Abnormal glucose metabolism in men with alcohol withdrawal

Transkrypt

Abnormal glucose metabolism in men with alcohol withdrawal
PRACE ORYGINALNE
Dorota Pach1
Monika Radomska2
Barbara Groszek2
Piotr Hydzik3
Aleksandra Gilis-Januszewska1
Janusz Pach4
Abnormal glucose metabolism in men with
alcohol withdrawal syndrome
Department of Endocrinology, Jagiellonian
University Medical College, Kraków, Poland
Head:
Prof. Alicja Hubalewwska-Dydejczyk, MD, PhD
The aim of the study was to evaluate the glucose metabolism in patients
suffering from ethanol withdrawal syndrome. The study group comprised 88
alcohol dependent men aged 21- 50 y
(mean 39.18 years, SD ±7.78), treated at
the Clinical Toxicology Ward. Alcohol
dependence was diagnosed according to the criteria of the International
Statistical Classification of Diseases
and Related Human Problems (ICD-10).
The degree of alcohol withdrawal syndrome was assessed according to the
scale CIWA-Ar. The blood ethanol concentration, and glucose serum concentration were measured on admission.
On the next post-admission day blood
glucose were determined after fasting
and at the 0, 60th and 120th minute of
an oral glucose tolerance test (OGTT)
using 75 g glucose. Basing on the
recommendations of Polish Diabetes
Association (2013y) the patients were
classified into one of groups according
to their glucose tolerance test results.
Results: Mean duration of alcohol
dependence was 10.56 years ± 7.78. A
mean CIWA-Ar scale score was 23.95
points ± 2.81. Mean BMI was 24.65
±3.74, overweight and obesity were
determined in 35.22% examined men.
Normal glucose tolerance were found
in 54.55%, abnormal fasting glucose
and/or abnormal glucose tolerance
were noted in 23.87%, diabetes in
10.23%, and hypoglycemia in 11.36%
of examined patients. Intensity of
withdrawal syndrome according to the
CIWA- Ar (OR - 1.59, p= 0.05) and duration of alcohol consumption (OR - 1.01,
p=0.03) were the risk factors of diabetes type 2 in examined group. Greater
BMI was a protective factor against
diabetes type 2 in the study group.
There was no significant correlation
between risk of hypoglycemia and age,
BMI, duration of alcohol consumption,
alcohol blood concentration on admission, intensity of withdrawal syndrome
according to the CIWA- Ar scale. A
higher frequency of hypoglycemia was
found in patients who declared vodka
drinking in interview (at the borderline
of statistical significance OR - 7.43,
p=0.06). Conclusions: 1. In the study
group of alcohol-dependent men, the
1
Clinical Toxicology and Internal Diseases
Ward
Rydygier Hospital, Kraków, Poland
Head:
Barbara Groszek, MD, PhD
2
Department of Toxicology, Jagiellonian
University Medical College, Kraków, Poland
Head:
Piotr Hydzik MD, PhD
3
Former Head of the Department of Toxicology,
Jagiellonian University Medical College,
Kraków, Poland and Head of the Clinical
Toxicology and Internal Diseases Ward,
Rydygier Hospital, Kraków, Poland
Institute of Health, State Higher Vocational
School in Nowy Sacz
Director:
Ryszard Gajdosz Md, PhD
4
Additional key words:
ethanol
withdrawal syndrome
glucose metabolism
Dodatkowe słowa kluczowe:
alkohol
zespół odstawienia
metabolizm glukozy
Adres do korespondencji:
Prof. Dorota Pach MD, PhD
Department of Endocrinology
Jagiellonian University Medical College
Kopernika 17, Krakow 31-501, Poland
Tel. 48 12 424 75 21
Fax. 48 12 424 73 99
e-mail: [email protected]
Przegląd Lekarski 2014 / 71 / 9
Zaburzenia gospodarki węglowodanowej u osób
z zespołem odstawiennym od alkoholu
Celem pracy była ocena gospodarki węglowodanowej u 88 mężczyzn
uzależnionych od alkoholu leczonych
z powodu zespołu abstynencyjnego
w Oddziale Toksykologii. Średni wiek
badanych wynosił 39,18 (SD ± 7,78) lat.
Rozpoznanie uzależnienia ustalono
na podstawie oceny psychologicznopsychiatrycznej, wg Międzynarodowej
Klasyfikacji Chorób i Problemów
Zdrowotnych, a stopień nasilenia
objawów zespołu odstawiennego wg
skali CIWA-Ar. W momencie przyjęcia
oznaczono stężenie etanolu we krwi
oraz stężenie glukozy w surowicy krwi.
Ponowne oznaczenie stężenia glukozy
we krwi przeprowadzano w następnej
dobie, na czczo. U osób, u których nie
rozpoznawano wcześniej cukrzycy,
po wytrzeźwieniu (stężenie etanolu
0,0 g/l), przeprowadzono oznaczenie
stężenia glukozy w 0, 60 i 120 minucie
doustnego testu obciążenia 75 g
glukozy (DTOG). Pacjentów zakwalifikowano do grup tolerancji glukozy
według wytycznych PTD 2013 Wyniki:
Średni czas uzależnienia od alkoholu w
badanie grupie wyniósł 10,56 lat ±7,78.
