Download Intragastrointestinal Alcohol Fermentation Syndrome: Report of Two

COMMENTARY
Intragastrointestinal Alcohol Fermentation
Syndrome: Report of Two Cases and
Review of the Literature
H KAJI,* Y ASANUMA, 0 YAHARA, H SHIBUE,
M HISAMURA,
N SAITO, Y KAWAKAMI and M MURAO
The First Department of Medicine, Hokkaido University School of
Medicine, Nishi-7, Kita-1.5, Kita-ku, Sapporo 060, Japan
Abstract
Two patients with frequent attacks of alcohol intoxication
following the intake of an ordinary meal are presented. The
causative agents were Candida albicans and C. krusei in the
first case and C. albicans in the second. The essential factors of
this syndrome were abnormal proliferation of the causative
agent, abnormal stagnation of food in the alimentary tract,
intake of a carbohydrate diet as the substrate for the alcohol
fermentation and low threshold of the patient to alcohol.
Thirty-seven other cases have been reported in Japan since
1952, with patients aged from 1 to 75 years. All those concerned with alcohol intoxication, especially in the forensic
sciences, should bear this syndrome in mind. Key Words:
Alcohol intoxication; Endogenous alcohol; Gastrointestinal
moniliasis; Candida albicans; Intragastrointestinal alcohol fermentation.
Journal of the Forensic Science Society 1984; 24: 461-471
Received 11 October 1983
Introduction
Increases in alcohol dependence, road casualties and crimes under the
influence of alcohol and inebriate driving are worldwide social problems
especially from the toxicological, medicolegal and criminological points of
view. In postmortem examinations it is necessary to determine whether the
source of blood ethanol is putrefactive alcohol production or antemortem
alcohol consumption. As more sensitive analyses come into general use,
trace amounts of alcohol are easily detectable in human body fluids. Thus,
Harger reports normal body alcohol levels of up to 0.25 mgldl [I] and Lester
* Present address: Health Examination Center, Workmen's Accident Compensation Hospital of
Iwamizawa, 4-jo, Higashi 16-chome, Iwami~awa068, Japan.
461
reports that concentrations of up to 0.15 mgldl may be present, but whether
this alcohol is endogenous is unresolved [2]. Recently, a significant increase
in lower aliphatic alcohols has been demonstrated in the 24-hour urine of
diabetic patients [3,4] and there may be ethanol production in infected urine
[51.
On the other hand, some cases have been reported with repeated attacks of
alcoholic intoxication without prior intake of alcohol, what may be called
the intragastrointestinal alcohol fermentation syndrome. This is a type of
moniliasis in which patients become inebriated after the intake of an
ordinary carbohydrate meal. It is caused by excessive production of ethanol
by carbohydrate fermentation due to yeasts, mainly those belonging to the
Candida group, which have proliferated abnormally in the gastrointestinal
tract. Thus far, 37 cases have been reported in Japanese literature since the
first report appeared [6]. Although, to the best of the authors' knowledge,
no such case has been reported in other countries, clinician, toxicologist and
forensic scientist should be aware of the significance of the syndrome.
In the present communication, two further cases of the syndrome are
presented, and the characteristics of the pertinent causative factors in 39
Japanese cases are analyzed.
Methods
Measurement of ethanol concentration in breath, blood and urine
The ethanol concentrations were measured by a gas chromatograph (Model
GC-SAPFFp, Shimadzu, Kyoto, Japan), equipped with a flame ionization
detector. Breath ethanol concentration was measured by the direct analysis
of 5ml of expired alveolar air [7]. Blood, plasma and urine ethanol
concentrations were also measured by GC using aqueous solutions of
acetonitrile or n-propanol (Wako, Osaka, Japan) as the internal standard
[8-101.
Isolation and identification of the causative agents
Stomach juice, duodenal juice and faecal specimens were serially cultured
using Sabouraud's glucose agar. Candida colonies appearing on this agar
were purified on Sabouraud's blood agar. Thereafter, Candida groups were
identified by morphological and biological examinations [ll].
Alcohol fermentation test in vitro
Purified Candida was precultured on potato-glucose agar at 27°C for 7 days.
Each suspension was adjusted to a cell number of either 4 x lo7 or 8 x lo7
in 3 ml and then innoculated into 3 ml of fermentation test medium
containing 3% of yeast extract. After incubation for between 20 and
100 hours at 27°C or 37"C, the degree of alcohol fermentation activity was
determined [ll].
