I.

INTRODUCTION
Upper gastrointestinal bleeding (UGB) is a life threatening complication of
gastrointestinal diseases. Even though bleeding is the common symptom different
causes of gastrointestinal bleeding are significantly different. Not only the
gastrointestinal tract itself, but also lesions in adjacent organs and systemic diseases
contribute to bleeding. Therefore, realization ofthe etiology and characteristics is
essential for doctors to diagnose and treat the disease. Peptic ulcer remains the most
common cause of UGB, representing approximately half of all cases. Esophageal
varicose and gastritis, gastric carcinoma and benign tumors of the digestive tract are
also common causes of UGB. There are many case reports of unusual causes of UGB,
hencewidening our understanding into the etiology of UGB. On the other hand, UGB
of rare diseases can also be thereason for misdiagnosis and sometimes leads to fatal
on sequences.1
Upper gastrointestinal (GI) bleeding is usually defined by a bleeding source
proximal to the ligament of Treitz although some authors may also include a bleeding
source in the proximal jejunum. Many upper GI bleeding cases (e.g. erosive gastritis
and esophagitis, angiodysplasia, gastric antral vascular ectasia or watermelon
stomach, Cameron erosions,portal hypertensive gastropathy and small ulcers) cause
iron-deficiency anemia but do not usually present as emergencies. Upper GI bleeding
emergencies are characterized by hematemesis, melena, hematochezia (if the bleeding
is very massive and risk) and evidence of hemodynamic compromise such as
dizziness, syncope episodes and shock. They are often caused by major hemorrhage
from ulcers, varices, Dieulafoy lesions,Mallory-Weiss tears and neoplasms. Rare
causes include hemobilia and hemosuccus pancreaticus as well as enteric fistula
connecting with major blood vessels.1,2
Hookworm infections have a worldwide distribution, with approximately 600
million people being affected globally according to the latest estimates; it is ranked
one of the most common parasitic infections of humans. The highest prevalence is
reported in southeast Asia, sub-Saharan Africa, and the Indian subcontinent,

1
especially in rural areas with low socioeconomic status, poor sanitary facilities, and
indiscriminate defecation habits that allow larvae to develop in the soil. 3
In 2010, it was estimated that 117 million individuals in sub-Saharan Africa
were infected with hookworms, as well as 64 million in East Asia, 140 million in
South Asia, 77 million in Southeast Asia, 30 million in Latin America and the
Caribbean, 10 million in Oceania, and 4.6 million in the Middle East and North
Africa. Oceania has the highest prevalence (49%), followed by sub-Saharan Africa
(13%), Southeast Asia (12.6%), South Asia (8.6%), East Asia (5%), and Latin
America/Caribbean (5%). These represent approximately 20% decreases in
prevalence from 2005 WHO estimates. 4

II. CASES
The first case, A 39 year old housewife came with a complaint from the
black stools 3 days before getting the hospital. Black stools with a frequency of 1
times a day with a volume of 100-200 cc in one of defecate. Black stools liquid and
sticky as asphalt and according to the patient's family is difficult when doused with
water. Nausea and vomiting are not there, no hematemesis. The patient complained of
pale since two month ago. Patient also complained of loss of appetite in the last one
week. Patients were only able to spend 5-6 spoons of rice in a meal. Weight loss does
not exist.No fever and cough. Urinate in the normal range, the patient urin 1000-1200
cc in 24 hours. A history of jaundice was not there before. A history of anti-pain
medication consumption there 2 years ago because joint pain, but only for one week
since that time the patient complained of headache. Patient referrals from Pidie
General Hospital with the diagnosis of upper gastrointestinal bleeding and has been
hospitalized for 2 days and had received a transfusion 1 kolf PRC.
She was composmentis and his blood pressure was 110/70 mmHg, pulse 92
beats/ minute, respiratory rate 18 breaths/ minutes, temperature 36,5o C. On physical
examination of head, conjunctiva palpebrae inferior was pale, ear,nose,and mouth
within normal limits. While examination of the lung, heart and stomach were normal

