Depression and Pancreatic Cancer

Oncology Unit, Third Department of Medicine, Athens School of Medicine,
Sotiria General Hospital. Athens, Greece.
Department of Clinical Oncology,
Yale School of Medicine and Cancer Center. New Haven, CT, USA
Although pancreatic carcinoma and depression have been linked for many years, the prevalence and relationship of these two entities
are still poorly understood. Published studies reviewing this issue have found that many patients with pancreatic cancer are
depressed. A clinical gestalt asserts that many patients present with depression before pancreatic carcinoma is diagnosed. If the
definition of depression is broadened to include mild depression in addition to major depression, these numbers may increase.
Depression in pancreatic cancer is a condition that must be diagnosed and treated, as studies have shown that depression is a
detrimental factor in the last stages of life of cancer patients as patients with high score of depression have worse survival rates in
breast and hepatobiliary cancers. Treatment for depression has also been shown to impact quality of life and may bring increased
comfort during end of life. This article reviews the literature linking pancreatic carcinoma to depression as well as the appropriate
therapeutic approach. In addition, for the first time, it fully underlines the key role of a social worker as a key participant throughout
the cancer continuum: at time of diagnosis, treatment, relapse, survivorship, end of life and bereavement in the management of
pancreatic cancer patients.
Several studies, dating back as early as the 1930s, have
been conducted in order to examine the association
between depression and pancreatic cancer [1]. A study
in 1967 showed that more than half of patients with
pancreatic cancer had psychological symptoms
occurring as early as 43 months before physical
symptoms [2]. When depression is considered a normal
phenomenon in cancer patients, its impact on the
quality of life is trivialized. This review studies the
literature regarding the association between depression
and pancreatic cancer as well the appropriate
therapeutic approach.
Depression has long been known to have greater
incidence in pancreatic cancer patients than in patients
with other malignancies. Fras et al. [2] conducted a
study based on patients admitted for possible
pancreatic or colon cancer and found that 76% of
patients with pancreatic cancer had depressive
symptoms prior to surgery as compared to 20% of
colon cancer patients. A retrospective study comparing
patients diagnosed with pancreatic and gastric cancers
reached the conclusion that depression was initially
present in 14% of patients with pancreatic cancer but in
only 4% of stomach cancer patients [3]. In 1986, two
prospective studies concerning the incidence of
depression in gastrointestinal tract malignancies were
conducted. Joffe et al. [4] concluded that 50% of
patients who were finally diagnosed with pancreatic
cancer met the criteria for the diagnosis of depression
while none of the patients that were finally diagnosed
with gastric cancer met the criteria. Holland et al. [5]
found that patients with pancreatic cancer in advanced
stages have more severe depression, anxiety and total
mood disturbance as compared to patients with other
advanced abdominal neoplasms. In 1993, 52 pancreatic
cancer patients were studied, out of which 71% had
depressive symptoms and 48% had “anxiety-related”
symptoms [6]. According to Massie et al. [7], the
prevalence of depression in people with pancreatic
cancer ranges from 33% to 50%.
Since the 1930s, a triad of symptoms has been
described preceding or accompanying the diagnosis of
pancreatic cancer of pancreatic cancer: depression,
Key words Depression; Epidemiology; Pancreatic Neoplasms;
/physiopathology; Therapeutics
Abbreviations MAOI: monoamine oxidase inhibitor; SSRI:
selective serotonin re-uptake inhibitor
Correspondence Muhammad Wasif Saif
Division of Medical Oncology, 333 Cedar Street, FMP 116, New
Haven, CT 06520, USA
Phone: +1-203.737.1569; Fax: +1-203.785.3788
Document URL

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anxiety and a sense of impending doom [1]. Symptoms
of clinical depression may include anorexia and weight
loss, but there might also be cachexia-related
symptoms misattributed to depression [8, 9, 10]. Other
common symptoms are negative thoughts and
behaviour, sleep disturbances, loss of interest and joy
in many aspects of daily life and feeling of
hopelessness. Level of fatigue has been found to
correlate significantly with depression levels [11, 12].
Symptoms may also include panic, social isolation or
even suicidal ideation [13]. Cognitive impairment may
be present, a phenomenon called depressive
pseudodementia, in which the patient’s results on the
Mini Mental State Examination (MMSE) are better
than expected [14]. Most studies have been based on
newly diagnosed patients, so there is danger of recall
bias influencing their psychological status.