462
Case reports
Case 1. A 24-year-old nurse, previously in good health, had, over a period
of 5 months developed symptoms of faintness, nausea and sometimes
vomiting 1 to 2 hours after eating. Occasionally she had fallen asleep during
her night duty or fallen down while shopping in the daytime. She had
deliberately avoided overeating because of the appearance of these signs and
symptoms after a meal. Her diet averaged about 1800Cal per day,
consumed in the Nurses' Home, with a carbohydrate content of about 78%.
Two hours after an ordinary breakfast, she complained of general malaise
and faintness, became unconscious and was admitted to hospital in a
comatose state about 3 hours later. Her breath had a strongly alcoholic
odour and the level of consciousness corresponded to stupor. The symptoms
of drunkenness continued for 3 days. She thereafter had repeated attacks
more frequently and occasionally fell into delirium or coma accompanied by
urinary incontinence. She had had constipation lasting maximally for six
days alternating with bouts of diarrhoea. Usually, the degree of intoxication
lessened after defaecation. Maximal breath ethanol concentration was
1208 pgll and that in blood 254 mgldl, which indicated marked intoxication.
Figure 1 illustrates the increase in the blood ethanol concentration after a
meal. The X-ray examination of the alimentary tract revealed slight
dilatation of the duodenum and frequent backward movement of duodenal
contents into'the stomach. The pH of the stomach juice was 1-40.
Serial cultures of the stomach juice, duodenal juice and faecal specimens
showed numerous colonies of Candida, notably in the faeces. The maximum
live cell count of Candida in the watery stool specimen after the attack of
inebriation was 2.3 X lo5 per gram of wet faeces. The average total counts
5
:loo
m
FIGURE 1 Ethanol concentration in expired alveolar air, and blood, after a normal meal
(Case 1).
463
of Candida in the stomach and the duodenal juice were 640 per ml. Candida
albicans and C . krusei were identified on Sabouraud's glucose agar.
C . albicans showed strong alcoholic fermentation activity, but the activity of
C. krusei was only weak (Figure 2).
Since C. albicans was considered the main causative agent, an antifungal
agent, Cabimicina (TrichomycinB), 10 x lo4 to 80 x lo4 unitslday, was
administered orally [12, 131. Laxatives were also used and, at the same time,
carbohydrates in the diet were restricted for five days from the beginning of
the treatment. The drunk-like symptoms disappeared completely with this
treatment.
Case 2. A 35-year-old cook had been complaining of an alcoholic odour in
his breath and drunklike symptoms, such as difficulty in articulation, blurred
vision and staggering or weaving gait, but denied having taken alcohol.
Although these symptoms appeared several times a week sometimes lasting
until midnight, they disappeared spontaneously. Seven months later, the
symptoms recurred and on several occasions he lapsed into unconsciousness.
Four months later he was admitted to Hospital A. Based on a provisional
diagnosis of "the intragastrointestinal alcohol fermentation syndrome" he
was treated with an antifungal agent, Nystatinum, 3 x lo6 unitslday orally
for 11 days, and was discharged free of symptoms.
Shortly after the discharge, however, his symptoms reappeared and he was
"1
(b)
(a)
20 .
B
.B 1 5 .
A
s
f
B
. A
$'
V
10.
.-5
F
.+8
m
.scm
5..
c.
Candida albicans
Candida albicans
8
I
Candida krusei
Candida krusei
0
0 10 20 30 40 50 60 70 80 90 100
0 10 20 30 40 50 60 70 80
Incubation time in hours
FIGURE 2 Alcoholic fermentation test in vitro (Case 1). (a) Incubation at 27'C. (b)
Incubation at 37°C.
admitted to our clinic. He had a past history of appendectomy at the age of
15. Physical and biochemical examinations revealed no abnormal findings
except for a slight alcoholic odour in his breath. The X-ray examination of
the alimentary tract revealed no abnormal findings. The pH of the stomach
juice was 6.80.