2
limits..we found pain in apigastrium regio. We found pale extremities on both hands
and feet. In rectal toucher we found spincter ani tight, slick mucosa , ampulla recti
filled with feces, and on handscoon visible feces chocolate and sticky.
RSUZA of laboratory results at the time of initial entry on 28th of July 2017
obtained haemoglobin 3,9 g/dL, erythrocyte 2,5 million/mm3, hematocrit 14 %,
leukocytes 7500/mm3, platelets 345.000 /mm3, MCV 55 fL, MCH 16 pg, MCHC 29
%, difttell eosinofil 8, basofil 0, netrofil batang 0, netrofil segmen 68, limfosit 16,
monosit 8, HbSAg negative, liver function test and elektrolit was normal limits. Urea
17 mg/dL, creatinin 0,50 mg/dL. On July 30th, 2017 we do routine stool examination
and we found the worm eggs ancylos 2-3 / LPB
On August 3th, 2017 EGD was performed and the result is gastric ulcer and
Ancylostoma.. On chest x-ray photo and USG abdomen showed within normal limits.
Patients received IV therapy Prosogan 30 mg / 12 hours, Sucralfate syrup 3xC1, and
transfusion PRC 1 kolf / day until Hb 10 g / dl. After the results of routine stool found
the patients treated with Albendazole 1x400 mg sigle dose and combination with
pyrantel pamoate 10 mg / kg / single dose. After therapy, we do routine feses and
found negative worm eggs. The patient has clinical improvement and allowed to
outpatient on 8th days treatment
The second case, A 57 year old housewife came with a complaint from the
black stools 10 days before getting the hospital. Black stools with a frequency of 1
times a day with a volume of 100-200 cc in one of defecate. Black stools liquid and
sticky as asphalt and according to the patient's family is difficult when doused with
water. Nausea and vomiting are not there, no hematemesis. Patients also complained
of loss of appetite in the last one week. Patients were only able to spend 4-6 spoons of
rice in a meal. Weight loss does not exist.No fever and cough. Urinate in the normal
range, the patient urin 1000-1500 cc in 24 hours. A history of jaundice was not there
before. A history of anti-pain medication consumption there 1 years ago because joint
pain, but only for one week since that time the patient complained of headache.

3
Patient referrals from Pidie Jaya General Hospital with the diagnosis of gastric ulcers
and has been hospitalized for 5 days and had received a transfusion 2 kolf PRC.
She was composmentis and his blood pressure was 120/70 mmHg, pulse 80
beats/ minute, respiratory rate 20 breaths/ minutes, temperature 36,5o C. On physical
examination of head, conjunctiva palpebrae inferior was pale, ear,nose,and mouth
within normal limits. While examination of the lung, heart and stomach were normal
limits.. We found pale extremities on both hands and feet. In rectal toucher we found
spincter ani tight, slick mucosa , ampulla recti filled with feces, and on handscoon
visible feces black and sticky.
RSUZA of laboratory results at the time of initial entry on 2nd of July 2017
obtained haemoglobin 2,5 g/dL, erythrocyte 1,9 million/mm3, hematocrit 9,6 %,
leukocytes 4400/mm3, platelets 314.000 /mm3, MCV 48 fL, MCH 12,5 pg, MCHC
26 %, difttell eosinofil 8, basofil 0, netrofil batang 0, netrofil segmen 68, limfosit 15,
monosit 9, HbSAg negative, liver function test and elektrolit was normal limits. Urea
15 mg/dL, creatinin 0,60 mg/dL.
On July 6, 2017 EGD was performed and the result is gastric ulcer and
Ancylostoma. On July 7, 2017 we do routine stool examination and we found the
worm eggs ancylos 3-4 / LPB. On chest x-ray photo showed within normal limits and
genue X-ray photo showed osteoartritis genuae dextra. Patients received IV therapy
Prosogan 30 mg / 12 hours, 3x500 mg Paracetamol, Sucralfate syrup 3xC1, and
transfusion PRC 1 kolf / day until Hb 10 g / dl. After the results of routine stool found
the patients treated with mebendazole 2x100 mg for 3 days and combination with
pyrantel pamoate 10 mg / kg / single dose. After therapy, we do routine feses and
found negative worm eggs. The patient has clinical improvement and allowed to
outpatient on 7th days treatment
The third case, A 74 year old farmer came with a complaint from the black
stools 14 days before getting the hospital. Black stools with a frequency of 2 times a
day with a volume of 100-150 cc in one of defecate. Black stools liquid and sticky
as asphalt and according to the patient's family is difficult when doused with water.