Pain should be the first to be assessed and controlled
[14]. It has been found that it is a presenting symptom
in 80% of pancreatic cancer patients and has occurred
at some point of the disease in 90% of patients [15].
Kelsen et al. [16] concluded that increasing pain and
depressive symptoms were strongly correlated and that
patients awaiting to start chemotherapy had higher
levels of measured depression than did patients
awaiting surgery.
Diagnosis of Depression in Cancer Patients
Depression has been found to worsen a patient’s pain
and should not be considered “normal” in the
terminally-ill [17, 18, 19, 20]. After the diagnosis of
cancer, there is usually a process that patients go
through in order to cope: initial shock and denial of
diagnosis, anxiety and depressive symptoms, impaired
cognitive ability, a decreased appetite and a disrupted
sleep pattern. In 50% of patients, these symptoms
subside within 10 days with family support and
treatment that offers hope [14, 19]. The actual level of
psychological distress experienced by the patient
depends on:
1. medical factors: advanced disease, treatment, pain,
physical disability, family history of depression;
2. psychological factors: such as a patient’s coping
ability or history of depression. The patient’s
perception of cancer and its manifestations is
significant, mainly fear of losing control over body
functions and of painful death;
3. social factors: whether emotional and financial
support from family and friends is available (Table 1)
[13, 14, 19].
The physician should be able to recognize when this
distress exceeds “normal”. Intervention is needed when
depressive symptoms are highly disruptive or when
their intensity and duration are greater than expected,
provided that these do not qualify for diagnosis of a
depressive episode (Diagnostic and Statistical Manual
IV) [19]. Major depressive disorder is 4 times more
often in cancer patients [13].
While diagnosis of depression in physically healthy
patients is based on symptoms like anorexia, weight
loss and fatigue, which are common in cancer,
psychological or cognitive symptoms of depression
(hopelessness, loss of self-esteem, anhedonia, guilt,
suicide ideation) are the basis for diagnosing
depression in cancer patients [14, 19]. A physician
should not be afraid to ask a patient about suicidal
ideation out of fear of “giving him the idea”, because,
on the contrary, this gives him the chance to talk about
his feelings and these thoughts are justified [13, 14].
Some sub-threshold forms of depression, which go
undiagnosed and untreated, are often observed in
cancer patients. These can be prodromes of major
depression, residual symptoms post treatment or a new
medical condition altogether [21].
Paraneoplastic Syndrome Depression
Depression may be a manifestation of a more
generalized paraneoplastic syndrome, which consists of
remote effects of the tumor without direct metastatic
activity. Depressive symptoms are found in 58% of
paraneoplastic limbic encephalitis cases [22].
Paraneoplastic limbic encephalitis is also characterized
by anxiety, irritability, hallucinations, memory loss,
seizures, episodes of depersonalization and, sometimes,
dementia [22, 23]. It is most common in lung, breast
and testis cancer. Paraneoplastic limbic encephalitis’s
symptoms usually precede the diagnosis of cancer
while the tumor might still be undetectable. Thorough
testing must be performed until the malignancy is
diagnosed [24]. Diagnosis of paraneoplastic limbic
encephalitis requires neuropathological exams or the
presence of the four following criteria:
1. compatible clinical presentation;
2. interval of less than 4 years between the
development of neurological symptoms and cancer
3. exclusion of other neuro-oncological problems;
4. at least one of the following: cerebrospinal fluid
with inflammatory changes but no positive cytology,
MRI with temporal lobe abnormalities or EEG with
epileptic activity in the temporal lobe [22].
Pathophysiology is believed to be immunological with
cancer-induced auto-antibodies attacking the patient’s
central nervous system [24].
Table 1. Factors that influence the level of emotional distress in
coping with cancer diagnosis.
Medical factors
advanced disease, poor prognosis, tumor site
(i.e. oral pharyngeal, lung, breast),
uncontrolled pain, use of steroids (mood
Psychological factors prior depression or psychosis, ability to
modify plans, fear of painful death, disability,
changes in appearance, loss of body function
Social factors
support from family, friends, co-workers,
financial concerns, stigma- fear of being
socially ostracized (in developing countries)

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The main question consists of whether pancreatic
cancer causes depression or whether depression and its
treatments can cause pancreatic cancer. It is believed
that the main link between depression and cancer in
general is immune dysregulation. In cancer, cytokines
are locally produced in the brain and become mediators
of neurologic manifestations. They can have a direct
effect on brain mechanisms (by altering neuronal
processes) or indirect (by altering brain chemistry)
[25]. Cytokine dysregulation due to malignancy
involves increase of pro-inflammatory cytokines, such
as IL-1beta, TNF-alpha, Il-6, IL-18. Studies have
shown that, in depressive disturbances, there is a
compromised cell-mediated immune function as well
as changes in the hypothalamic-pituitary-adrenal axis
activity [21]. Increased levels of cytokines in the
hypothalamus play a vital role in the cachexia-anorexia
syndrome in cancer. Studies on tumor-bearing rodents
have shown that peripheral tumor development
activates paracrine interactions within the brain. These
sustain cytokine production, independently of cytokine
concentration in body circulation [25].
