- Volume 13, Issue 2
Irritable bowel syndrome, chronic gastritis, smoking, depression,
haemorrhoids and urolithiasis
Onder Tonyali (1)
Mustafa Yaprak (1)
Mustafa Cem Algin (2)
Abdulrazak Abyad (3)
Lesley Pocock (4)
(1) Specialist of Internal Medicine, MD
(2) Specialist of General Surgery, MD
(3) Middle-East Academy for Medicine of Aging, MD
(4) medi+WORLD International
:Mehmet Rami Helvaci, MD
07400, ALANYA, Turkey
Received: January 2019; Accepted: February 2019; Published:
April 1, 2019
Citation: Helvaci M. R. et al. Irritable bowel syndrome,
chronic gastritis, smoking, depression, haemorrhoids
Middle East Journal of Nursing 2019; 13(2): 29-34. DOI:
Background: We tried to understand whether
or not there are some significant relationships between
irritable bowel syndrome (IBS), chronic gastritis (CG),
smoking, depression, haemorrhoids, and urolithiasis
in the present study.
Method: IBS is diagnosed
according to Rome II criteria in the absence of red
flag symptoms including pain and diarrhea that awakens/interferes
with sleep, weight loss, fever, and abnormal physical
examination findings which are not compatible with IBS.
Results: The study included
647 patients with the
IBS and 340 control cases. Mean age of the IBS patients
was 41.4 ± 14.4 (15-86) years. Interestingly,
64.2% of the IBS patients were female. Prevalence of
CG (78.3% versus 15.0%), history of antidepressant use
(48.0% versus 15.5%), smoking (36.4% versus 20.5%),
haemorrhoids (36.1% versus 7.0%), and urolithiasis (23.3%
versus 9.4%) were all significantly higher in the IBS
group (p<0.001 for all).
Conclusion: IBS may
be a low-grade inflammatory process being initiated
with infection, inflammation, smoking, anxiety, depression,
sleep disorders, cancer fear, or death fear-like stresses,
and eventually terminates with dysfunctions of the gastrointestinal
and genitourinary tracts of the body. Probably there
are highly significant relationships between IBS, CG,
smoking, depression, haemorrhoids, and urolithiasis.
Key words: Irritable
bowel syndrome, chronic gastritis, smoking, depression,
Recurrent upper abdominal discomfort may be the cause of nearly
half of applications to Internal Medicine Polyclinics (1).
Although gastroesophageal reflux disease, esophagitis, duodenal
or gastric ulcers, erosive gastritis or duodenitis, celiac
disease, chronic pancreatitis, and malignancies are found
among possible causes, irritable bowel syndrome (IBS) and
chronic gastritis (CG) may be two of the most frequently diagnosed
disorders among all. Flatulence, periods of diarrhea or constipation,
repeated toilet visits due to urgent evacuation or early filling
sensation, excessive straining, feeling of incomplete evacuation,
frequency, urgency, reduced feeling of well-being, and eventually
disturbed social life are often reported by the IBS cases.
According to literature, 10-20% of general population have
IBS, and it is more common in females with yet unknown reasons
(2). Although many patients relate onset of symptoms to intake
of food, and often incriminate specific food items, a meaningful
dietary role is doubtful both in the IBS and CG. Although
smoking is more common in males (3), psychological factors
and smoking seem to precede onset or exacerbation of gut symptoms,
and many potentially psychiatric disorders including anxiety,
depression, sleep disorders, cancer fear, or death fear frequently
coexist with the IBS (4, 5). For example, thresholds for sensations
of initial filling, evacuation, urgent evacuation, and utmost
tolerance recorded via a rectal balloon significantly decreased
by focusing the examiners attention on gastrointestinal
stimuli by reading pictures of gastrointestinal malignancies
in the IBS patients (6). So although IBS is described as a
physical instead of a psychological disorder according to
Rome II guidelines, psychological factors, cancer fear, death
fear, and smoking may be crucial for triggering of the physical
changes in the body. IBS is actually defined as a brain-gut
dysfunction according to the Rome II criteria, and it may
have more complex mechanisms affecting various systems of
the body with a low-grade inflammatory process (7). For example,
IBS may even terminate with CG, haemorrhoids, and urolithiasis
in a significant proportion of patients (8-10). Similarly,
some authors studied the role of inflammation via colonic
biopsies in 77 patients with the IBS (11). Although 38 patients
had normal histology, 31 patients demonstrated microscopic
inflammation and eight patients fulfilled criteria for lymphocytic
colitis. However, immunohistology revealed increased intraepithelial
lymphocytes as well as increased CD3 and CD25 positive cells
in lamina propria of the group with normal histology.
