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120 J. Allen and P. C. Belafsky
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endoscopy. Given that self-reported questionnaires
are noninvasive, simple, and cheap, they may be
instituted easily in practice. Broadly speaking,
instruments may be symptom severity rating scales or
quality of life scales. We will discuss only three
scales as a representative sample.
8.1.1 Reflux Disease Questionnaire
Designed to act as a diagnostic tool for GERD, the
12-item Reflux Disease Questionnaire (RDQ) has
now been used as both an outcome measure and a
diagnostic tool (Shaw et al. 2001, 2008; Nocon et al.
2008; Dent et al. 2010) (see Appendix). Developed by
Shaw et al. (2008), it is a 12-item scale grouped into
three subscales—heartburn, regurgitation, and dyspepsia. It is validated and has been tested for
responsiveness. The RDQ has subsequently been
translated and validated in Swedish and Norwegian. It
has been used as a symptom survey to monitor
symptom severity over time in patients enrolled in the
ProGERD study in Europe, showing useful stability
and reproducibility (Nocon et al. 2008) and in the
Diamond study comparing diagnostic tools in reflux
disease (Dent et al. 2010). One interesting aspect of
this survey instrument is the lack of use of the word
‘‘heartburn.’’ Initial development suggested that this
word was poorly understood by patients, and that a
‘‘word picture’’ was better in conveying the symptom,
i.e., burning rising up from the stomach behind the
breastbone (Dent et al. 2010). The primary advantages of this survey are its conciseness, short completion time, adapted patient wording describing
symptoms clearly, and cross-cultural validation. The
primary limitations are inclusion of more than one
disease profile (i.e., GERD and dyspepsia), long recall
period, uncontrolled treatment in the patient validation population, a diagnostic accuracy equal to that of
physician assessment, and variable scoring system.
8.1.2 Gastro-oesophageal Reflux Disease
Impact Scale
Jones et al. (2007) proposed the Gastro-oesophageal
Reflux Disease Impact Scale (GIS) as a management
tool for primary care physicians (see Appendix). The
survey aims to assist patients in conveying GERD
severity and impact, and to prompt clinicians to
enquire about reflux-related symptoms. GIS is a nineitem scale with a 1-week recall period that can be
completed in a matter of minutes. It has been
validated, and tested for responsiveness. Primary care
physicians using the scale found it helped direct
treatment decisions and assess treatment effectiveness. It has been utilized and reported by Gisbert et al.
(2009), as part of the multinational European RANGE
(Retrospective Analysis of GERD) study. Louis et al.
(2009) reported the GIS correlated well with physician-assessed GERD severity, and was sensitive to
treatment changes over time. The primary advantages
of this survey are the multidimensionality of the
survey (symptoms and impact of GERD) and the
brevity of the survey. The primary limitations of this
survey are the tendency for results clusters and lack of
diagnostic precision (GER vs dyspepsia vs functional
heartburn).
8.1.3 Reflux Symptom Index
The Reflux Symptom Index (RSI) is a nine-item self
administered survey that asks patients to rate on a
scale of 0–5, with 0 being no problem and 5 being all
the time, how much a particular symptom bothered
them over the past month (Belafsky et al. 2002)
(see Appendix). Total scores range from 0 to 45. In
validation studies, the upper limit of 95% confidence
intervals in normal controls was 13.6. Scores greater
than 13 may suggest LPR playing a significant role in
symptom production. Despite conflicting studies in
support of and against the use of the RSI, it remains a
simple, cheap, and reproducible tool, which most
patients can answer in an expeditious fashion. It
includes most of the accepted symptoms that are
thought to be associated with LPR. Criticisms of the
RSI have included the lack of frequency modifiers and
missing symptom items such as throat pain and
burning, and bundling of more than one symptom
together. The review of Musser et al. (2010) of rating
scales in extraesophageal reflux, although critical of
the predictive value of the RSI, actually demonstrated
significant correlation of the RSI with reflux area
index at pH 4, a new proposed measure that normalizes frequency, duration, and acidity of reflux
episodes for the total time of the study.