On the other hand, it seems possible that depression
may increase the risk of subsequent cancer. Depression
impairs cell-mediated immunity and the body’s defense
against malignancy. Therefore, there seems to be a bi-
directional relationship between depression and
immunological dysregulation in cancer patients [21]. A
meta-analysis based on 13 prospective studies showed
a small but increased cancer risk after depression. This
result was shown only after reviewing studies with a
follow-up of ten years or more. Possible patho-
physiological mechanisms are the following:
1. depression indicates physical changes related to
the first stages of oncogenesis;
2. depression and cancer are related to common or
adjacent genes;
3. greater cancer risk has mainly been proven in
breast cancer studies, which can be explained by the
fact that depressed women are less likely to have many
4. antidepressants have been suggested to be
carcinogenic, but more research is necessary to
establish this [26].
Some of the confounding factors in the relation
between depression and cancer are smoking and
alcohol, obesity and family history. These affect a
person’s immune system and risk of developing cancer
[26, 27].
Review of literature regarding pancreatic cancer
showed that nearly 50% of patients with this kind of
cancer experience depressive symptoms before
diagnosis [6, 27]. This study also showed that
diagnosis of depression is made approximately 1.5
years before the pancreatic cancer diagnosis and,
therefore, it is unlikely to mask physical symptoms of
pancreatic cancer, as symptoms appear only 10 weeks
before cancer diagnosis [27]. Many theories have been
proposed in order to explain the pathophysiology of
depression preceding pancreatic cancer (Figure 1):
1. immunological: pancreatic tumor cells release a
protein inducing the production of antibodies that block
central nervous system serotonin receptors or anti-
idiotypic antibodies act as alternate receptors and make
serotonin less available in synapses [3, 28, 29];
2. hormonal: urinary excretion of 5-hydro-
indoleacetic acid (5-HIAA), 5-hydroxytryptophan (5-
HTP) or 5-hydroxytryptamine (5-HT:serotonin) has
been found in some pancreatic tumors. Increased
serotonin secretion depletes serotonin stores and causes
depression [28];
3. paraneoplastic: the tumor might produce a false
neurotransmitter which alters the patient’s mood and
leads to non-suppression of the dexamethazone
suppression test [4, 28];
4. biochemical: acid-base abnormalities, anemia, and
metabolic abnormalities are possible but they are not
present in all patients [6, 28, 30]. It is thought that
tumors of the gastro-intestinal tract, which is rich in
neuropeptides, may lead to production of biogenic
amines that alter the psychological state [5].
Scales for Screening
Several depression scales have been developed for
routine screening and for mood change evaluation
during treatment, but they are not useful for diagnosis
[21, 31]. Such scales are the Beck Depression
Inventory [32], the Distress Thermometer [31], the
Hospital Anxiety and Depression Scale (HADS)
questionnaire [33], the Brief Edinburgh Depression
Scale (BEDS) [34], and the Cancer Communication
Assessment Tool for Patients and Families (CCAT-PF)
scale [35]. By using these tools, physicians are alerted
when patients have depressive symptoms, and referral
to mental health counseling should be routine
Impact of Depression on Survival
Depression has been found to have a significant impact
on morbidity in patients with advanced metastatic
cancer rendering effective intervention imperative.
Figure 1. Pathophysiology of depression in pancreatic cancer.

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Breast cancer patients with high score of depression
have worse survival rates [18] and this has also been
shown in patients with hepatobiliary carcinoma [36].
Several reviews have reached the same conclusion for
cancer patients in general [37, 38].