These features were more evident in the microscopic inflammation
group who additionally revealed increased neutrophils, mast
cells, and natural killers. All of these immunopathological
abnormalities were the most evident in the lymphocytic colitis
group who also demonstrated HLA-DR staining in the crypts
and increased CD8 positive cells in the lamina propria (11).
A direct link between the immunologic activation and IBS symptoms
was provided by work of some other authors (12). They demonstrated
not only an increased incidence of mast cell degranulation
in the colon but also a direct correlation between proximity
of mast cells to neuronal elements and pain severity in the
IBS (12). In addition to these findings, there is some evidence
for extension of the inflammatory process behind the mucosa.
Some authors addressed this issue in 10 patients with severe
IBS by examining full-thickness jejunal biopsies obtained
via laparoscopy (13). They detected a low-grade infiltration
of lymphocytes in myenteric plexus of nine patients, four
of whom had an associated increase in intraepithelial lymphocytes
and six demonstrated evidence of neuronal degeneration. Nine
patients had hypertrophy of longitudinal muscles and seven
had abnormalities in number and size of interstitial cells
of Cajal. The finding of intraepithelial lymphocytosis was
consistent with some other reports in the colon (11) and duodenum
(14). On the other hand, smoking is a well-known cause of
chronic vascular endothelial inflammation even in the gastrointestinal
and genitourinary tracts of the body. We tried to understand
whether or not there are some significant relationships between
IBS, CG, smoking, depression, haemorrhoids, and urolithiasis
in the present study.
The study was performed in the Internal Medicine Polyclinic
of the Dumlupinar University between August 2005 and March
2007. Consecutive patients with upper abdominal discomfort
were taken into the study. Their medical histories including
smoking habit, alcohol consumption, urolithiasis, and already
used medications including antidepressants at least for a
period of six-month were learned. Patients with devastating
illnesses including eating disorders, malignancies, acute
or chronic renal failure, cirrhosis, hyper- or hypothyroidism,
and heart failure were excluded. Current daily smokers at
least for six months and cases with a history of five pack-year
were accepted as smokers. Patients with regular alcohol intake
(one drink a day) were accepted as drinkers. A routine check
up procedure including C-reactive protein, serum albumin,
serum creatinine, thyroid function tests, hepatic function
tests, markers of hepatitis A virus, hepatitis B virus, hepatitis
C virus, and human immunodeficiency virus, serum IgA, urinalysis,
fresh fecal sample examination, a posterior-anterior chest
X-ray film, an electrocardiogram, an abdominal ultrasonography,
an abdominal X-ray graphy in supine position, recto-sigmoidoscopy
in cases symptomatic for haemorrhoids, and a questionnaire
for IBS was performed. IBS is diagnosed according to Rome
II criteria in the absence of red flag symptoms including
pain and diarrhea that awakens/interferes with sleep, weight
loss, fever, and abnormal physical examination findings which
are not compatible with IBS. An upper gastrointestinal endoscopy
was performed, and sample biopsies were taken in case of requirement.
CG is diagnosed histologically, and infiltration of neutrophils
and monocytes into gastric mucosa is the hallmark of CG (15).
Additionally, microscopic examination shows stereotypical
changes in epithelium such as degeneration, focal intestinal
metaplasia, dysplasia, and glandular atrophy (15). An intravenous
pyelography was performed just in suspected cases from presenting
urolithiasis as a result of urinalysis and abdominal X-ray
graphy. So urolithiasis was diagnosed either by medical history
or as a result of current findings. Because of highly variable
clinical severity of celiac disease and high sensitivity and
specificity of endomysial antibody (EMA), EMA was used as
a screening test for celiac disease and jejunal biopsy was
planned just for EMA positive cases to be able to see absence
of villi and elongated crypts. Eventually, all patients with
the IBS were collected into the first, and age and sex-matched
controls were collected into the second groups. Prevalence
of smoking, antidepressant use, CG, haemorrhoids, and urolithiasis
were detected in each group and compared in between. Mann-Whitney
U test, Independent-Samples T test, and comparison of proportions
were used as the methods of statistical analyses.
The study included 647 patients with the IBS and 340 control
cases, totally. The mean age of the IBS patients was 41.4
± 14.4 (15-86) years. Interestingly, 64.2% (416) of
the IBS cases were female. Prevalence of CG (78.3% versus
15.0%), history of antidepressant use (48.0% versus 15.5%),
smoking (36.4% versus 20.5%), haemorrhoids (36.1% versus 7.0%),
and urolithiasis (23.3% versus 9.4%) were all significantly
higher in the IBS patients (p<0.001 for all) (Table 1).