Nasilenie objawów odstawiennych wg
skali CIWA-A wynosiło 23,95 pkt ± 2,81.
Średnia wartość BMI wynosiła 24,65
± 3,74, nadwagę i otyłość stwierdzono u 35,22% badanych. Prawidłową
tolerancję glukozy stwierdzono u
54,55% badanych, zaburzenia tolerancji
glukozy obejmujące nieprawidłową
glikemię na czczo i/lub nietolerancję
glukozy rozpoznano u 23,87% badanych, cukrzycę u 10,23%, hipoglikemię u
11,36%. W badanej grupie czynnikiem
ryzyka wystąpienia cukrzycy typu 2
było nasilenie objawów odstawiennych według skali CIWA-A (OR =
1,59, p = 0,05), długość trwania ciągu
alkoholowego (OR = 1,01, p = 0,03).
Wielkość wskaźnika BMI w badanej
grupie ma działanie protekcyjne w
wystąpieniu cukrzycy (OR = 0,49,
p = 0,02). Nie wykazano w badanej
grupie istotnego statystycznie związku
pomiędzy ryzykiem wystąpienia hipoglikemii względem: wieku, wskaźnika
BMI, długości ciągu alkoholowego,
stężenia etanolu we krwi w chwili
przyjęcia, nasilenia objawów odstawiennych określonych wg skali CIWA-A.
469
risk of diabetes was inversely proportional to BMI value. 2.
The risk factors of type 2 diabetes in the alcohol-dependent
group included the duration of lasting alcohol drinking and
the intensity of withdrawal symptoms according to the
CIWA- Ar scale. 3. According to the preference of alcohol
type, a higher frequency of hypoglycemia was confirmed
only in persons preferring to drink vodka.
Introduction
The U shaped relationship between
daily ethanol consumption and the risk of
abnormal glucose metabolism and type 2
diabetes is described. The risk of abnormal
fasting blood glucose concentration and
type 2 diabetes in severe drinkers has
been reported in some study [1-3]. In the
others the influence of ethanol on glucose
metabolism was not observed [4-6]. A many
biologically active factors (adipokines) are
secreted by the adipose tissue. Some of
them: TNFα, IL-6, MCP-1 and adiponectin
play an important role in regulation of insulin
sensitivity caused by ethanol abuse. RBP4
(Retinol binding protein 4) is considered
to link insulin resistance with obesity and
type 2 diabetes but not with metabolic
syndrome of ethanol etiology. Adipokines
have also proinflammatory and endocrine
properties by enhancing the adipose tissue
infiltration to macrophages. Some relation
between insulin resistance and enhanced
macrophages inflow to adipose tissue and
resultant changes in cytokines expression
was shown in the study. Ethanol abuse
leads to higher serum concentration of
diols (2,3-butenediol and 1,2-propenediol),
a chemical compounds responsible in vitro
for adipocytes insulin resistance, decrease
in glucose utilization and glycogen synthesis
in the myocardium and muscles. A lower
GLUT4 gene expression in adipose tissue
and abnormal stimulation of GLUT4 by
insulin - characteristic to insulin resistance
were also shown in the study [7-10]. Both
the hyper - and the hypoglycemia can be
caused by ethanol [11,12]. A decreased
glycogen store and the inhibition of liver
gluconeogenesis even for few hours can
cause hypoglycemia [9,13]. Activation of
adrenergic system can be also involved in
hypoglycemia - activation of β2-adrenergic
receptors shorten a hypoglycemic state [14].
Diabetes can be caused not only by ethanol
disturbances in glucose metabolism but
also by the liver and pancreas impairment
[15,16]. The aim of the study was to evaluate
the glucose metabolism in patients suffering
from ethanol withdrawal syndrome.
Materials and methods
The study group comprised 88 alcohol
dependent men aged from 21 - 50 years
(mean 39.18 ± 7.78), treated for alcohol
withdrawal in Toxicology Ward in Rydygier
Hospital in Kraków. A diabetes, liver, pancreas or kidney insufficiency, mixed dependence on alcohol and the other psychoactive
substance (but not a nicotine) or the patients
in whom the glucose preparations were ad470
Wykazano, na granicy istotności statystycznej, picie wódki
w wywiadzie jako czynnik ryzyka wystąpienia hipoglikemii
(OR = 7,43, p = 0,06). Wnioski: 1. W grupie mężczyzn
uzależnionych od alkoholu ryzyko wystąpienia cukrzycy
jest odwrotnie proporcjonalne do wartości wskaźnika BMI.
2. Czynnikami ryzyka cukrzycy typu 2 w badanej grupie
jest długość trwania ciągu alkoholowego przed przyjęciem
do leczenia i nasilenie objawów odstawiennych określone
wg skali CIWA-A. 3. Uwzględniając rodzaj spożywanego
alkoholu, w grupie mężczyzn uzależnionych od alkoholu,
istotnie statystycznie częstsze występowanie hipoglikemii
stwierdzono jedynie u osób pijących wódkę.
ministered were excluded. A standardized
interview and medical examination were performed on admission. Alcohol dependence
was diagnosed according to the criteria of
the International Statistical Classification
of Diseases and Related Human Problems
(ICD-10) [17]. The degree of alcohol withdrawal syndrome was assessed according
to the scale CIWA-Ar (Clinical Institute Withdrawal Assessment Alcohol revised) [18-20].