The greatest contribution of self-reported scales is
their role in reflecting changes over time in the same
patient, whether treatment is given or not. Subjectivity of symptom reporting differs hugely between
patients, but will be more consistent in the same
patient, and reflects the patient’s level of disease
burden. Reflux is a symptom-driven disease and what
Gastroesophageal Reflux Disease, Globus, and Dysphagia 121
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matters most is how the patient feels. Use of symptom
indices and endoscopic grading systems in treatment
outcome studies is necessary to allow comparison of
relative disease severity (in selected test and control
populations), and response to intervention.
8.2 pH Studies
Currently considered the gold standard for diagnosing
both GERD and LPR, the pH study is expensive,
relatively hard to perform or at least time-consuming,
and not by any means 100% sensitive or specific for
reflux disease (Vaezi et al. 2006; Arevalo et al. 2011).
Inclusion of impedance studies is now advocated for
detection of nonacid reflux and volume reflux that
may cause symptoms aside from those due to drop in
pH (Arevalo et al. 2011). pH and impedance studies
may be more specific but are poorly sensitive in this
remitting disease, and the appropriate diagnostic criteria remain unclear. Detection of these conditions in
the pharynx is poor, and the study may be poorly
tolerated in many patients. Patients may find the
probe uncomfortable and unsightly and may alter
daily behaviors, which reduces the reliability of the
test. One in eight patients will remove the probe
before a complete study can be recorded (Kotby et al.
2010). In the performance of the study, placement of
the probe remains controversial, and probe-related
artifacts from drying can be an issue. In diagnosis of
GERD, established normative data suggest that prolonged acid times (more than 4% of 24 h spent at
pH \ 4) are associated with increasing mucosal
injury (Vaezi et al. 2006; Arevalo et al. 2011).
However, it is apparent that a group of patients with
normal acid contact times still have symptoms related
to reflux, and this group has been termed ‘‘sensitive
esophagus’’ (Arevalo et al. 2011). Furthermore,
abrupt esophageal distension that may occur in liquid
or gaseous/liquid reflux may also give rise to symptoms via mechanoreceptors (Arevalo et al. 2011), and
without impedance testing these episodes are unlikely
to be detected. In a recent metanalysis, Kotby et al.
(2010) quoted an overall sensitivity of pH studies in
the range of 50–80%. Almost one third of patients
with endoscopically visualized esophagitis will have
completely normal findings in a pH study. Are the
norms asserted for the esophagus applicable to the
pharynx? The increasing body of literature in this
area suggests not. It is likely that much higher pHs
(i.e., those closer to neutral) are still injurious to the
laryngopharynx (Postma 2000; Merati et al. 2005).
8.3 Proton Pump Inhibitor Trial
Empirical trial of PPI medication may appear to be an
appealing option. If acid production and its reflux
were the cause of symptoms, then a potent inhibitor of
gastric acid secretion should produce definitive
symptom control. Good quality, randomized controlled trials of PPI in treatment of pH-documented
GER still fail to show an unequivocal benefit in terms
of symptoms or objective endoscopic findings. Only
60% of patients with erosive esophagitis treated with
PPI show a complete symptomatic response (Arevalo
et al. 2011). In patients with nonerosive esophagitis,
the response rate is a dismal 40% (Arevalo et al.
2011; Mainie et al. 2006). In a multicenter study using
combined multiluminal impedance and pH monitoring, 37% of 168 patients with persisting symptoms
despite twice daily PPI treatment had a significant
symptom association with nonacid reflux episodes
(Mainie et al. 2006). Even more important, 11% of
patients demonstrated symptoms with continued acid
reflux on combined multiluminal impedance and pH
monitoring, suggesting that PPI cannot control gastric
acid secretion completely in some individuals (Mainie
et al. 2006). Numans et al. (2004) undertook a metaanalysis of studies reporting the ‘‘PPI test.’’ This
demonstrated that the PPI test showed a low likelihood ratio and specificity of only 54% in diagnosing
GERD (Numans et al. 2004). Qadeer et al. (2006)
undertook a meta-analysis of randomized controlled
trials of PPI in treatment of reflux. They found only a
modest nonsignificant improvement in symptoms
with PPI therapy (Qadeer et al. 2005, 2006).
Acid is not the only component of refluxate that
may cause injury. Other gastric refluxate components,
including bile acids and pepsin, and the mere volume
itself may result in dysfunction (Johnston et al. 2004,
2007; Galli et al. 2002; Tack 2005; Strugala et al.