What must be determined is whether there are
underlying organic causes of the depression by
conducting thorough physical, endocrinological,
neurological and cognitive testing. Causes of organic
depressive disorders in cancer patients are:
- metabolic (i.e., hypercalcemia);
- hematologic (i.e., anemia, that should be corrected
with recombinant human erythropoietin);
- endocrinologic (i.e., hyperthyroidism, corticosteroid
- infections (i.e., Epstein-Barr virus infection) and
antibiotics (i.e., amphotericin);
- nutritional (i.e., vitamin B12 deficiency);
- biologic therapies (i.e., interferon and interleukin);
- whole-brain radiation;
- drug side-effects (i.e., b-adrenergic antagonists,
chemotherapeutic agents, such as vinca alkaloids,
procarbazine, asparaginase, tamoxifen, intrathecal
methotrexate) [14, 19, 21, 39]. Chemotherapy can also
cause depression and cognitive deficits after its
completion, a phenomenon called “chemobrain”. It
consists of impairment of attention, psychomotor
functions and memory and is caused by vascular injury,
inflammation, neuronal and oxidative damage [40].
In any of the above cases, the organic disorder must be
treated first. We often start antidepressant
administration concurrently when the treatment is
estimated not to suffice, when depression is caused by
a drug that cannot be discontinued (i.e.,
chemotherapeutic drug) or in order to have more rapid
results [14]. Administration of various antidepressant
drugs is effective but no individual drug has been
proven to be relatively more effective than the rest,
partly because few studies have been conducted
regarding the effectiveness of antidepressants in cancer
patients [19, 41].
Choice of antidepressant therapy should rely on:
- the patient’s overall clinical presentation (i.e. hepatic
- cognitive functions;
- other concomitant psychiatric condition;
- main target symptoms in each patient (i.e., insomnia,
- family history of psychiatric disorders and previous
personal response to antidepressants;
- the need to avoid side-effects caused by
- tolerability by the patient;
- potential interaction with other co-administered
drugs; and
- patient’s preference [19, 21, 41].
Pharmacologic Therapy
The treatment can consist of one of the following or a
combination (Table 2).
1. Tricyclic antidepressants (i.e., amitriptyline,
doxepin, imipramine, nortriptyline, doxapine,
protryptyline) are the most commonly used drugs to
Table 2. Antidepressant drugs and criteria for selection in cancer patients.
Tricyclic antidepressants
1. Choose according to target symptoms and side-effects:
- agitation, insomnia: amitriptyline, doxepin;
- cognitive impairment: desipramine, protryptiline;
- neuropathetic pain: imipramine, doxepin, amitriptyline.
2. Their effect begins in 2 weeks.
3. Great caution when administering to elderly with cardiac problems.
4. Weight gain.
Heterocyclic antidepressants
1. Administered when patient does not respond to tricyclic antidepressants.
2. Extrapyramidal symptoms usual side-effect.
Atypical antidepressants
1. Less cardiotoxic.
2. Increased risk of seizures, priapism, and weight fluctuations.
Selective serotonin re-uptake inhibitors (SSRIs) 1. Less cardiotoxic and sedative. Less anticholinergic effects.
2. Initial period: nausea, insomnia.
3. Weight loss, sexual dysfunction.
4. SSRI overdose rarely fatal.
Lithium carbonate
1. Less sedative. Narrow therapeutic index.
2. Can cause tremor, ataxia, seizures.
Monoamine oxidase inhibitors (MAOIs)
1. Administered when patient non-responsive or allergic to other antidepressants.
2. Avoid tyramine-containing foods (i.e., aged cheese, liver, alcohol, soy).
3. Do not co-administer with SSRI, tricyclic antidepressants or sympathomimetic drugs.
1. Increased energy levels, less fatigue.
2. Rapid action onset-gradually increase dose.
3. Tolerance may develop.
4. Insomnia, tremor, agitation, cardiac arrythmias, decreased appetite are possible side-effects.
1. Indicated when anxiety symptoms are present. Sedative effect.
2. Rapid action onset.
3. Addiction can develop. Withdrawal symptoms upon abrupt discontinuation.
4. Do not administer in case of severe hepatic dysfunction.

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treat depression in cancer patients in general, and
pancreatic cancer in particular. These drugs are
initiated at low doses and their doses are slowly
increased until adequate response is achieved. It has
been noticed that cancer patients show a therapeutic
response at much lower doses than usually required but
the reason for this remains unknown [14, 19]. The
choice of a specific drug of this category is mainly
based on the target symptoms and side-effects. If the
patient is experiencing agitation and insomnia, a
tricyclic antidepressant with sedating effects (i.e.,
amitriptyline or doxepin) is preferred. If there is
psychomotor dysfunction, compounds with less
sedating effect are preferred (i.e., protryptyline or
desipramine). If there is concomitant neuropathetic
pain, then imipramine, doxepin, amitriptyline or
desipramine are administered as they have been proven
effective in this kind of pain [14, 21, 28]. Nortriptyline
is preferred for patients with hepatic dysfunction [19].