On the 13th day after admission, he felt faint during the morning and mildly
drunk throughout the day. These symptoms abated by noon of the 14th day
(Figure 3). During this time, microbiological examinations of stomach juice,
duodenal juice and faeces were performed. The live cell counts of Candida
were 1750, 820, 620 and 300 per ml in the stomach juice, 1470 per ml in the
duodenal juice, and 7.4 x lo4 per gram of wet faeces. Candida colonies on
Sabouraud7s glucose agar were identified as C. albicans Robins Berkhout
(1853) which proved to be resistant to the Nystatinum which had been used
in Hospital A. The symptoms did not re-appear in spite of taking an
ordinary meal, and he was discharged without treatment, but three months
later he was readmitted because of severe inebriation. This time, the live
cell count of C . albicans in stomach juice was 3560 per ml. He was treated by
oral administration of 1-5 x 10' unitslday of Cabimicina (TrichomycinB) for
45 days. Thereafter organisms of the Candida group were not detected in
stomach juice and faeces and he is now quite healthy and completely free
from the previous symptoms.
0
J
-I
9
lOpm
Time
I
I
1
6
7
8
I
9 am
FIGURE 3 Serial ethanol concentrations in an attack of inebriation (Case 2). A -.-.
breath, 0--3 plasma, X----X
urine.
465
A
C. albicans
C. albicans
C. albicans & Brown yeast
C. stelloidea
C. tropicalis
Saccharomyces
C. albicans
C. albicans
C. tropicalis & Brown
yeast
C. albicans
Saccharomyces cervisiae
C. guilliermondii
C. albicans
C. albicans
41 Male
28 Female
37 Male
43 Male
75 Female
30 Male
61 Male
51 Male
39 Female
1 Female
45 Male
28 Female
28 Female
15 Male
3 Female
Muramoto*
Miyaishi*
Fujisawa*
Ezaki [25]
Hashimoto [26]
Tanaka*
Ito*
1962 Maeda (20)
1963 Kameya*
Ishibashi*
Kawabata [27]
Yoshikawa*
1964 Kunishima*
Tsukahara*
Makunai*
1961 Kikuoka [24]
C. albicans
41 Male
Takasugi [23]
C. albicans
-
C. albicans
46 Male
1960 Takasugi [23]
Candida fukuoka Sato
Causative agents
46 Male
Age and sex
1952 Sato [6]
Case report
-
intestinal tuberculosis, atonia of stomach and
duodenum
dilatation of duodenum
congenital stenosis of upper jejunum
cholecystectomy (cholelithiasis), normo-acidity,
penicillin and streptomycin administration
-
pylorostenosis (stomach cancer), dilatation
of stomach, normo-acidity
gastrojejunostomy
exploratory laparotomy, pylorostenosis
(ulcus duodeni), penicillin orally, an-acidity
gastrectomy (Billroth 11), ampulla formation of
intestine, normo-acidity
gastrectomy (ulcus ventriculi), ampulla
formation at gastrojejunostomy
ulcus ventriculi, penicillin and chloramphenicol orally
intestinal tuberculosis, stenosis and
dilatation of small intestine
gastrojejunostomy, reversed peristalsis of
duodenal C-loop, an-acidity
gastrojejunostomy
gastrojejunostomy, partial dilatation of
small intestine, an-acidity
gastrectomy (Billroth 11), intestinal tuberculosis,
ampulla formation after anastomosis
gastrectomy (Billroth I), dilatation of duodenum
History of abdominal operation, gastrointestinal abnormalities, and related matters
-
resection of stenosis
-
gastrojejunostomy
Trichomycin
gastrectomy &
Trichomycin
Trichomycin
NK 458, mycostatin
Nystatin
Trichomycin
Trichomycin
Gentiana violet
Trichomvcin
(Cabimicina)
resection of
ampullar region
Treatment
TABLE 1. Summary of cases of 39 patients with the intragastrointestinal alcohol fermentation syndrome (Japanese Meitei-sho)
P
8
Torulopsis glabrata
C. albicans
19 Female
46 Male
52 Female
48 Male
64 Male
68 Female
36 Male
53 Male
2 Female
40 Female
Noborisaka*
1968 Mihara*
1969 Tajima*
Wakana*
Miura*
1971 Sakakiyama [22]
Takahashi*
1974 Yamashita [29]
1978 Kawanaka [30]
Kanaya*
T. glabrata
C. tropicalis
C. albicans & C. krusei
C. albicans
70 Male
70 Male
24 Female
35 Male
pylorostenosis, gastrojejunostomy
Candida in bile, an-acidity
blind loop formation after gastrojejunostomy,
malabsorption syndrome, an-acidity
duodenal dilation after duodenojejunostomy
due to congenital stenosis of duodenum
laparotomy, resection of colon descendens, postoperative stenosis of jejunum, dilatation of
stomach
duodenal dilation after gastrectomy
hypo-acidity, ulcus ventriculi, irradiation,
cancer chemotherapy and steroid treatment for
lung cancer and dermatomyositis
dilatation and reversed peristalsis of duodenum,
chloramphenicol and colimycin orally, constipation,
normo-acidity
hypo-acidity
-
none
cholecystectomy, stomach cancer, anacidity
laparotomies (4 times) including gastrectomy,
blind loop formation
pylorostenosis
none
none
gastrectomy (Billroth I), stenosis of duodenum
(pars horizontalis), chloramphenicol orally, hypo-acidity
none
dilatation of duodenum
pancreatitis (due to intestinal moniliasis?)