Table 1: Comparison of patients with irritable bowel syndrome
and control cases
Although the presence of some social drinkers, there was not
any patient with regular alcohol intake among the study cases.
Additionally, we were not able to detect any patient with
Gastric acid is probably not involved in the etiology of CG
but psychological factors and smoking seem to be crucial for
the development. The highly significant relationship between
IBS, CG, and smoking in the present study and already known
importance of psychological factors in the development of
IBS and CG also support this hypothesis. Additionally, a meaningful
dietary role in CG is doubtful. Although some dietary habits
may trigger CG, these relationships may not always be seen
even in the same patients. The most important etiologic factor
of CG is chronic infection by bacillus Helicobacter pylori
(H pylori). Although H pylori is linked to CG, peptic ulcer,
gastric carcinoma, and mucosa-associated lymphoid tissue-
lymphoma (16), and it is recognised as a class I gastric carcinogen
(17), and it affects more than 50% of world population, just
a small subset of affected individuals experience H pylori-associated
disorders. Some possible symbiotic relationships may take
role between H pylori and the human body. In another definition,
H pylori infection may be beneficial for the human body to
some extent. This hypothesis is based on increased prevalence
of gastroesophageal reflux disease, Barretts esophagus,
and adenocarcinoma of esophagus after eradication of H pylori
in some countries (18). A recent study showed that H pylori
infection protects against gastroesophageal reflux and esophageal
carcinoma (18). So there may be a nearly symbiotic and balanced
relationship between the bacterium and the human body. The
colonization may either be beneficial or with a low biological
cost to the host. Eventually, the role of H pylori in CG is
obvious but why every patient with CG does not need
to visit a doctor? or why the patients are not
always symptomatic during the infection? are unknown.
We think that CG may actually be just one of the several end-points
of the IBS (9, 10). Although there is absence of a meaningful
dietary role in IBS, many patients relate onset of symptoms
to intake of food and often incriminate specific food items,
which may actually be a result of the significant association
of IBS with CG.
Urolithiasis is also an extremely
common pathology in society. For example, lifetime risk of
urolithiasis is around 15% for a white man and around 6% for
a white woman with a lifetime recurrence rate of up to 50%
(19). Approximately 80% of stones are composed of calcium
oxalate (CaOx) and calcium phosphate, and CaOx is their main
constituent. the remaining 10% of stones are struvite and
9% are uric acid stones. The majority of CaOx stone formers
do not suffer from any systemic disease (20). It is often
thought that oxalate is the primary problem in these patients
since excess oxalate is absorbed through the inflamed bowel
wall. Similarly, low-grade vascular endothelial inflammation-induced
increased absorption rate of oxalate may be one of the development
mechanisms of urolithiasis in the IBS. Since although indirectly,
increased oxalate absorption-induced urolithiasis was also
shown, previously (21, 22). We detected ratios of urolithiasis
as 15% in men and 13% in women prior(8). Interestingly, some
authors reported that relative risk of developing IBS was
detected as 2.48 times higher in patients with urinary stone
disease, and urinary stone disease should be considered as
an etiological factor of IBS (23). But actually we think of
IBS as a cause of urolithiasis instead of a result due to
its prolonged nature and frequently reported accompanying
urinary and gynecological symptoms (8). Although there is
male predominance of urolithiasis (19) against the female
predominance of IBS (2), the relationship between IBS and
urolithiasis may still be significant (8), and IBS may actually
be a cascade of many physiological events, being initiated
with infection, inflammation, smoking, and psychological disturbances
like many stresses, and eventually terminating with gut dysfunction.
So urolithiasis may be one of the several end-points of the
physiological events cascade, IBS. By this way, the
huge gap about the underlying etiologies of most of urolithiasis
cases may be explained by the high prevalence of IBS in society.
On the other hand, haemorrhoids are engorged fibrovascular
cushions lining the anal canal. Constipation, increased intra-abdominal
pressure, and prolonged straining predispose to haemorrhoids.
Almost one-half of Americans older than 50 years experience
symptomatic haemorrhoids (24). Bright red, painless rectal
bleeding just after defecation is the most common symptom.
It was detected that beside bleeding, pain, soiling, and prolapse,
many patients with grade 3-4 haemorrhoids have concomitant
functional bowel symptoms, possibly associated with IBS (25).