4
Nausea and vomiting are not there, no hematemesis. Patients also complained of loss
of appetite in the last one week. Patients were only able to spend 3-4 spoons of rice in
a meal. Weight loss does not exist but patients feel faint. No fever and cough. Urinate
in the normal range, the patient urin 1000-1500 cc in 24 hours. A history of jaundice
was not there before. A history of anti-pain medication consumption there 4 years
ago, but only for one week since that time the patient complained of headache.
Patient referrals from Sigli General Hospital with the diagnosis of gastric ulcers and
has been hospitalized for 14 days and had received a transfusion 4 kolf PRC.
He was composmentis and his blood pressure was 130/70 mmHg, pulse 82
beats/ minute, respiratory rate 20 breaths/ minutes, temperature 36,5o C. On physical
examination of head, conjunctiva palpebrae inferior was pale, ear,nose,and mouth
within normal limits. While examination of the lung, heart and stomach were normal
limits.. We found pale extremities on both hands and feet. In rectal toucher we found
spincter ani tight, slick mucosa , ampulla recti filled with feces, and on handscoon
visible feces black and sticky.
th
RSUZA of laboratory results at the time of initial entry on 28 of October
2016 obtained haemoglobin 4,5 g/dL, erythrocyte 2 million/mm3, hematocrit 16 %,
leukocytes 5400/mm3, platelets 605,000 /mm3, MCV 76 fL, MCH 22 pg, MCHC 29
%, difttell eosinofil 7, basofil 0, netrofil batang 0, netrofil segmen 69, limfosit 15,
monosit 9, HbSAg negative, liver function test and elektrolit was normal limits. Urea
13 mg/dL, creatinin 0,70 mg/dL.
On August 30, 2016 EGD was performed and the result is gastric ulcer and
Ancylostoma. On August 31 th 2016 we do routine stool examination and we found
the worm eggs ancylos 2-3 / LPB. On chest x-ray and genue photo showed within
normal limits. Patients received IV therapy Prosogan 30 mg / 12 hours, 3x500 mg
Paracetamol, Sucralfate syrup 3xC1, and transfusion PRC 1 kolf / day until Hb 10 g /
dl. After the results of routine stool found the patients treated with mebendazole
2x100 mg for 3 days and combination with pyrantel pamoate 10 mg / kg / single

5
dose. After therapy, we do routine feses and found negative worm eggs. The patient
has clinical improvement and allowed to outpatient on 15th days treatment

Tabel 1. Clinical manifestation

Case 1 Case 2 Case 3
Sex Female Female Male
Age 39 yo 57 yo 64 yo
Addres Pidie Pidie jaya
Clinical manifestation
Black stool Yes Yes Yes
Nausea No No No
Vomiting No No No
Hematemesis No No No
Pale Yes ( 2 month Yes (1 month)
Loss appetite Yes Yes
Weight loss No No No
Fever No No No
Cough No No No
Urinate Normal Normal Normal
History of joundice No No No
History of anti-pain / NSAID consumption No No No
History of transfusion (PRC) Yes ( 1 kolf) Yes (2 kolf) Yes ( 1 kolf)

Tabel 2. Laboratory result and investigation

Case 1 Case 2 Case 3
Haemoglobin 3,9 2,5 4,5
Erythrocyte 2,5 x 106 1,9 x 106 2x106
Hematocrit 14 % 9,6 % 16%
Leucocyte 7.5 x 103 4,4 x 103 5,4x103
Platelets 345x103 314x103 605x103
MCV/MCH/MCHC 55/16/29 48/12/26 54/16/28
Diftell ( E/B, SN, BN, L,M) 8/0/0/68/16/8 6/0/0/70/16/8 7/0/0/69/15/9
HbSAg Negative Negative Negative
LFT Normal Normal Normal
Electrolite Normal Normal Normal
Urea 17 15 13
Creatinin 0,50 0,4 0,70
Routine stool worm egg No worm worm egg
ancylos egg ancylos
Yes (2-3 LBP) Yes (3-4 LBP)
EGD Gastric ulcer, Gastric ulcer, Gastric ulcer,
Ancylostoma Ancylostoma Ancylostoma
Chest X-ray Normal Normal Normal
USG Abdomen Normal Normal Normal