* Abstract of the case report cited from the Japana Centra Revuo Medicina.
1980 Takahashi*
Shy [311
C. tropicalis
C. albicans
C. albicans
27 Male
32 Male
22 Male
Nagai*
Ideuchi*
1967 Tanaka [28]
C. tropicalis
C. tropicalis
C . albicans, C. stelloidea
& Saccharomyces
C. albicans
Saccharomyces
Saccharomyces
C. albicans
Candida
C. albicans
C. albicans
C. albicans & C. krusei
20 Female
48 Male
21 Female
1965 Yokota*
Fukaura*
1966 Iyo [21]
-
Trichomycin
Trichomycin
Nystacin
-
gastrectomy (Billroth I)
gastrojejunostomy
gastrectomy (Billroth I)
Trichomycin
gastrectomy
Trichomycin
-
Trichomycin, Amphotericin B, Nystatin
Nystatin
-
Trichomycin
re-operation (Billroth
11)
Discussion
Although 39 cases have been reported in Japan since 1952, including our
two cases, the syndrome has not yet been recognized outside the country.
The syndrome is called "Meitei-sho" in Japanese, which means "the
intragastro intestinal alcohol fermentation syndrome", "the alcohol autointoxication syndrome" or "the endogenous alcohol intoxication syndrome".
A summary of case details is given in Table 1. The age distribution ranged
from 1 to 75 years. The male to female ratio was 23: 15 but females
predominated in the age group under 29, viz. 10 of 13 cases (76.9%),
whereas males outnumbered females in patients over 30, viz. 20 out of 25
cases (80.0%).
In order to rule out surreptitious drinking, patients were strictly and
continuously monitored by doctors or nurses in the sickroom for 24 hours.
The patterns of ethanol concentrations in blood and in urine would seem to
be of value for the differential diagnosis of intragastrointestinal fermentation
from surreptitious drinking. There are several reports demonstrating breath,
blood and/or urine alcohol concentration patterns following ingestion of 200,
300 and 400 ml of Japanese Sake which contains 16% vlv of ethanol. In such
cases, the blood ethanol concentration reaches a peak in an hour following
ingestion [14-161, but as shown in Figure 4, in the cases reported here, the
blood ethanol concentration peaks two hours following the intake of an
ordinary Japanese meal [15].
1
loo
Meal
I/
ingestion
of Sake
0
5
2
1
6
7
Time
3
8
4
9
300 ml (n = 7)
200 rnl (n = 59)
5 hrs
10 pm
FIGURE 4 Plasma ethanol concentration curve after a normal Japanese meal (Case I),
superimposed upon the blood ethanol concentration curves after ingestion of 200, 300 and
400 ml of Japanese Sake in healthy males [15].
Candida albicans was recovered in the majority of cases. Causative agents in
descending order are: C. albicans, 21 cases; C. tropicalis, 6; Saccharomyces,
4; Torulopsis glabrata and brown yeast, 2 each; C. fukuoka Sato, C. krusei,
C. guilliermondii and C. stelloidea, 1 each. As C. albicans is one of the
normal flora in the human gastrointestinal tract and its presence increases in
several gastrointestinal disorders [17-191, we must consider factors which
appear to play important roles in the abnormal proliferation of the agents
and marked alcohol fermentation occurring in certain hosts.
Most cases described have shown various gastrointestinal abnormalities.
