очередь, в значительной степени снижает эффективность лечения и способствует
возникновению побочных реакций.
Нами проведено изучение обмена аскорбиновой кислоты и закономерностей
динамики клинического течения острой пневмонии у 140 больных, леченных только
одними антибиотиками и теми же антибиотиками, но в сочетании с аскорбиновой
кислотой. Все больные — мужчины, в возрасте от 20 лет до 61 года.
Больные были разделены на две равные группы, Первой группе (70 чел.)
назначались антибиотики в средних терапевтических дозах, но без аскорбиновой
кислоты (из них пенициллин получали 25 человек, стрептомицин—15, пенициллин +
стрептомицин—15, тетрациклин —15).
Вторая группа (70 чел.) получала те же ан¬тибиотики и в такой же дозировке, как
и больные первой группы, но 39 человек из них дополнительно получали внутрь
аскорбиновую кислоту из расчета 50 мг на 100 тыс. ЕД. антибиотика —- то есть
минимальную дозу аскорбиновой кислоты * и 31 больной получал аскорбиновую
кислоту из расчета 100 мг на 100 тыс. ЕД. антибиотика — то есть оптимальную дозу
аскорбиновой кислоты (Н. И. Мочалкин).
Антибиотики и витамины назначались в первые десять суток. Суточная доза
пенициллина составляла 6 млн. ME, стрептомицина — 500 тыс.—1 млн. ЕД.
внутримышечно, тетрациклина (окситетрациклина) — 600 тыс. ЕД. внутрь.
В качестве эффективности лечения в обеих группах учитывались в динамике
сроки нормализации, температуры, РОЭ, количество лейкоцитов в периферической
крови, сроки исчезновения влажных хрипов, длительность рассасывания
рентгенологически определяемых пневмонических очагов и срок лечения.
Изучение динамики изменений содержания аскорбиновой кислоты в плазме крови
(в мг%) и выделения ее с мочой (в мг/час) начиналось с определения исходного уровня.
Затем назначались антибиотики; на 5—10—15—20-й и 30-й дни проводилось
определение концентрации аскорбиновой кислоты в плазме (по видоизмененному
методу Фармера и Абта) и моче (по методу Н. С. Железияковой).
• Минимальная и оптимальная дозы аскорбиновой кислоты, предотвращающие развитие ее
дефицита в организме при антибиотикотерашш, выработаны нами экспериментально на животных и
проверены в условиях клиники.
