Asian Journal of Bio-Medical Research

Original Article

Pattern of Hemoglobin and Anemia in Patients Seen with

Symptoms of Bladder Outlet Obstruction (BOO) at First
Presentation and Review of Possible Causes of Anemia in
BOO Patients
Elijah Udoh1, Felix Olisaeke2
Urology Unit, Department of Surgery,University of Uyo Teaching Hospital, Uyo, Akwa Ibom State, Nigeria, 2Department of Obstetrics and
Gynaecology, University of Uyo Teaching Hospital, Akwa Ibom State, Nigeria
1

Address for Correspondence:

Dr.Elijah A. Udoh,
Urology Unit, Department of
Surgery, University of Uyo
Teaching Hospital, Uyo, Akwa
Ibom State, Nigeria.
Tel: 08085551239
E-mail: elijah_udoh@yahoo.com.

Submission : 01-09-2015
Revision : 16-10-2015
Publication : 19-11-2015
URN: pmi:jr:0019ajbr.v1i2.8579
How to Cite this Article:
Udoh, Elijah Asuquo; Olisaeke,
Felix. Pattern of Hemoglobin
and anemia in patients seen with
bladder outlet obstruction (BOO)
at first presentation and review
of possible causes of anemia in
BOO patients.Asian Journal of
Bio-Medical Research (ISSN:24546275), [S.l.], v. 1, n. 2, oct. 2015.
ISSN 2454-6275. Available
at: <http://pmindexing.com/
journals/index.php/AJBR/article/
view/857>.

ABSTRACT
Objective: To study the pattern of hemoglobin levels in patients seen with symptoms of
bladder outlet obstruction at first presentation to our facility and to review the possible causes
of low hemoglobin in this group of patients. Materials and Methods: Aretrospective study of
hemoglobin levels in 110patient who presented between January 1, to December 31, 2014, aged
between 50 and 85years. Information were retrieved from case notes. Hemoglobin was tested
on presentation and was classified based on National Cancer Institute grading of anemia into,
no anemia, mild, moderate, severe and life threatening anemia. Patients were predominantly
diagnosed with benign prostatic hyperplasia, cancer of the prostate, bladder cancer and urethral
stricture. Results: Of the 110 patients evaluated for hemoglobin levels and classified into
different levels of severity of anemia, 30patients were normal while 80patients were anaemic;
comprising 34patients (31.0%) with mild, 27patients (24.5%) with moderate, 11patients (10.0%)
with severe and 8patients with life threatening anemia respectively. Conclusion: Low level of
hemoglobin or anemia can be manifested in the setting of bladder outlet obstruction from any
cause. Possible pathophysiological mechanisms have been known and well studied.

Keywords: Hemoglobin, Anemia, Bladder outlet obstruction, National cancer institute grading
of anemia

Introduction
Hemoglobin (Hb) is the red oxygen carrying pigment in the red
blood cells of vertebrates. It has a molecular weight of 64,450 and
is made up of 4 sub-units. Each of these sub-units contains a haem
moiety conjugated to a polypeptide. Haem is iron containing while
the polypeptide is the globin portion of the hemoglobin. There
are two types of polypeptide namely the -chain and the -chain
containing 141 and 146 amino acids respectively. This is the adult
hemoglobin. Other variants of Hb in adults are HbA2 and HbA1c.
HbA1c has glucose attached to the terminal valine in each -chain
and it is important in glucose monitoring in diabetics. When the Hb

level is low and hence its oxygen carrying capacity is insufficient to

meet the bodys physiologic needs, it is termed anemia.
Bladder outlet obstruction from any cause can lead to low
levels of Hb and hence its oxygen carrying capacity. In this study,
the various causes of bladder outlet obstruction were; cancer of the
prostate, benign prostatic hyperplasia, urethral stricture and cancer
of the bladder. In the literature review, the possible causes of low
Hb or anemia in patients with bladder outlet obstruction ranged
from blood loss, anemia of chronic disease, chronic renal failure
and bone marrow infiltration by malignant cells thereby halting
erythropoiesis.