AST and ALT activity higher than a normal
limit at least fivefold or incorrect indices the
blood coagulation (excluding the platelets)
were considered as a biochemical marker
of the liver injury. The blood and urine amylase activity was used to evaluation of pancreas. The abdomen ultrasonography was
performed in all the patients and assessed
according to USG scale introduced by the
Department of Clinical Toxicology previously
[21]. The glucose serum concentration was
determined on admission. The glucose
concentration higher than 7.8 mmol/L was
accepted as a cut limit for glucose intolerance and the value of 3 mmol/L or lower for
hypoglycemia. On the next post-admission
day blood glucose was determined before
eating at the 0, 60th and 120th minute of an
oral glucose tolerance test (OGTT) using
75 g glucose. Basing on the 2013 y recommendations of Polish Diabetes Association
[22] the patients were classified into one of
groups according to their glucose tolerance
test results:
1. Diabetes mellitus (DM) - fasting plasma glucose ≥7.0 mmol/L or a levels above
11.2 mmol/L at 2 hours OGTT acc. WHO.
2. Impaired glucose tolerance - blood
plasma glucose between 7.8 – 11 mmol/L
at 2 hours OGTT.
3. Impaired fasting glycaemia - fasting
plasma glucose 5.6 - 6.9 mmol/L.
4. Normal glucose tolerance - fasting
plasma glucose 3.4 - 5.5 mmol/L, at 2 hours
glucose level <7.8 mmol/L.
Hypoglycaemia - plasma glucose ≤3
mmol/L at 2 hours OGTT.
The patients with impaired glucose tolerance and with abnormal fasting glycaemia
were taken together to statistical evaluation.
BMI was calculated for each the patient and
evaluated according to WHO recommendation: normal weight: 18.5 – 24.9; overweight:
25 – 29.9, obesity: BMI ≥30 [23]. A control
group was comprised of 89 men, 35 - 50
years of age, occasionally drinkers (no
often than 4 times a week, no more than
4 standardized doses of ethanol on one
occasion).
Statistical evaluation: A mean value
and standard deviation were calculated for
independent variables and the percentage
characteristics was applied to the dependent
variables. The χ2 test or an more accurate
Fisher test for a small groups were used
for comparison of depended variables. A
Mann-Whitney or Kruskal-Wallis test were
applied to analysis of independent variables.
A rang Spearman test was used to evaluate
a correlation between variables analyzed. A
level of p <0.05 was accepted as a statistical
significance. A calculations were performed
using STATA 8.0 package.
Results
Characteristics of 88 examined men is
presented in table I
Vodka (61.36%) followed by bear
(59.09%) were a dominant alcohol beverages declared by the men examined. No
serious changes in biochemical indices of
liver injury were found. A fatty liver in 59%,
hepatitis in 23% and the liver cirrhosis in
12% of examined men were found in abdominal USG.
BMI was normal in most (63.64%) of
Table I
Parameters related to alcohol addiction in the study group.
Parametry związane z uzależnieniem w grupie badanych mężczyzn.
Parameter
mean
SD ±
Min
Max
Age [years]
39.18
7.78
21
50
BMI
24.65
3.74
18.3
38.4
Duration of ethanol addiction [years]
10.56
7.17
0.5
30
Duration on a daily basis drinking [days]
118.75
198.52
2
1200
Ethanol units* per day
19.34
11.10
2
60
Blood ethanol concentration on admission [g/L]
0.82
1.04
0
3.55
CIWA-Ar [points]
23.95
2.81
16
31
*ethanol unit - 10 g alcohol
D. Pach i wsp.
men, the overweighed (27.27%) together
with obese men (7.95%) constituted 35.22%
of the group examined. BMI below 18.49
was stated in the one case only.
In table II glucose concentration on
admission, fasting glucose and results of
OGTT are presented.
A normal glucose tolerance was stated
in 54.55%, abnormal glucose tolerance
(abnormal fasting glucose or/and impaired
glucose tolerance at 2 h of OGTT together)
in 23.87%, and diabetes mellitus in 10.23%
of examined men. Hypoglycaemia at 2 h of
OGTT was diagnosed in 11.36% of the group examined. None of the patient presented
hypoglycaemia on admission.
Frequency of glucose intolerance and
diabetes mellitus was significantly correlated
with an ethanol concentration on admission
(p=0.033) and CIWA-Ar scores obtained
(p=0.02) - table III, and with withdrawal
syndrome intensity according to CIWA-Ar
(p=0.003) (table III). Consumption of vodka
was related to significantly lower incidence
of glucose tolerance disorders and diabetes
mellitus (p=0. 03) - table IV.
No overweight nor obesity was found in
the group of diabetic men, no underweighted patients were found in hypoglycaemic
patients at 2 h of OGTT (figure 1).
Significant relation between lower BMI
and higher frequency of diabetes mellitus
was shown (p=0.05).
The age, BMI, glucose tolerance di-
Rycina 1
The frequency of overweight, obesity and normal weight in particular group of glucose tolerance disturbances
of OGTT in the group of ethanol dependent patients.