If our main concern is to avoid urinary retention and
constipation, if there is stomatitis or if drugs with
anticholinergic properties are concomitantly used,
desipramine or nortriptyline are prescribed, as they
have the least anticholinergic effects. If a patient is
unable to swallow pills, antidepressant is administered
as an elixir (amitriptyline, nortriptyline or doxepin) or
by intramuscular route (amitrityline, imipramine) [14,
19]. There are also drugs in this category that can be
administered parenterally (amitriptyline, imipramine
and clomipramine) in case of absent swallowing reflex,
intestinal obstruction or gastric tube. Close monitoring
of cardiac conduction is needed when using the
parenteral route [14].
2. Heterocyclic antidepressants (i.e., maprotiline,
amoxapine). These are prescribed when the patient is
not responsive to tricyclic antidepressants or there are
serious side-effects. Maprotiline increases the risk of
seizures whereas amoxapine can cause extrapyrimidal
symptoms if taken with other dopamine blockers, such
as antiemetics [14, 19].
3. Atypical antidepressants (i.e., trazodone,
buproprion). These are less cardiotoxic than tricyclic
antidepressants. Buproprion increases the risk of
seizures. Trazodone is strongly sedating and therefore
preferred in insomnia but must be administered with
great caution in male patients as it can cause priapism
[14, 19, 28].
4. Selective serotonin re-uptake inhibitors (SSRIs)
(i.e., paroxetine, sertraline, fluoxetine, fluvoxamine,
citalopram). These drugs have fewer sedative and
autonomic effects than tricyclic antidepressants [14,
19, 28]. Pancreatic tumors have been found to have
increased serotonin secretion. This exuberant
metabolism decreases the serotonin in the central
nervous system thereby resulting in depression [27].
For a brief initial period, SSRIs can cause nausea,
headache, somnolence, insomnia, increased anxiety
and appetite suppression [14, 19, 28]. There is no
evidence of interaction between SSRIs and
chemotherapy in inducing nausea [33]. Paroxetine and
sertraline have shorter half-life than fluoxetine, which
is important in order to avoid drug accumulation [14].
SSRIs are also co-administered with interferon in
treatment of melanoma, in order to achieve targeted
prevention of depression secondary to interferon, but
also because studies have shown that sertraline
downregulates the anti-apoptotic Akt molecule.
Therefore, they might improve the efficacy of
interferon [32, 42].
5. Lithium carbonate. If the cancer patient had
bipolar disorder before the diagnosis, lithium should be
continued with fluid and electrolyte monitoring. It can
be nephrotoxic if co-administered with cisplatin [14].
6. Monoamine oxidase inhibitors (MAOIs) (i.e.,
phenelzine, isocarboxazid, tranylcypromine). If a
patient is already on MAOI with good response, it
should be continued. Caution should be exercised in
their administration. Tyramine-containing foods should
be avoided. If co-administered with narcotic
analgesics, there may be myoclonus and delirium,
whereas sympathomimetic drugs combined with
MAOIs can cause hypertensive crisis [14, 19]. MAOIs
have significant interactions with tricyclic
antidepressants increasing their concentration [43].
7. Psychostimulants
dextroamphetamine). These drugs are energizing,
improve attention span, and decrease weakness. They
have rapid action onset and counteract sedation caused
by narcotic analgesics enhancing their analgesic effect
[14, 19, 28]. The dose is gradually increased until
adequate response or side-effects appear (nervousness,
insomnia, blood pressure increase, dyskinesia,
psychosis). Tolerance may develop and in this case
dose should be adjusted. Pemoline is available in
chewable form and it is absorbed by the buccal
mucosa. It is useful in patients with difficulty
swallowing or intestinal obstruction but must be
avoided in renal impairment [14, 19].
8. It is suggested that when rapid effect is needed, we
start with an initial dose of methylphenidate, 2.5 mg
orally increased every couple of days up to a maximum
dose of 30 mg. When the patient has a greater life span,
SSRIs are administered, as they may take up to 4-6
weeks to become effective. They can be given
concurrently with psychostimulants that are
progressively tapered as antidepressants start to have
therapeutic effect [20, 44]. A specialist must be
consulted when the patient does not respond after 4-6
weeks of antidepressant therapy or if depression
relapses concurrently [33].