Udoh and Olisaeke: Pattern of hemoglobin and anemia

Materials and Methods

This was a retrospective study of hemoglobin level of patients who
presented to us with symptoms of bladder outlet obstruction from
January 1stto December 31st, 2014. Information was retrieved from
their case notes. They were seen either in Accident and Emergency
or Surgical Outpatient Department. Their hemoglobin levels were
determined on first presentation and used for this study. Atotal of
110patients were seen and blood samples taken for Hb estimation.
They were all males ranging from 50 to 85years with a mean age of
67.5years.
The pattern of Hb and anemia was classified according to the
National Cancer Institute classification and grading of anemia1 as
follows:
Grade

Degree of anemia

Hemoglobin values (g/dl)

Within normal limits

12.016.0(women)

Table1: Patients classification based on degree of severity of

anemia
Grade of anemia
0(within normal range)
1(mild)

Hb level
(g/dl)

Number of
patients

Percentage
of patients

>14.0

30

27.3

10.013.9

34

31.0

2(moderate)

8.09.9

27

24.5

3(severe)

6.57.9

11

10.0

<6.5

7.2

110

100

4(life threatening)

14.018.0(men)
1

Mild

10.0to levels within

Moderate

8.010.0

Severe

6.57.9

Life threatening

<6.5

Normal limits

Results
Analysis showed that, of the 110patients; 30patients representing
27.3% had Hb levels above 14.0g/dl and were not classified as anemic
while 80patients representing 72.7% were classified anemic at
various levels of severity. Further analysis of the latter group showed
that 34 patients (31.0%), 27 patients (24.5%), 11 patients (10.0%)
and 8patients (7.2%) were classified as mild, moderate, severe and
life threatening anemic patients respectively Table 1, Figures 1 and 2.

Discussion

Figure 1: % comparison between normal and anaemic patients

Hemoglobin (Hb) concentration in the body can be affected

adversely by both genetic and acquired conditions. In bladder outlet
obstruction (acquired condition) characterized by difficulty with
emptying of urinary bladder content and subsequent complications
in the bladder, ureters and kidneys can affect the Hb concentration
of the blood. The mechanism is multifactorial. Back pressure of
urine to the kidneys causing hydronephrosis will lead to progressive
atrophy of the renal parenchyma and renal failure. Patients suffering
from renal failure almost invariably develop anemia to a greater or
lesser extent which is largely due to inappropriate erythropoietin
production. Erythropoietin is produced by the peritubular cells of
the kidney. In renal insufficiency, the cells are gradually lost and
hence the ability of the kidneys to respond to a progressively anemic
state is reduced. This in turn causes a reduction in erythroid cell
proliferation and differentiation in the bone marrow and eventually
a low circulating red cell mass.
In addition to low levels of erythropoietin in this set of patients,
there are many other factors contributing to the anemia of renal
failure. These include; haematinic deficiency; particularly iron and
folic acid, low grade haemolysis, blood loss particularly from the
gastrointestinal tract and suppression of erythropoiesis by uraemic
inhibitors.2 The concepts of uraemic inhibitors have been a subject
of much current interest. These substances inhibit erythropoiesis
2

Figure 2: Percentage of patients and grades of anemia

and include polyamines, parathyroid hormone and some of the

inhibitory cytokines. The role of these substances remains a mystery.
Since the early 1970s, it has been suggested that polyamines may play
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Udoh and Olisaeke: Pattern of hemoglobin and anemia

a role in the pathogenesis of anemia in renal failure3. Polyamines are

series of organic cations; and include substances such as spermine,
spermidine, putrescine and cadaverine. They are believed to play a
role in cellular proliferation and differentiation.4 It is also known
that they accumulate in the plasma of patients with chronic renal
failure and have been found to reduce proliferation and maturation
of erythroid cells.5 There is reasonable evidence to suggest that
polyamines may exert a specific inhibitory affect on erythropoiesis.
This suppression of bone marrow activity seemed fairly specific to
the erythroid lineage since leucopenia and thrombocytopenia are
not usually seen in renal failure.6
The role of parathyroid hormone either directly or indirectly
modulating erythropoiesis has also been a subject of clinical debate. In
renal failure patients, it has been suggested that hyperparathyroidism
is one of the causes of poor response to erythropoietin therapy, and
possible explanations for this phenomenon include development of
marrow fibrosis and a direct effect of parathormone in suppressing
erythroid colony growth.7 Inflammatory cytokines have also been
implicated as modulators of erythropoiesis in uraemic patients.
These cytokines; interleukin-2(IL-2), interleukin-3(IL-3), insulinlike growth factor-1(IGF-1) may enhance erythropoiesis by
promoting the differentiation of primitive erythroid cells from
the precursor stem cells thus increasing the pool of cells on which
erythropoietin can act on.8 The pro-inflammatory cytokines, on
the other hand, namely interleukin-1(IL-1), tumour necrosis
factor- (TNF-) and interferon-(IF-) have inhibitory effects on
erythropoiesis. Allen et al demonstrated that the inhibitory effect of
uraemic serum on human erythroid colony growth could be partially
or completely reversed by pre-exposure to a polyclonal antibody
against tumour necrosis factor- or interferon-. The combination
of these antibodies was additive, suggesting that both cytokines may
be involved in this process.9
Urinary tract stones caused by precipitation of crystals in the
kidneys, ureters or bladder consequent upon stasis from bladder
outlet obstruction can cause microhaematuria in about 85% of cases
but gross haematuria tends to be rare.10
A case of acute haemolytic anemia caused by E Coli Urinary
tract infection was reported by Herbert T. et al11 in which cessation
of haemolytic process was demonstrated to coincide with the
introduction of appropriate antibiotic therapy. This could co-exist
in patients with bladder outlet obstruction who present with low
hemoglobin. Aside from the general effects of stasis and back pressure
of urine to the kidneys caused by bladder outlet obstruction, specific
actiologies of bladder outlet obstruction can pose specific problems.
In carcinoma of the prostate (Cap) especially in advanced stage,
anemia could be caused by androgen deprivation, bone marriow
replacement, anemia of chronic disease, inflammatory cytokines,
haematuria and poor nutrition. Some of the patients seen with
prostate cancers must have been previously exposed to androgen
deprivation before presenting to us and androgen deprivation
therapy (ADT) is a well documented cause of anemia as testosterone
is required for enhancement of erythropoietin formation in the
kidneys as well as bone marrow action of erythropoiesis.12 Jeffrey
et al also pointed out that replacement of bone marrow with cancer
cells also contribute to low hemoglobin in men with cap due to
impaired haematopoiesis.12
Anemia of chronic disease is a form of anemia seen in chronic
infection, chronic immune activation and malignancy. These
conditions also produce massive elevation of interleukin-6(IL-6). In
AJBR Vol 1 Issue 2 2015