Twenty-one were cases of abdominal surgery, namely: gastrectomy (13);
laparotomy (6); and cholecystectomy (2). Organic or functional disturbances
of the passage of the gastrointestinal tract are also important factors, such as
post-operative blind loop formation, dilatation of the duodenum or small
intestine, and backflowing of duodenal content into the stomach. These
abnormalities cause the stagnation of digested foods and, at the same time,
possibly offer a favourable site for abnormal proliferation of the related
agents and alcohol fermentation. On rare occasions, however, no gastrointestinal abnormality was detectable. Secondary disturbances of the normal
intestinal flora due to the frequent medical use of antibiotics seems to be
another factor.
The optimum pH for C. albicans activity lies between 2-8 and 6.0, and it
utilizes glucose, maltose and sometimes galactose as the substrates for
alcohol fermentation. Therefore, hypoacidity of the stomach, the predigestion of carbohydrates and the back flow of duodenal contents into the
stomach or the stagnation of substrate in the intestine all provide a
favourable environment.
In contrast to normal gastrointestinal moniliasis, histopathological changes
have not been detected [20-311. This syndrome is therefore characterized as
gastrointestinal parasitism of microflora and so, in most cases, it is easily
cured by the administration of antifungal agents such as Trichomycin,
Amphotericin B or Mycostatin. In some cases, the symptoms disappear
spontaneously. Surgical treatment to remove the site of fermentation can be
effective (10 out of 39 cases).
As stated above, the intragastrointestinal alcohol fermentation syndrome
consists of the following essential factors: parasitism and abnormal
proliferation of the causative agent, mainly the Candida group, which is
capable of alcohol fermentation in the alimentary tract; abnormal stagnation
of foods caused by organic or functional disorders of the alimentary tract;
intake of a carbohydrate diet as the substrate for the alcohol fermentation;
and a low threshold of the host patient to alcohol.
At present, such cases have been rarely reported outside Japan. Although
not a scientific paper, there was a newspaper report of an American man's
memoirs in 1977, indicating he had the syndrome [32]. Additional cases
should exist in many other countires. All those concerned with alcoholic
intoxication in clinical toxicology and in forensic medicine must bear this
syndrome in mind and should consider mycological examination as well as
sensitive biochemical analyses.
References
1. Harger RN. Perennial claims of endogenous alcohol or alcohol-like substances. In:
Proceedings of the Fourth International Conference on Alcohol and Traffic Safety.
Bloomington: Indiana University, 1965: 182-189.
2. Lester D . The concentration of apparent endogenous alcohol. Quarterly Journal of
Studies on Alcohol 1962: 23: 17-25.
3. Liebich HM, Al-Babbili 0 , Zlatkis A and Kim K. Gas chromatographic and mass
spectrometric detection of low molecular weight aliphatic alcohols in urines of normal
individuals and patients with diabetes mellitus. Clinical Chemistry 1975; 21: 12941296.
4. Liebich HM, Buellow HJ and Kallmayer R. Quantification of endogenous aliphatic
alcohols in serum and urine. Journal of Chromatography 1982; 239: 343-349.
5. Ball W and Lichtenwalner M. Ethanol production in infected urine. New England
Journal of Medicine 1979; 301: 614.
6. Sato M. On moniliasis of the alimentary tract with alcoholic fermentation produced
therein. Fukuoka Acta Medica 1952; 43: 1013-1029.
7. Kaji H , Ide H, Aikawa T and Murao M. Evaluation of the fasting level of the expired
alveolar acetone concentration. Journal of the Japan Diabetic Society 1974; 17:
453-456.
8. Baker RN, Alenty A L and Zack JF, Jr. Simultaneous determination of lower alcohols,
acetone and acetaldehyde in blood by gas chromatography. Journal of Chromatographic Science 1969; 7: 312-314.
9. Palo V and Ilkova H. Direct gas chromatographic estimation of lower alcohols, acetaldehyde, acetone and diacetyl in milk products. Journal of Chromatography 1970; 53:
363-367.
10. Jain NC. Direct blood-injection method for gas chromatographic determination of
alcohols and other volatile compounds. Clinical Chemistry 1971; 17: 82-85.
11. Lodder J and Kreger-van Rij NJW. The yeast; a taxonomic study. Amsterdam: North
Holland Publishing Company, 1952.