9. Benzodiazepines (i.e., diazepam, alprazolam,
flurazepam, temazepam, triazolam). They are
administered when the patient has anxiety symptoms
[14, 28].
10. Electroconvulsive therapy. This kind of therapy is
indicated for patients with depression refractory to
antidepressant drugs, with suicidal or psychotic
features or when antidepressants are contraindicated
[14, 19, 21]. Psychotic depression includes delusions,

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hallucinations or grossly disorganized behavior. In
these cases, antipsychotic drugs are co-administered
(preferably high potency antipsychotics to minimize
risk of delirium and anticholinergic effects) [14, 19].
Support, and Role of the Social Worker
When cancer occurs, patients may experience any
combination of fear, sadness, anxiety and/or
depression. Family members may also experience such
feelings. Anger over the reality of a diagnosis,
concerns about shifting roles and responsibilities,
foreseeable economic burdens and questions about
doing what is needed often surface. These feelings may
appear at any time in the course of the illness, even
after treatment ends. While these feelings may be
predictable, there are times when feelings can
overwhelm and take control over aspects of daily life.
Social workers play an important role in helping the
patient and family manage these symptoms, through
short-term counseling or cognitive-behavioral stress
management therapy. The patient and family should be
taught coping strategies, so that he and his relatives can
cope more effectively and the feeling of helplessness
diminished [13, 19, 33, 41]. The target is to help the
patient return to his earlier psychological baseline [19].
Anti-depressants are co-administered, if necessary [45].
It is also important to address the potential need for
treatment of family members. It has been shown that
survival rates are greater in cancer patients after
psychotherapy but other studies have shown no
significant improvement [38]. Planning of treatment for
psychosocial intervention must take into account
factors that determine a patient’s emotional distress,
such as individual temperament and family support, as
discussed earlier. When faced with a limited prognosis,
transition to hospice care should be implemented.
These services may take place at home or at a free-
standing or in-patient facility. Psychosocial care
continues to be provided to both the patient and his/her
family. This allows the patient to be reassured that
he/she will not die alone or in pain [14, 19, 28] and will
assist the family in coping with their grief (Figure 2).
Social workers are the key participants throughout the
cancer continuum: at time of diagnosis, treatment,
relapse, survivorship, end of life, and bereavement.
Clinical social workers are uniquely qualified to
manage these challenges for the patient and family, as
well as address the concrete concerns that may arise,
which often result in referrals to community resources.
As part of the standard of care, the social worker
should be introduced on the initial visit and participate
in the discussion that the physician has with the patient
and family after examination. This normalizes the role
of the social worker and validates the need for
subsequent sessions. Although patients and families
may not need to consult with the social worker on
every visit, it allows for a connection to the social
worker and subsequent increased comfort
communicating with the social worker when a crisis
does occur. One model of care that should be
considered is that of continuity of care. The same
social worker is able to provide therapeutic
intervention regardless of site of care (in-patient,
infusion units, diagnostic imaging, etc.) and be a
consistent presence throughout the course of illness.
The ability to obtain mental health counseling within
the medical setting takes into account a patient’s
fatigue and allows them to receive comprehensive care
in one setting, without necessitating extra
appointments, potential rides or other resources.
According to the Institute of Medicine (IOM) [46],
many providers do not consistently ask about
psychosocial issues nor do they provide an adequate
link to resources, which has a detrimental impact on
patients. It also recommends that all patients with
cancer have a psychosocial treatment plan.
Depression in pancreatic cancer is a condition that
must be diagnosed and treated, as studies have shown
that depression is a detrimental factor in the last stages
of life of cancer patients. Treatment for depression has
also been shown to impact quality of life and may
bring increased comfort during end of life.
Conflict of interest None
Helsinki declaration Conformed
1. Yaskin JD. Nervous symptoms at earliest manifestations of
cancer of the pancreas. JAMA 1931; 96:1664-8.
2. Fras IL, Litin EM, Pearson JS. Comparison of psychiatric
symptoms in carcinoma of the pancreas with those in some other
intra-abdominal neoplasms. Am J Psychiatry 1967; 123:1553-62.