The low-grade inflammatory process all over the gastrointestinal
tract, smoking, excessive straining, repeated toilet visits,
and periods of constipation may be considered among possible
causes of haemorrhoids in the IBS patients (9).
Smoking-induced vasculitis may be
the most common type in society. Smoking is a major risk factor
for the development of atherosclerotic end-points including
coronary heart disease (CHD), peripheric artery disease, chronic
obstructive pulmonary disease (COPD), cirrhosis, chronic renal
disease, and stroke (26). Its atherosclerotic effects are
the most obvious in Buergers disease. Buergers
disease is an obliterative disease characterized by inflammatory
changes in small and medium-sized arteries and veins, and
it has never been reported in the absence of smoking in the
literature. Although there are well-known strong atherosclerotic
effects of smoking, some studies reported that smoking in
humans and nicotine administration in animals are associated
with a decreased body mass index (BMI) (27). Evidence revealed
an increased energy expenditure during smoking both on rest
and light physical activity (28), and nicotine supplied by
patch after smoking cessation decreased caloric intake in
a dose-related manner (29). According to an animal study,
nicotine may lengthen intermeal time and simultaneously decrease
amount of meal eaten (30). Additionally, BMI seems to be the
highest in the former, the lowest in the current and medium
in never smokers (31). Smoking may be associated with postcessation
weight gain but evidence suggests that risk of weight gain
is the highest during the first year after quitting and declines
over the years (32). Similarly, although CHD was detected
with similar prevalence in both genders in a previous study
(33), prevalence of smoking and COPD were higher in males
with CHD against the higher prevalence of BMI, white coat
hypertension, low density lipoproteins, triglycerides, hypertension,
and diabetes mellitus in females with CHD as the other atherosclerotic
risk factors. This result may indicate both the strong atherosclerotic
and weight decreasing roles of smoking (34). Similarly, the
incidence of a myocardial infarction is increased six-fold
in women and three-fold in men who smoke at least 20 cigarettes
per day (35). In other words, smoking is more dangerous for
women regardingthe atherosclerotic endpoints probably due
to the higher BMI and its consequences in them. Parallel to
the above results, the proportion of smokers is consistently
higher in men in the literature (3). So smoking is probably
a powerful atherosclerotic risk factor with some suppressor
effects on appetite. Smoking-induced weight loss may be related
to the smoking-induced chronic vascular endothelial inflammation
all over the body, since loss of appetite is one of the major
symptoms of inflammation in the body. Physicians can even
understand healing of their patients from their normalizing
appetite. Several toxic substances found in cigarette smoke
get into the circulation via the respiratory tract, and cause
a vascular endothelial inflammation until their clearance
from the circulation. But due to the repeated smoking habit
of the individuals, the clearance process never terminates.
So the patients become ill with loss of appetite, permanently.
In another explanation, smoking-induced weight loss is an
indicator of being ill instead of being healthy (29-31). After
smoking cessation, appetite normalizes with a prominent weight
gain in the patients but the returned weight is actually their
There may be several mechanisms terminating
with IBS, CG, haemorrhoids, and urolithiasis in smokers (36).
First of all, smoking-induced chronic vascular endothelial
inflammation all over the body may even disturb epithelial
function both for absorption and excretion in the gastrointestinal
and genitourinary tracts. These functional problems may terminate
with loose stool, diarrhea, constipation, and urolithiasis.
Secondly, diarrheal losses-induced urinary changes may even
terminate with urolithiasis (8, 9). Thirdly, smoking-induced
sympathetic nervous system activation may cause motility disorders
in the gastrointestinal and genitourinary tracts. Fourthly,
immunosuppression secondary to smoking-induced chronic vascular
endothelial inflammation all over the body may even cause
gastrointestinal and genitourinary tract infections causing
loose stool, diarrhea, and urolithiasis since some types of
bacteria can provoke urinary supersaturation and modify the
environment to form crystal deposits in the urine. In fact,
10% of urinary stones are struvite stones which are built
by magnesium ammonium phosphate-produced
during infection with bacteria that possess the enzyme, urease.
Similarly, prevalence of urolithiasis was significantly higher
in the IBS group in the present study (23.3% versus 9.4%,
As a conclusion, IBS may be a low-grade
inflammatory process being initiated with infection, inflammation,
smoking, anxiety, depression, sleep disorders, cancer fear,
or death fear-like stresses, and eventually terminates with
dysfunction of the gastrointestinal and genitourinary tracts
of the body. Probably there are highly significant relationships
between IBS, CG, smoking, depression, haemorrhoids, and urolithiasis.
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