Częstość występowania nadwagi, otyłości i prawidłowej masy ciała w poszczególnych grupach tolerancji glukozy w
grupie pacjentów uzależnionych od alkoholu.
Table II
Serum glucose concentration in the study group of alcohol dependent men.
Wartości glikemii w badanej grupie mężczyzn uzależnionych od alkoholu.
Parameters
mean
SD ±
Min
Max
Glycaemia on admission [mmol/L]
5.48
0.95
3.5
8.7
Fasting glycaemia 0 OGTT [mmol/L]
4.80
0.61
3.4
6.6
Glycaemia at 2 h OGTT [mmol/L]
6.32
3.18
1.8
15.57
Table III
Parameters of alcohol dependence in relation to glucose tolerance.
Charakterystyka parametrów związanych z uzależnieniem w poszczególnych grupach tolerancji glukozy w badanej grupie.
Glucose tolerance impairment (IGF and IGT)
Normal
Parameters
Diabetes
p
mean
SD ±
mean
SD ±
mean
SD ±
Duration of ethanol dependence [years]
9.44
7.02
11.76
6.72
10.89
6.15
NS
Continous daily drinking [days]
85.25
110.94
151.95
269.05
220.45
309.86
NS
Blood ethanol concentration on admission [g/L]
0.59
0.85
0.96
1.24
1.74
1.12
0.033
Ethanol units per day*
19.87
10.79
15.48
9.42
20.34
13.04
NS
CIWA-Ar [points]
23.7
2.63
23.54
2.76
24.28
3.02
0.02
* ethanol unit - 10 g alcohol
Table IV
Alcohol beverage preference declared in interview, intensity of withdrawal syndrome and BMI in particular groups of glucose tolerance.
Rodzaj preferowanego alkoholu, nasilenie objawów zespołu odstawiennego oraz BMI w poszczególnych grupach tolerancji węglowodanów.
Parameter
Hypoglycaemia
Normal glucose
N
%
N
Vodka
9
16.67
32
59.26
Bear
5
9.62
28
Liquers
0
0
2
Impaired glucose tolerance
%
N
Diabetes
p
%
N
%
10
18.52
3
5.56
0.03
53.85
12
23.08
7
13.46
NS
50
1
25
1
25
NS
13
25.49
0
0.00
0.003
8
21.62
9
24.32
Kind of alcoholic beverage
CIWA-Ar
≤24 points
6
11.76
32
62.75
≥25 points
4
10.81
16
43.24
BMI [kg/m ]
2
≤18.49
0
0.00
0
0.00
0
0.00
1
100.0
18.5- 24.99
7
12.50
27
48.21
14
25.00
8
14.29
25.0- 29.99
3
12.50
15
62.50
6
25.00
0
0.00
≥ 30.00
0
0.00
6
85.71
1
14.29
0
0.00
Przegląd Lekarski 2014 / 71 / 9
NS
471
Table V
BMI and frequency of glucose tolerance disturbances in 0th and 120th minute of OGTT in the group of ethanol
dependent patients and the control group.
Porównanie BMI, częstości występowania zaburzeń tolerancji glukozy na czczo i w 120 min DTOG.
Examined group
Parameter
N
%
Control group
N
%
p
BMI
≤18.49
1
1.12
0
0
18.5 - 24.99
57
63.04
25
28.41
25 - 29.99
24
26.97
44
50.00
≥30
7
7.87
19
21.59
Hypoglycaemia
10
11.36
6
6.90
p<0.001
OGTT
Normal
48
54.55
29
33.33
Impaired glucose tolerance
21
23.86
49
56.32
Diabetes
9
10.23
3
3.45
p<0.001
Table VI
BMI and age as the risk factor of type 2 diabetes (one dimensional logistic regression analysis).
Regresja logistyczna jednowymiarowa wpływu BMI i wieku na ryzyko wystąpienia cukrzycy typu 2 przeprowadzona
na grupie kontrolnej.
Diabetes
Odds Ratio (OR)
95% CI
p
BMI
0.99
0.72 - 1.34
NS
Overweight
0.59
0.03 - 9.33
NS
Obesity
1.41
0.08 - 24.18
NS
Age [years]
1.40
0.86 - 2.29
NS
Table VII
BMI, age, parameters of alcohol addiction as the risk factor of type 2 diabetes in the study group of alcohol
dependent men in the regression analysis model.
Regresja logistyczna jednowymiarowa wpływu BMI, wieku, parametrów związanych uzależnieniem na ryzyko wystąpienia cukrzycy typu 2 przeprowadzona na grupie mężczyzn uzależnionych od alkoholu.
Diabetes
Odds ratio (OR)
95% CI
p
BMI
0.63
0.43 - 0.92
0.01
Age
0.98
0.90 - 1.07
NS
35-45 years
1.92
0.34 - 10.78
NS
45-50 years
0.88
0.11 - 6.79
NS
CIWA-Ar [points]
1.43
1.07 - 1.91
0.01
Duration on a daily basis drinking [days]
1.00
0.99 - 1.00
NS
Diuration of ethanol addiction [years]
1.01
0.91 - 1.11
NS
Blood ethanol concentration on admission [g/L]
2.29
1.20 - 4.36
0.01
Vodka
0.27
0.06 - 1.18
NS
(0.08)
Bear
2.64
0.52 - 13.54
NS
Table VIII
BMI, age, intensity of withdrawal syndrome assessed in CIWA-Ar scale, days of continuous drinking and the
blood ethanol concentration on admission as the risk factors for type 2 diabetes in the study group of alcohol
dependent men (one-dimensional regression analysis).