[PMID 4381627]
3. Jacobsson L, Ottosson JO. Initial mental disorders in carcinoma
of pancreas and stomach. Acta Psychiatr Scand Suppl 1971; 221:120-
7. [PMID 5286323]
Figure 2. Algorithm for treatment of patient with pancreatic cancer
and depression.

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JOP. J Pancreas (Online) 2009 Jan 8; 10(1):69-76.
JOP. Journal of the Pancreas - - Vol. 10, No. 1 - January 2009. [ISSN 1590-8577]
4. Joffe RT, Rubinow DR, Denicoff KD, Maher M, Sindelar WF.
Depression and carcinoma of the pancreas. Gen Hosp Psychiatry
1986: 8:241-5. [PMID 3744031]
5. Holland JC, Korzun AH, Tross S, Silberfarb P, Perry M, Comis
R, Oster M. Comparative psychological disturbance in patients with
pancreatic and gastric cancer. Am J Psychiatry 1986; 143:982-6.
[PMID 3524279]
6. Green AI, Austin CP. Psychopathology of pancreatic cancer. A
psychobiologic probe. Psychosomatics 1993; 34:208-21. [PMID
7. Massie MJ. Prevalence of depression in patients with cancer. J
Natl Cancer Inst Monogr 2004; 32:57-71. [PMID 15263042]
8. Savage C, Butcher W, Noble D. Psychiatric manifestations in
pancreatic disease. J Clin Exp Psychopathol 1952; 13:9-16. [PMID
9. Perlas AP, Faillace LA. Psychiatric manifestations of carcinoma
of the pancreas. Am J Psychiatry 1964; 121:182. [PMID 14194218]
10. Karliner W. Psychiatric manifestations of cancer of the pancreas.
N Y State J Med 1956; 56:2251-2. [PMID 13334839]
11. Visser MR, Smets EM. Fatigue, depression and quality of life in
cancer patients: how are they related? Support Care Cancer 1998;
6:101-8. [PMID 9540167]
12. Hann DM, Denniston MM, Baker F. Measurement of fatigue in
cancer patients: further validation of the Fatigue Symptom Inventory.
Qual Life Res 2000; 9:847-54. [PMID 11297027]
13. Mishra SK, Mohapatra PK, Bhattacharya K, Gupta T, Agarwal
JP. Prevalence of psychiatric disorder in asymptomatic or minimally
symptomatic cancer patients on treatment. J Cancer Res Ther 2006;
2:136-9. [PMID 17998693]
14. Massie MJ, Gagnon P, Holland JC. Depression and suicide in
Patients with Cancer. J Pain Symptom Manage 1994; 9:325-40.
[PMID 7963785]
15. Foley KM. Pain assessment and cancer pain syndromes. In:
Doyle D, Hanks GWC, MacDonald N, Eds. Oxford Textbook of
Palliative Medicine. 2nd ed Oxford, New York: Oxforfd University
16. Kelsen DP, Portenoy RK, Thaler HT, Niedzwiecki D, Passik
SD, Tao Y, et al. Pain and depression in patients with newly
diagnosed pancreas cancer. J Clin Oncol 1995; 13:748-55. [PMID
17. Barkwell DP. Ascribed meaning: a critical factor in coping and
pain attenuation in patients with cancer-related pain. J Palliat Care
1991; 7:5-14. [PMID 1941361]
18. Watson M, Haviland JS, Greer S, Davidson J, Bliss JM.
Influence of psychological response on survival in breast cancer: a
population-based cohort study. Lancet 1999; 354:1331-6. [PMID
19. Passik SD, Breitbart WS. Depression in patients with pancreatic
carcinoma. Diagnostic and treatment issues. Cancer 1996; 78:615-26.
[PMID 8681300]
20. Block SD. Perspectives on care at the close of life.
Psychological considerations, growth, and transcendence at the end
of life: the art of the possible. JAMA 2001; 285:2898-905. [PMID
21. Spoletini I, Gianni W, Repetto L, Bria P, Caltagirone C, Bossù
P, Spalletta G. Depression and cancer: an unexplored and unresolved
emergent issue in elderly patients. Crit Rev Oncol Hematol 2008;
65:143-55. [PMID 18068997]
22. Cornelius JR, Soloff PH, Miewald BK. Behavioral
Manifestations of Paraneoplastic Encephalopathy. Biol Psychiatry
1986; 21:686-90. [PMID 3011132]
23. Gultekin SH, Rosenfeld MR, Voltz R, Eichen J, Posner JB,
Dalmau J. Paraneoplastic limbic encephalitis: neurological
symptoms, immunological findings and tumour association in 50
patients. Brain 2000; 123:1481-94. [PMID 10869059]