2009). PPI will not abrogate the effects of these
components. Johnston et al. (2007) have demonstrated
endocytosis of pepsin into laryngeal epithelium, and
activity of pepsin up to pH 6.5. In fact, pepsin is not
irreversibly deactivated until it is exposed to pH 8.
This may explain some of the negative effects of
122 J. Allen and P. C. Belafsky
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nonacid or weakly acid reflux. There is ongoing
debate about the dose and duration of treatment of PPI
medication, and more concerning, new evidence
suggesting that PPIs are not as benign as we once
thought. Significant decrease in calcium absorption
has been documented in women receiving long-term
treatment, with increase in osteoporosis and hip
fracture risk in those taking PPI for prolonged periods. These medications interact with some drugs,
including the platelet inhibitor clopidogrel, and alone
they have a side effect profile that includes gastric
upset, bloating, rash, myalgia, and depressed mood.
They also remain expensive medications, especially
newer-generation formulations.
Finally, it has now become clear that use of a PPI
can result in reflex acid hypersecretion when treatment is terminated, which then leads to false-positive
reinforcement to the patient that he or she is indeed
suffering from acid reflux (Reimer et al. 2009). This
rebound effect may last as long as 4 weeks and may
be induced by only 8 weeks of therapy. Trial of
medications (primarily PPI) runs the risk of medication side effects, lack of therapeutic effect in nonacid
reflux or with other gastric refluxate components, and
inducing rebound hypersecretion.
have demonstrated characteristic dilated intercellular
spaces in esophageal biopsies of patients with laryngeal symptoms only, and with both laryngeal and
typical GER symptoms, compared with normal controls. Identification of pepsin in tissue or fluid aspirates (e.g., from middle ear, lung) has been suggested
as a surrogate marker for reflux, and may well prove
to be useful over time (Johnston et al. 2003, 2004,
2004; Knight et al. 2005; Tasker et al. 2002; Fox
2011). A new test kit, the Peptest lateral flow device
(RD Biomed, Hull, UK) uses a latex bead monoclonal
antibody to identify pepsin in saliva in the manner of
a pregnancy test. Results take only 5 min to obtain
and it may be more useful in primary practice as a
diagnostic tool for reflux (Fox 2011). Further testing
is awaited.
A history consistent with GERD or LPR and
examination findings of laryngopharyngeal inflammation or complications of reflux disease support a
clinical diagnosis of reflux. At this point clinicians
differ in their view as to what is the most appropriate
next step.
9 Investigation
8.4 Endoscopy and Biopsy
Looking at tissue from the area affected at a microscopic and cellular level would, on the face of it,
appear to be a definitive diagnostic process. However,
ulceration, inflammation, eosinophilia, fibrosis,
metaplasia, and dysplasia may be suggestive of reflux
damage but are not pathognomonic or diagnostic of
reflux on light microscopy (Wada et al. 2009). Many
biopsies from patients with typical reflux symptoms
show completely normal findings. Endoscopy has
weak correlation with symptoms. It is a good screen
for reflux complications but has low diagnostic sensitivity. The site of biopsy—the pharynx, upper
esophagus, distal esophagus—may affect findings.
Acquiring tissue is mildly uncomfortable, may require
sedation, is relatively time intensive and expensive,
and requires highly specialized tools and practitioners. Esophageal electron microscopy studies suggest
that dilated intercellular spaces are correlated with
GER (Park et al. 2010; Fox 2011). Park et al. (2010)
The options for investigation include those mentioned
earlier—pH-metry, manometry, endoscopy, and
VFSS. Peng et al. (2010) reported 469 Chinese
patients presenting with typical symptoms of GERD
(heartburn or regurgitation). All patients underwent
early endoscopic evaluation, with 38.4% demonstrating clinically significant endoscopic findings
(esophagitis, Barrett’s metaplasia, peptic ulcer, carcinoma). Peng et al. (2010) recommended early
endoscopy for both diagnosis and identification of
complications. In-office endoscopic screening is well
tolerated, safer, and cheaper than a sedated esophagoscopy, and these findings support early TNE in the
management of GER and LPR (Postma et al. 2005;
Rees 2007; Belafsky and Rees 2009). Contrast
imaging studies are widely used in the diagnosis of
dysphagia. Videofluoroscopy for diagnosis of GERD,
however, is poorly sensitive and its use is not routinely indicated without other symptoms being present. Provocative testing during VFSS may
demonstrate active GER but will rarely demonstrate
LPR.