Regresja logistyczna wielowymiarowa związku pomiędzy BMI, wiekiem, nasileniem objawów odstawiennych w skali
CIWA-Ar, długością trwania ciągu alkoholowego i stężeniem etanolu przy przyjęciu a ryzykiem wystąpienia cukrzycy
typu 2 przeprowadzona na grupie mężczyzn uzależnionych od alkoholu.
472
Cukrzyca
Odds ratio (OR)
95% CI
p
BMI
0.49
0.26 - 0.93
0.02
Age [years]
1.09
0.94 - 1.26
NS
CIWA [points]
1.60
1.00 - 2.55
0.05
Duration on a daily basis drinking [days]
1.01
1.00 - 1.01
0.03
Blood ethanol concentration on admission [g/L]
1.50
0.62 - 3.60
NS
sorders in the group of ethanol dependent
patients suffering from withdrawal syndrome
and in the control group are presented in
table V.
In the group of ethanol dependent
patients a normal body weight was found
in 63.04% vs. 28.4% in the control group;
the overweighed men comprised 50%, and
obese 21.59% of the control. Difference
between BMI was statistically significant
(p<0.001). In the group of ethanol dependent patients more often than in the control
group hypoglycemia (11.36%) and diabetes mellitus (10.23%) were noted. In the
control group more often than in the study
group incorrect fasting glucose or impaired
glucose tolerance at 2 h of OGTT (56.32%
vs. 23.86%) was noted. The difference was
statistically significant (p<0.001).
The one-dimensional regression analysis
did not show any significant relation between
the risk of type 2 diabetes and BMI index or
age in the control group (table VI).
The results of such analysis for the study
group is presented in table VII.
The blood ethanol concentration on
admission (OR = 2.29; p=0.01) and degree
of alcohol withdrawal syndrome according
to CIWA-Ar scale (OR=1.43; p=0.01) were
significant risk factors for type 2 diabetes in
the group examined. The higher BMI was
a protective factor for type 2 diabetes in
that group of ethanol dependent patients
(R=0.63; p=0.01). Any significant relations
between hypoglycaemia and age, duration
of ethanol dependence, days of continual
daily drinking, bear consumption were
noted in the examined group. A vodka as a
kind of alcohol beverages consumed was
at the borderline of statistical significance
(OR=0.27; p=0.08).
Multi-dimensional regression analysis
was also performed to assess the risk factor
for type2 diabetes in examined ethanol dependent patients suffering from withdrawal
syndrome (table VIII).
Degree of withdrawal syndrome according to CIWA-Ar scale and duration of
continual daily drinking were revealed as
a statistically significant risk factor for type
2 diabetes by multi-dimensional regression
analysis (OR=1.59; p=0.05 and OR = 1.01;
p=0.03) respectively. A BMI was a protective
factor in that group examined (OR = 0.49,
p = 0.02).
Multi-dimensional regression analysis
performed to assess such a risk factors for
hypoglycaemia did not show any significant
relation (table IX). A vodka consumption declared in a medical interview was a risk factor
at the borderline of statistical significance
(OR=7.44; p=0.06).
Discussion
The mean age of the examined group
was 39.18 ± 7.78 y. The proportion of young
(20-34 y) ethanol dependent men in our
study group is relatively high and confirm
indirectly a common observation of early initiation and extensive binge alcohol drinking
by a youngsters [24,25].
Vodka and the other strong alcohols
were a most frequent alcohol beverages
declared by the study patients (61.36%).
More than half of them (59.09%) declared
D. Pach i wsp.
Table IX
BMI, age, intensity of withdrawal syndrome assessed in CIWA-Ar scale, days of continuous drinking, blood
ethanol concentration on admission and a vodka as preferred alcohol beverage as the risk factors for type 2
diabetes in the study group of alcohol dependent men (multi regression analysis).
Regresja logistyczna wielowymiarowa związku pomiędzy BMI, wiekiem, nasileniem objawów odstawiennych w skali
CIWA-Ar, długością trwania ciągu alkoholowego, stężeniem etanolu przy przyjęciu i piciem wódki w wywiadzie a
ryzykiem wystąpienia hipoglikemii przeprowadzona na grupie mężczyzn uzależnionych od alkoholu.
Hypoglycaemia
Odds ratio (OR)
95% PU
p
BMI [25,0-29,99]
1.01
0.21 - 4.86
NS
Age [years]
1.05
0.94 - 1.17
NS
CIWA [points]
0.93
0.68 - 1.25
NS
Duration on a daily basis drinking [days]
1.00
0.99 - 1.00
NS
Blood ethanol concentration on admission [g/L]
1.14
0.52 - 2.52
NS
Vodka as preferred alcohol beverage
7.44
0.86 - 64.46
NS
(0.06)
also a bear drinking what can indicate on
changes in cultural habits, influence of TV
promotion or behavior related to ethanol
abuse rather (drinking vodka and bear together). A general approval for low-alcohol
beverages drinking by youngsters and a
young adults is unfortunately very common
in our society [26,27].