response to increasing interleukin-6 production, the liver produces

increased amount of hepcidine which in turn causes increased
internalization of ferroportin molecules in cell membrane which
prevents release of iron stores. Inflammatory cytokines also appear
to affect other important elements of iron metabolism including
decreasing ferroportin expression and probably directly blunting
erythropoiesis by decreasing the ability of the bone marrow to
respond to erythropoietin.13
In anemia of cancer as in anemia of chronic disease, multiple
mechanisms can interfere with normal erythrocyte production.
The cytokines TNF-, TGF-, IL-1, IL-6 and interferon- are likely
most prevalent as inhibitory mechanisms. This network of cytokines
probably modulates iron metabolism and the erythropoietin effect
may be blunted by TNF- among others. An anti-TNF- antibody
may abrogate this effect and has been demonstrated in rheumatoid
arthritis.14 Moreover, activation of macrophages can lead to a shorter
erythrocyte half-life and a decrease in iron utilization. Drug therapy
further aggravates anemia in cancer patients such as radiotherapy
and chemotherapy.
Nutritional decline may also lead to low hemoglobin in patients
with cancer. Haematuria can contribute to this phenomenon
due to cancer infiltration of the urethra and bladder wall as in
prostate cancers and bladder cancer with consequent sloughing
and bleeding. In BPH as well as in prostate cancer, grossly, there is
increased density of the micro-vessels in the prostate and in a 2002
cross sectional study, had a self reported rate of haematuria in 2.5%
of subjects with BPH.15
In our study as well as other studies reviewed, patients
presentation is usually late and most of these mechanisms
causing low hemoglobin level go on unchecked. Only 30 patients
representing 27.3% of all patients evaluated had their hemoglobin
levels within normal limits while 72.7% were anemic at various
levels of severity. Severe and life threatening anemia seen in
17.2% of the population studied carry grave consequences if not
adequately addressed especially in other poor resource centres
with no facilities for blood transfusion. The progressive nature of
the pathologies, even in the mild to moderate groups, is a cause
for concern. In all of these situations, addressing the underlying
pathologies early and promptly and correction of anemia is the key
to successful management.

Conclusion
Low hemoglobin in patients with bladder outlet obstruction causes
significant morbidity. It impairs virtually every organ and tissue
of the body leading to multiple function disturbances, decreasing
mental and physical performance capacity. Most of the patients
in the study presented late and the underlying pathophysiological
changes continue unannounced untill bladder outlet obstructive
symptoms brought them to our facility.
With the knowledge of this study, awareness campaign can
evolve to sensitize men in this age group to seek medical care at
the earliest notice of symptoms to forstall attendant morbidity and
mortality that come with late presentation accessioned by high
prevalence of low hemoglobin and other complications.

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Author Contribution: EU : Concept and design of the study, reviewed the literature,
manuscript preparation, statistically analysed and interpretation of draft manuscript and
critical revision of the manuscript. FO : Data collection, review of literature and helped in
preparing first draft of manuscript.
Source of Support: Nil. Conflict of Interest: None declared.

AJBR Vol 1 Issue 2 2015