Gastroesophageal Reflux Disease, Globus, and Dysphagia 123
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Table 5 Lifestyle modifications recommended in gastro-
esophageal and laryngopharyngeal reflux disease
Elevate head of bed (more than
10 cm)
Smoking cessation
Avoid lying down within 2 h of
meal
Sleep on left side
Weight loss and regular exercise
Chew gum (sugar free)
Small frequent meals
Avoid refluxogenic
foods
Alcohol
Fatty foods
Chocolate
Spicy food
Tomato products
Peppermint
Citrus fruits
10 Management
Therapeutic options for reflux disease begin with lifestyle modifications (Table 5). Avoidance of refluxogenic foods, alcohol, caffeine, and smoking is
recommended. Positioning with the head elevated
during sleep, ensuring gastric emptying by not lying
down for at least 2 h after meals, and regular exercise
with weight loss may help symptomatic reflux. As yet
there are no randomized controlled trials demonstrating efficacy of lifestyle changes alone.
10.1 Medications
The most potent and effective medications for GERD
are PPIs. These reduce stomach intraluminal acid
secretions by blocking end-organ function (H
ATPase pumps). No tolerance effect is seen; however,
rebound hypersecretion can occur if use of these
medications is discontinued abruptly, leading to a flare
of symptoms. This may occur after only 8 weeks of
therapy (Qadeer et al. 2005). The dose and duration of
therapy are debated and different depending on whether the patient is deemed to have GERD or LPR. In
GERD, response to therapy is seen at lower doses
often with once daily regimens; however, in LPR
patients twice daily administration is usually required,
with higher doses at each time point (Park et al. 2005).
The rate of response in nonerosive reflux disease may
be lower than expected, with one study demonstrating
only 40% response to PPI treatment in patients diagnosed with nonerosive reflux disease (Dean et al.
2004). Randomized controlled trials have failed to
show unequivocal improvement in LPR patients
+/K+
receiving PPIs however, and debate remains over the
appropriate duration of treatment (ranging from 4 to
12 weeks) (Postma et al. 2002; Koufman 2002;
Noordzij et al. 2001; Steward et al. 2004). Histamine
type 2 receptor antagonists (H2RA) reduce gastrin
secretion and therefore overall acid secretion in the
stomach. H2RAs have a short onset of action (less than
1 h) but also reduced effective period (less than 12 h).
They are effective in healing esophagitis in approximately 50% of cases, but are less effective than PPIs in
the resolution rate of symptoms, ulcer healing, and
relapse of both mucosal disease and symptoms
(Meneghelli et al. 2002; Caro et al. 2001; Farley et al.
2000). Patients taking these medications develop
tachyphylaxis or a drug tolerance effect with longterm usage. Instituting a ‘‘drug holiday’’ such as a
week off therapy every 3 weeks may limit this effect.
Although acid suppression with PPI treatment is
profound, these medications do not prevent reflux—
rather they only make it nonacid. Physical reflux
barriers such as magnesium sulfate or aluminium
sulfate suspensions, alginates, and sucralfate may
provide protection against volume reflux (Strugala
et al. 2009; Tang et al. 2005; McGlashan et al. 2009;
Dettmar et al. 2006). McGlashan et al. (2009) demonstrated equivalent success in treating symptoms of
LPR with liquid alginate alone compared with PPIs.
Dettmar et al. (2006) demonstrated faster onset of
action with liquid alginate than with either H2RAs or
PPI. Alginates are polysaccharide copolymers that
form a meshlike gel structure which can act as a
biological sieve (Strugala et al. 2009). The properties
of the gel can be altered by changing the relative
proportions of guluronic acid and mannuronic acid in
the mix. This adjusts the cross-linking and changes
the pore sizes within the gel mesh, critically changing
the permeability of the substance (Strugala et al.