Duration of ethanol dependence declared by our patients was from 6 months
to 30 years (mean 10.56 ± 7.17y). A 2 to
1200 days (mean: 118.75 ± 198.52 days)
of continua, daily drinking were declared by
the patients in medical interview. A moderate
withdrawal syndrome using the CIWA-Ar
scale was diagnosed most frequently (mean
23.95 ± 2.81 scores). Basing on the individual CIWA-Ar scores a medical treatment with
a proper administration of sedatives, mostly
benzodiazepines was introduced [19,28].
No serious changes in biochemical indices of liver injury were found in the group
of patients suffering from acute withdrawal
syndrome. Hepatic USG revealed a signs of
a fatty liver in 59% of our ethanol dependent
patients. This the most frequent alcohol-related liver disease is caused by the changes in
hepatocyte redox reactions, oxidative stress,
increased lipid peroxydation and hepatic
lobule hypoxia [29-31].
A malnutrition was stated in the one
case only (1.14%), a normal body weight or
overweight in the rest (98.86%) of ethanol
dependent patients, what confirm a common
observation that incidence of malnutrition
among alcoholics is not so high at present
[32].
The men from the control group more
often than the study group suffered from
impaired glucose tolerance (56.32% vs.
23.86%; p<0.001). Incidence of hypoglycaemia and diabetes was higher in the study
group of ethanol dependent patients. In that
group incidences of diabetes and hypoglycaemia at 2 h of OGTT were similar (11.36%
vs. 10.23%).
The U shaped relationship between alcohol consumption and the risk of abnormal
glucose metabolism and type 2 diabetes is
described in literature [33-35]. The prospective Rancho Bernardo Study [5] and Atherosclerosis Risk in Communities Study
(ARIC) [36] show that a moderate alcohol
consumption reduces the incidence of T2D,
however, binge drinking seems to increase
Przegląd Lekarski 2014 / 71 / 9
the incidence. In the Kao study an increased
risk of diabetes incidence was higher in
men who consumed more than 21 drinks a
week compared with those who consumed
not more than 1 drink. It was consistent
with common opinion that heavy drinking
increase the risk of diabetes in mean aged
men [36]. The lower type 2 diabetes risk in
moderate but not a heavy alcohol consumption (bear, wine or vodka) was also shown
in Swedish study performed in population of
mean aged men [32,37].
A higher blood ethanol concentration
on admission (OR = 2.29, p = 0.01) and the
degree of withdrawal syndrome assessed by
CIWA-Ar score (OR = 1.43, p = 0.01) were
a significant risk factor for diabetes shown
in our study by logistic regression model. A
vodka consumption compared with other
alcoholic beverages was connected with
higher incidence of hypoglycaemia (OR =
7.43, p = 0.06; at the borderline of statistical significance) in our study. A relationship
between vodka consumption and incidence
of hypoglycaemia is consisted with the other
study. Some of them recommend to drink a
vodka with a fruit juice or meal to prevent
hypoglycemia [32,38] however results of
OGTT obtained in our study do not feet it.
A lowest body mass index was found in
those ethanol dependent men in whom diabetes was diagnosed (BMI = 21.96±2.02); in
the group with hypoglycaemia at 2 h OGTT
all the patients had a normal body weight or
overweight. The higher BMI was a protective factor for type 2 diabetes in that group
of ethanol dependent patients (R=0.63;
p=0.01) as was shown by multi-dimentional regression analysis in our study. The
incidence of overweight and obesity was
higher in the control group (50% vs. 26.97%
and 21.59% vs. 7.87% respectively). A
malnutrition was not stated in any men from
the control group. Our ethanol dependent
patients were more slim than the men from a
control, although the style of feeding among
alcoholics has in general improved.
Tsumura and others Japanese authors
have shown that a higher BMI together with
moderate alcohol consumption was related
to lower risk of type 2 diabetes, whereas
a lower BMI together with heavy drinking
increased a risk of type 2 diabetes [39-41].
A meta-analysis of relationship between incidence of diabetes ethanol consumption and
BMI undertaken by Sieke [42] has confirmed
these observations.
The U shaped relationship between risk
of hydrocarbons intolerance and type2 diabetes and ethanol consumption was shown
in Nakanishi study. A genetic differences between the Japanese and Caucasian related
to mitochondrial aldehyde dehydrogenase
gene 2 must be considered in the results
interpolation [35].
The Carlsson study performed on 22 778
Finnish twins has shown that moderate alcohol consumption was related to lower risk
of type 2 diabetes incidence in obese and
overweighed people (BMI>25), whereas in
normal weighed people and with malnutrition
alcohol consumption was related to higher
incidence of diabetes [43].
Conclusions
The incidence of overweight and obesity was significantly lower in the group of
ethanol dependent patients compared to the
control. In that group of alcohol-dependent
men, the risk of diabetes was negatively
correlated with BMI value.