12. Hosoya S, Komatsu N, Soeda M, Yuwaguchi T and Sonoda Y. Trichomycin, a new
antibiotic with trichomonacidal and antifungal activities. Antibiotics 1952; 5: 564-566.
13. Waksman SA and Lechevalier HA. The actinomycetes. Volume 111. Baltimore: The
Williams and Wilkins Company, 1962: 397.
14. Fukui Y. Gas chromatographic determination of acetaldehyde in the expired air after
ingestion of alcohol. Japanese Journal of Legal Medicine 1969; 23: 24-40.
15. Hishida S, Kinoshita M, Ijiri I, Okada T , Adachi J and Mizoi Y. Studies on the ratio
between alcoholic concentrations in urine and blood. Japanese Journal of Legal
Medicine 1973; 27: 295-306.
16. Lindros KO, Stowell A , Pikkarainen P and Salaspuro M. Elevated blood acetaldehyde
in alcoholics with accelerated ethanol elimination. Pharmacology, Biochemistry and
Behavior 1980; 13 (Supplement 1): 119-124.
17. Donaldson RM, Jr. Normal bacterial populations of the intestine and their relation to
intestinal function. New England Journal of Medicine 1964; 270: 938-945, 994-1001,
1050-1056.
18. Takahashi K. Etiology and pathogenesis of so-called "drunkenness disease". Report of
the Hokkaido Institute of Public Health (Sapporo) 1968; 18: 50-57.
470
Finegold SM. Intestinal bacteria. The role they play in normal physiology, pathologic
physiology and infection. California Medicine 1969; 110: 455-459.
Maeda M, Kobayashi J, Hashimoto H, Yabuso S, Wakamatsu M and Yanagisawa T . A
case of drunkenness disease in the patient without operation of the stomach. Internal
Medicine and Pediatrics (Tokyo) 1962; 17: 77-82.
Iyo S, Ikeda M, Ohashi I, Asai T , Takashima T and Yokohama S. On so-called
Meitei-sho. Japanese Journal of Internal Medicine (Tokyo) 1966; 17: 881-888.
Sakakiyama Y, Shiramatsu K, Tozuka M and Suzuki A. Drunkenness disease induced
by the alcoholic fermentation in the alimentary tract (stomach). Journal of the
Japanese Practical Surgeon Society 1971; 32: 434-438.
Takasugi T and Takada T. Meitei-sho caused by the overgrowth of Candida albicans in
the intestinal tract. Clinical All-round (Osaka) 1960; 9: 2092-2095.
Kikuoka H, Masaoka T and Akagi M. A case of Meitei-sho caused by the intragastrointestinal alcohol fermentation. Japanese Journal of Clinics (Osaka) 1961; 19: 197-202.
Ezaki H, Funaoka H , Fukuma A and Saito H. Meitei-sho caused by the yeasts. Surgical Diagnostics and Treatment (Tokyo) 1961; 3: 1529-1534.
Hashimoto K, Matsuno H, Kato H and Tsuchiya N. A case of Meitei-sho caused by the
overgrowth of Saccharomyces in the intestine. Chemotherapy (Tokyo) 1961; 9: 24-25.
Kawabata K, Sugawara M, Hiraga H and Takahashi K. Drunkenness-like syndrome.
Japanese Transportation Medicine (Tokyo) 1963; 19: 308-314.
Tanaka K, Ideuchi H, Sakamoto S, Adachi S and Kitayama S. A case of gastrointestinal
Candidiasis with elevated blood and urinary amylase values and drunk-like symptoms.
Japanese Journal of Internal Medicine (Tokyo) 1967; 20: 359-362.
Yamashita Y, Inoue N, Shirabe T, Ohnishi A and Kuroiwa Y. A case of malabsorption
syndrome, "Meiteisho" (endogenous ethanol intoxication) and polyneuropathy. Clinical Neurology (Tokyo) 1974; 14: 17-23.
Kawanaka T , Nozaki T . Nakamura K, Kajimoto T, Asai T and Kanayama T . A
2-year-old surgically treated female case of so-called Meitei-sho. Operation (Tokyo)
1978; 32: 1249-1252.
Shy CY, Sugiyama M, Eto S, Tsuchiya S and Nagaoka H. A case of gastric Candidiasis
with alcoholemia. Japanese Journal of Gastroenterology (Tokyo) 1982; 79: 13181321.
National Enquirer. 30586-2. November 1, 1977.