2009; Tang et al. 2005). Tang et al. (2005) demon-
strated that adhered alginate gel significantly reduced
both proton (acid) diffusion and pepsin diffusion in a
dose-dependent fashion. Strugala et al. (2009) showed
reduced pepsin diffusion in alginate, by up to 82%
compared with controls. Furthermore, the alginate
used in their study significantly retarded diffusion of
bile acids as well. They simulated repeated reflux
events by using multiple 5-ml-aliquot exposures of
pepsin and bile acids. Even after ten exposures,
alginate gel absorbed 50% of pepsin in the sample
(Strugala et al. 2009). Alginate gel will coat mucosal
124 J. Allen and P. C. Belafsky
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both no effect and a significantly beneficial effect of
fundoplication in selected patients presenting with
extraesophageal manifestations (Westcott et al. 2004;
Lindstrom et al. 2002; Swoger et al. 2006; Luostarinen 1993; Shaw et al. 2010; Catania et al. 2007).
Fundoplication may play an increasing role in treatment of nonacid reflux (Arevalo et al. 2011). Novel
procedures to reduce GER such as endoscopic suture
plication, radio-frequency energy treatment, and
injection of the lower esophageal sphincter are under
investigation but there are no long-term data to support their implementation at this time.
Fig. 8 Photomicrograph of hamster cheek pouch demonstrat-
ing three squamous cell carcinomas induced by pepsin and
7,12-dimethylbenz[a]anthracene, a known carcinogen
surfaces and can stay adherent for up to 60 min
without being washed off by saliva flow (Tang et al.
2005). Thus, alginate gel may act like gastric mucus,
forming a physical barrier to diffusion of acid and
pepsin, and preventing contact with the cell surface
and subsequent damage (Strugala et al. 2009; Tang
et al. 2005). Allen et al. (2011), using a hamster
model of carcinogenesis, demonstrated a significant
reduction in tumor growth and proliferation in hamsters treated with alginate versus controls (Fig. 8).
Use of prokinetics agents or c-aminobutyric acid B
agonists is under investigation. Treatment with baclofen has demonstrated increased lower esophageal
sphincter tone and reduced transient lower esophageal
sphincter relaxations (Ciccaglione and Marzio 2003;
Koek et al. 2003). Side effects include nausea, dizziness, and drowsiness which may improve over time.
10.2 Surgery
In refractory cases of GERD or LPR where medical
therapy is unhelpful, or in cases complicated by large
herniae, subglottic stenosis, brittle airway disease, or
cancer, consideration of surgical intervention is warranted. Fundoplication is successful in reducing
symptoms in the vast majority of patients with typical
GER symptoms (Mainie et al. 2006). In those with
extraesophageal symptoms, there is debate as to the
role of fundoplication. Studies have demonstrated
11 Globus
Globus is a symptom rather than a diagnosis. Previously considered a hysterical manifestation, it is now
recognized as being a symptom generated from
largely organic dysfunction. This is reflected by a
change in terminology to globus pharyngeus. Globus
pharyngeus may be used to describe a ‘‘lump in the
throat’’ sensation, throat irritation, fullness in the
throat, or even effortful swallowing. The cause of this
symptom is likewise varied. There may be an association with esophageal reflux and particularly proximal esophageal refluxate excursion. Both the
presence of material in the proximal esophagus and
slow distension of the proximal esophagus are known
to result in reflex contraction of the UES (Szczesniak
et al. 2010; Lang et al. 2001), whereas rapid distension may result in UES relaxation (Szczesniak et al.
2010). This protective contraction acts to prevent
refluxate escaping into the pharynx and subsequently
threatening the airway, whereas the relaxation of the
UES enables eructation. It is suggested that intermittent recurrent reflux episodes result in a state of
hypertension or hyperactivity in the UES, particularly
the cricopharyngeal component. This mechanism is
also proposed as the cause of cricopharyngeal bar.
Szczesniak et al. (2010) have demonstrated an
enhanced esophago-UES relaxation response in
patients with symptoms of reflux laryngitis and
suggested that this heightened belch response may
contribute to symptoms. The sensation of a lump in
the throat may be due to a lump in the throat.
Vallecula cysts, lingual tonsillar hypertrophy, long
uvula, and lingual thyroid tissue may all cause globus
sensation.