24. Farrugia ME, Conway R, Simpson DJ, Kurian KM.
Paraneoplastic limbic encephalitis. Clin Neurol Neurosurg 2005;
107:128-31. [PMID 15708228]
25. Plata-Salamán CR. Central nervous system mechanisms
contributing to the cachexia-anorexia syndrome. Nutrition 2000;
16:1009-12. [PMID 11054608]
26. Oerlemans ME, van den Akker M, Schuurman AG, Kellen E,
Buntinx F. A meta-analysis on depression and subsequent cancer
risk. Clin Pract Epidemol Ment Health 2007; 3:29. [PMID
27. Carney CP, Jones L, Woolson RF, Noyes R Jr, Doebbeling BN.
Relationship Between Depression and Pancreatic Cancer in the
General Population. Psychosom Med 2003; 65:884-8. [PMID
28. Shakin EJ, Holland J. Depression and Pancreatic Cancer. J Pain
Symptom Manage 1988; 3:194-8. [PMID 3057080]
29. Brown JH, Paraskevas F. Cancer and depression. Cancer
presenting with depressive illness : an autoimmune disease? Br J
Psychiatry 1982; 141:227-32. [PMID 6182940]
30. Alter CL. Palliative and Supportive Care of patients With
Pancreatic Cancer. Semin Oncol 1996; 23:229-40. [PMID 8623059]
31. Tuinman MA, Gazendam-Donofrio SM, Hoekstra-Weebers JE.
Screening and referral for psychosocial distress in oncologic practice:
use of the Distress Thermometer. Cancer 2008; 113:870-8. [PMID
32. Greenberg DB. Barriers to the Treatment of Depression in
Cancer. J Natl Cancer Inst Monogr 2004; 32:127-35. [PMID
33. Ballenger JC, Davidson JR, Lecrubier Y, Nutt DJ, Jones RD,
Berard RM; International Consensus Group on Depression and
Anxiety. Consensus statement on depression, anxiety, and oncology.
J Clin Psychiatry 2001; 62 (suppl 8):64-7. [PMID 12108825]
34. Lloyd-Williams M, Shiels C, Dowrick C. The development of
the Brief Edinburgh Depression Scale (BEDS) to screen for
depression in patients with advanced cancer. J Affect Disord 2007;
99:259-64. [PMID 17055588]
35. Siminoff LA, Zyzanski SJ, Rose JH, Zhang AY. The Cancer
communication Assessment Tool for Patients and Families (CCAT-
PF): a new measure. Psychooncology 2008; 17:1216-24. [PMID
36. Steel JL, Geller DA, Gamblin TC, Olek MC, Carr BI.
Depression, immunity, and survival in patients with hepatobiliary
carcinoma. J Clin Oncol 2007; 25:2397-405. [PMID 17557953]
37. Angelino AF, Treisman GJ. Major depression and
demoralization in cancer patients: diagnostic and treatment
considerations. Support Care Cancer 2001; 9:344-9. [PMID
38. Spiegel D, Giese-Davis J. Depression and cancer mechanisms
and disease progression. Biol Psychiatry 2003; 54:269-82. [PMID
39. el-Kamar FG, Grossbard ML, Kozuch PS. Metastatic pancreatic
cancer: emerging strategies in chemotherapy and palliative care.
Oncologist 2003; 8:18-34. [PMID 12604729]
40. Nelson CJ, Nandy N, Roth AJ. Chemotherapy and cognitive
deficits : Mechanisms, findings, and potential interventions. Palliat
Support Care 2007; 5:273-80. [PMID 17969831]
41. Rodin G, Katz M, Lloyd N, Green E, Mackay JA, Wong RK.
Treatment of depression in cancer patients. Curr Oncol 2007; 14:180-
8. [PMID 17938701]
42. Reddy KK, Lefkove B, Chen LB, Govindarajan B, Carracedo A,
Velasco G, et al. The antidepressant sertraline downregulates Akt
and has activity against melanoma cells. Pigment Cell Melanoma Res
2008; 21:451-6. [PMID 18710373]
43. Bernard SA, Bruera E. Drug Interactions in Palliative Care. J
Clin Oncol 2000; 18:1780-99. [PMID 10764440]
44. Ellison NM, Chevlen E, Still CD, Dubagunta S. Supportive care
for patients with pancreatic adenocarcinoma: symptom control and

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