A statistically higher incidence of type 2
diabetes and hypoglycaemia at 2 h OGTT
was found in the ethanol dependent men
compared to the control; duration of alcohol
dependence and intensity of withdrawal
symptoms according to CIWA-Ar scale were
a significant risk factors.
A significantly higher frequency of hypoglycaemia was noted in persons preferring
to drink vodka but not the other alcohol
beverages.
References
1. Avogaro A, Valerio A, Miola M, Crepaldi C, Pavan
P. et al: Ethanol impairs insulin-mediated glucose
uptake by an indirect mechanism. J Clin Endocrinol
Metab. 1996; 81: 2285-2290.
2. Mamcarz A: Alkohol w profilaktyce chorób układu
sercowo-naczyniowego - co wiadomo Anno Domini
2010? Kardiologia na co Dzień 2010; 5:119-125.
3. Howard AA, Arnsten JH, Gourevitch MN: Effect of
alcohol consumption on diabetes mellitus. Ann Intern
Med. 2004; 40: 211-224.
4. Flanagan DE, Pratt E, Murphy J: Alcohol consumption alters insulin secretion and cardiac autonomic
activity. Eur J Clin Invest. 2002; 32: 187-192.
5. Holbrook TL, Barrett-Connor E, Wingard DL: A
prospective population-based study of alcohol use
and non-insulin-dependent diabetes mellitus. Am J
Epidemiol. 1990; 132: 902-909.
6. Shelmet JJ, Reichard GA, Skutches CL, Hoeldtke
RD, Owen OE, Boden G: Ethanol causes acute
inhibition of carbohydrate, fat, and protein oxidation
and insulin resistance. J Clin Invest. 1988; 81:
1137-1145.
7. Kang L, Sebastian BM, Pritchard MT, Pratt BT,
Previs SF, Nagy LE: Chronic ethanol-induced
insulin resistance is associated with macrophages
infiltration into adipose tissue and altered expression
of adipocytokines. Alcohol Clin Exp Res. 2007; 31:
1581-1588.
8. Knip M, Ekman AC, Ekman M, Leppäluoto J, Vakkuri O: Ethanol induces a paradoxical simultaneous
increase in circulating concentrations of insulin-like
growth factor binding protein-1 and insulin. Metabolism 1995; 44: 1356-1369.
9. Orywal K, Jelski W, Szmitkowski M: Udział alkoholu
etylowego w powstawaniu zaburzeń metabolizmu
węglowodanów. Pol Merkur Lek. 2009; 27: 68-71.
10. Xu D, Dhillon AS, Abelmann A, Croft K, Peters
TJ, Palmer TN: Alcohol-related diols cause acute
insulin resistance in vivo. Metabolism 1998; 47:
1180-1186.
11. Heikkonen E, Ylikahri R, Roine R, Välimäki M,
Härkönen M, Salaspuro M: Effect of alcohol on
473
excercise-induced changes in serum glucose and
serum free fatty acids. Alcohol Clin Exp Res. 1998;
22: 437-443.
12. Pach D, Szurkowska M, Szafraniec K, Targosz D,
Sułek M. i wsp: Zaburzenia gospodarki węglowodanowej w ostrych zatruciach ksenobiotykami. Przegl
Lek. 2007; 64: 243-247.
13. Kaminsky YG, Kosenko EA: Blood glucose and
liver glycogen in rats. Effects of chronic ethanol
consumption and its withdrawal on the diurnal rythms.
FEBS Lett. 1986; 200: 217-220.
14. Park MJ, Guest CB, Barnes MB, Martin J, Ahmad
U. et al: Blocking of beta-2 adrenergic receptors
hastens recovery from hypoglycemia-associated
social withdrawal. Psychoneuroendocrinology 2008;
33: 1411-1418.
15. Czupryniak L, Loba J: Aktywność zawodowa i styl
życia w cukrzycy. [w]: Sieradzki J (red.): Cukrzyca
Kompendium. Via Medica Gdańsk 2009.
16. Jelski W, Szmitkowski M: Wpływ alkoholu etylowego
na zespół metaboliczny. Pol Arch Med Wewn. 2007;
117: 306-311.
17. Międzynarodowa Statystyczna Klasyfikacja Chorób
i Problemów Zdrowotnych. Rewizja dziesiąta. Vesalius, Kraków 1994.
18. Berge KH: Protocol-Driven Treatment of Alcohol Withdrawal in a General Hospital: When Theory Meets
Practice. Mayo Clin Proc. 2008; 83: 270-271.
19. Corfee FA: Alcohol withdrawal in the critical care unit.
Austral Critic Care 2011; 24 : 110-116.
20. Habrat B, Steinbarth-Chmielewska K, Baran-Furga
K: Zaburzenia psychiczne i zaburzenia zachowania
związane z przyjmowaniem substancji psychoaktywnych. [w]: Pużyński S, Rybakowski J, Wciórka
J (red): Psychiatria. Podstawy psychiatrii. Elsevier
Urban &Partner, Wrocław 2011.
21. Węgrzynek I, Żulikowska E: Przydatność badań
enzymatycznych, biochemicznych i ultrasonograficznych dla oceny hepatotoksycznego działania alkoholu
etylowego. Przegl Lek. 2001; 58: 301-305.