Gastroesophageal Reflux Disease, Globus, and Dysphagia 125
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behavioral changes such as sipping water, or reflux
12 Investigation
lifestyle modifications. In many cases patients require
aggressive antireflux therapy with medication. Muscle
Patients presenting with globus as a symptom require
full evaluation to ensure no obstructive lesion is
responsible. This may entail endoscopy, contrast
imaging studies, e.g., VFSS, or computed tomography,
depending on other symptoms. If the findings are normal, consideration of pH/manometrystudies to examine
the UES region looking for a hypertensive or poorly
compliant UES may be helpful. Esophageal disease
relaxant medications such as diazepam have been
used successfully in some patients and there are
anecdotal reports of empiric balloon dilation of the
UES showing promise (C.J. Rees, unpublished data).
If investigations suggest a cricopharyngeal bar or
hypertensive UES, consideration of balloon dilation,
botulinum toxin injection, and rarely cricopharyngeal
myotomy may be required.
commonly results in a feeling of discomfort in the cervical region. Smith et al. (1998) demonstrated that 58%
of patients with a marshmallow impacted at the distal
14 Conclusion
esophagus complained of cervical dysphagia. One third
of patients with globus, cough, or cervical dysphagia
have an esophageal cause (Smith et al. 1998).
Swallowing disorders are common and will increase
in prevalence in the coming decades. Dysphagia is
intimately related to GERD and globus, and investi-
gation and treatment of all conditions is best accom-
13 Treatment
plished by thorough investigation and appropriate
multidisciplinary-team-based therapy.
Treatment should be directed at the underlying cause
of globus. If there is a mass lesion present, this should
be addressed. Patients may benefit from reassurance,
15 Appendix
Table A.1 Ten-item Eating Assessment Tool (EAT-10) (Belafsky et al. 2008)
My swallowing problem has caused me to lose
weight
My swallowing problem interferes with my ability
to go out
Swallowing liquids takes extra effort 0 = no
Swallowing solids takes extra effort 0 = no
Swallowing pills takes extra effort 0 = no
Swallowing is painful 0 = no
The pleasure of eating is affected by my swallowing 0 = no
When I swallow food sticks in my throat 0 =
I cough when I eat 0 = no
Swallowing is stressful 0 = no
0 = no
problem
0 = no
problem
problem
problem
problem
problem
problem
no
problem
problem
problem
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
1 = slight 2 = mild 3 = moderate 4 = severe
126 J. Allen and P. C. Belafsky
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Table A.2 Reflux Symptom Index (RSI) (Belafsky et al. 2002)
In the last month how did the following problems affect you?
(1 = no problem, 5 = all the time)
Hoarseness or a problem with
your voice?
Clearing your throat 0–5
Excess throat mucus or postnasal drip 0–5
Difficulty swallowing food, liquids,
or pills
Coughing after you ate or after
lying down
Breathing difficulties or choking
episodes
Troublesome or annoying cough 0–5
Sensation of something sticking in your
throat or a lump in your throat
Heartburn, chest pain, indigestion,
or stomach acid coming up
0–5
0–5
0–5
0–5
0–5
0–5
Reflux Disease Questionnaire (RDQ) (Shaw et al.
2001)
Three domains (heartburn, regurgitation, dyspepsia)
Acid taste frequency
Acid taste severity
Movement of materials severity
Movement of materials frequency
Frequency of pain behind the breastbone
Frequency of burning behind the breastbone
Severity of burning behind the breastbone
Severity of pain behind the breastbone
Upper stomach burning severity
Upper stomach burning frequency
Upper stomach pain frequency
Upper stomach pain severity
Gastro-oesophageal Reflux Disease Impact Scale
(GIS) (Jones et al. 2007)
Subjects make one of four responses—daily, often,
sometimes, or never:
1. How often have you had the following symptoms:
Pain in your chest or behind the breastbone?
Regurgitation or acid taste in your mouth?
Pain or burning in your upper stomach?
Sore throat or hoarseness that is related to your
heartburn or acid reflux?
2. How often have you had difficulty getting a good
night’s sleep because of your symptoms?
3. How often have your symptoms prevented you
from eating or drinking any of the foods you like?
4. How frequently have your symptoms kept you from
being fully productiveinyour job or dailyactivities?
5. How often do you take additional medication other
than what the physician told you to take (such as
Tums, Rolaids, Maalox)?
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