22. Zalecenia kliniczne dotyczące postępowania u
chorych na cukrzycę, 2013. Stanowisko Polskiego
Towarzystwa Diabetologicznego. Diabetol Prakt.
474
2013; 12: supl. A. A1-A52.
23. World Health Organization: Obesity: preventing
and managing the global epidemic. Report of a
WHO consultation. (WHO Technical Report Series
894). Geneva, 2000.
24. Chassin L, DeLucia Ch: Picie w okresie dojrzewania.
[w]: Picie alkoholu w różnych okresach życia. Alkohol
a zdrowie nr 25, PARPA, Warszawa 2000.
25. Habrat B: Szkody zdrowotne spowodowane alkoholem. Springer PWN, Warszawa 1996.
26. Moskalewicz J, Wieczorek Ł: Dostępność, konsumpcja alkoholu i konsekwencje picia - trzy dekady
doświadczeń. Alkohol Narkom. 2009: 22: 305-337.
27. Ogonowska D, Pach D, Targosz D: Używanie
substancji psychoaktywnych przez uczniów szkół
średnich w Nowym Sączu. Przegl Lek. 2009, 66:
293-300.
28. Radomska M: Zespoły odstawienne. [w]: Pach J.
(red.): Zarys toksykologii klinicznej. Wydawnictwo
Uniwersytetu Jagiellońskiego, Kraków 2009.
29. Andersen BN, Hagen C, Faber OK, Lindholm J,
Boisen P, Worning H: Glucose tolerance and B cell
function in chronic alcoholism: its relation to hepatic
histology and exocrine pancreatic function. Metabolism 1983; 32: 1029-1032.
30. Mach T: Alkoholowa choroba wątroby. [w] Szczeklik
A (red.): Choroby wewnętrzne. Stan wiedzy na rok
2010. Medycyna Praktyczna, Kraków 2010.
31. Valtueña S, Numeroso F, Ardigò D, Pedrazzoni M,
Franzini L et al: Relationship between leptin, insulin,
body composition and liver steatosis in non-diabetic
moderate drinkers with normal transaminase levels.
Eur J Endocrinol. 2005; 153: 283-290.
32. Conigrave KM, Hu BF, Camargo CA Jr, Stampfer
MJ, Willett WC, Rimm EB: A prospective study of
drinking patterns in relation to risk of type 2 diabetes
among men. Diabetes 2001; 50: 2390-2398.
33. Fan AZ, Russell M, Stranges S, Dorn J, Trevisan
M: Association of lifetime alcohol drinking trajectories
with cardiometabolic risk. J Clin Endocrinol Metab.
2008; 93: 154-161.
34. Flanagan DE, Moore VM, Godsland IF, Cockington
RA, Robinson JS, Phillips DI: Alcohol consumption
and insulin resistance in young adults. Eur J Clin
Invest. 2000; 30: 297-301.
35. Nakanishi N, Suzuki K, Tatara K: Alcohol consumption and risk for development of impaired fasting
glucose or type 2 diabetes in middle-aged Japanese
men. Diabetes Care 2003; 26: 48-54.
36. Kao WH, Puddey IB, Boland LL, Watson RL, Brancati FL: Alcohol consumption and the risk of type 2
diabetes mellitus: atherosclerosis risk in communities
study. Am J Epidemiol. 2001; 154: 748-757.
37. Carlsson S, Hammar N, Efendic S, Persson PG,
Ostenson CG, Grill V: Alcohol consumption. Type
2 diabetes mellitus and impaired glucose tolerance
in middle-aged Swedish men. Diabet Med. 2000;
17: 776-781.
38. Baker SG, Joffe BI, Shires R, Viljoen M, Lamprey
JM, Seftel HC: Alcohol-potentiated reactive hypoglycemia depends on the nature of the carbohydrate
ingested at the same time. Alcohol Alcohol. 1984;
19: 45-49.
39. Tsumura K, Hayashi T, Suematsu C, Endo G, Fujii
S, Okada K: Daily alcohol consumption and the risk of
type 2 diabetes in Japanese men: the Osaka Health
Survey. Diabetes Care 1999; 22: 1432-1437.
40. Waki K, Noda M, Sasaki S, Matsumura Y, Takahashi Y. et al: Alcohol consumption and other risk
factors for self-reported diabetes among middle-aged
Japanese: a population-based prospective study
in the JPHC study cohort I. Diabet Med. 2005; 22:
323-331.
41. Watanabe M, Barzi F, Neal B, Ueshima H, Miyoshi
Y. et al: Alcohol consumption and the risk of diabetes
by body mass index levels in a cohort of 5 636 Japanese. Diabetes Res Clin Pract. 2002; 57: 191-197.
42. Seike N, Noda M, Kadowaki T: Alcohol consumption
and risk of type 2 diabetes mellitus in Japanese: a
systematic review. Asia Pac J Clin Nutr. 2008; 17:
545-551.
43. Carlson S, Hammar N, Grill V, Kaprio J: Alcohol
consumption and the incidence of type 2 diabetes:
a 20-year follow-up of the Finnish twin cohort study.
Diabetes Care 2003; 26: 2785-2790.
D. Pach i wsp.

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