6
 Tabel 3. Therapy patients
Case 1 Case 2 Case 3
iv. lansoprazole 2x30 mgs Yes
Sucralfat syr 3xCII Yes
Anti anchilostoma Albendazole
1x400 mg +
Pirantel
pamoat 10
mg/kgBB (
sigle doses)
Transfusion Yes

III. DISCUSSION
Hookworm infection in humans is caused by an infection with the helminth
nematode parasites Necator americanus and Ancylostoma duodenale and is
transmitted through contact with contaminated soil. It is one of the most common
chronic infections, with an estimated 740 million cases in areas of rural poverty in the
tropics and subtropics. Because hookworm infection occurs predominantly among the
worlds most impoverished people.1it holds a unique place in modern history.5
In Southeast Asia, almost 215 million women are estimatedto be anemic. In
Vietnam, the prevalence of anemia was 42.8% in 1995, 12 and a recent survey found
that 40% of non pregnant women were anemic. 13 The prevalence of hook worm
infection in northern Vietnam has previously been reported as 52%. 14 However, in
many districts of Vietnam, the prevalence of anemia, iron deficiency and hookworm
infection remains largely unknown. Thus, before the development and
implementation of strategies in Vietnam to control iron deficiency anemia, further
analysis of these parameters is necessary.6
For the patients whose first symptom presented as acute upper
gastrointestinal bleeding, but were found chronic microcytic, hypo chromic anemia, it
was especially important to consider multi-reason possibility. In this case, chronic
blood loss caused by hook warm infection could be the reasonable explanation of
unmatchable small volume of hemorrhage at the beginning and heavy grade of

7
microcytic, hypo chromic anemia. The attachment of hookworms' cutting organs to
the intestinal mucosa and submucosa and the subsequent rupture of intestinal
capillaries and arterioles cause blood loss .6,7

Table 1 : Etiology of upper gastrointestinal bleeding1

Diagnosis Percentge (%)
Peptic Ulcer 35-50
Erosion of stomach and duodenum 8-15
Esophagitis 5-15
Varicose vein 5-10
Mallory Weiss Syndrom 15
Malignant disease of the upper gastrointestinal tract 1
Vascular malformation 5
Rare reason 5

In the first case,we found female, 39 years old with the work of housewife
came with complaints blackstool 3 days before entering the hospital and pale since 2
month ago. In the second case,we found female, 57 years old with the work of
housewife came with complaints blackstool and pale 10 days before entering the
hospital and the third case a male, 76 years old with the work of farmer came with
complaints blackstool and pale since 14 days before entering the hospital. We
diagnosis as upper gastrointestinal bleeding with differential diagnosis ulcus gaster,
ulcus duodenal and gastritis erosif
The Life Cycles of Necator americanus and Ancylostoma duodenale Humans
acquire hookworm when third-stage infective larvae in soil either penetrate the skin
(as do both N. americanus and A. duodenale ) or when they are ingested (A.

8
duodenale only). The larvae are each approximately 600 m long and are
developmentally arrested. After entering the host, the larvae receive a host-derived
signal that causes them to resume development. The larvae then migrate through the
vasculature and are swept by the afferent circulation to the right side of the heart and
then to the pulmonary vasculature. From the lung capillaries, the larvae rupture and
enter the parenchyma, where they ascend the alveoli, bronchioles, bronchi, and
trachea. After being coughed up and swallowed, the larvae enter the gastrointestinal
tract, where they molt twice and develop to the adult stage. Approximately six to
eight weeks pass from the time the larvae first infect humans until they reach sexual
maturity and mate. Each female hookworm produces thousands of eggs daily.
Intestinal blood loss in the host begins just before egg production and release and
continues for the life of the hookworm. Hookworm eggs exit the body in feces. When
deposited in soil, with adequate warmth, shade, and moisture, the eggs hatch within
24 to 48 hours and develop into first-stage larvae. These larvae molt twice as they
develop to the third stage. The larvae are nonfeeding organisms that can live for
several weeks in the soil, until they exhaust their lipid metabolic reserves.
Transmission of hookworm is most prevalent in areas where there is high moisture
and appropriate soil conditions. 4

9
 Intestinal blood loss is the major clinical manifestation of hookworm
infection. In fact, hookworm disease historically refers to the childhood syndrome of
iron deficiency anemia, protein malnutrition, growth and mental retardation with
lethargy resulting from chronic intestinal blood loss secondary to hookworm infection
in the face of an iron deficient diet. Hookworms ingest and digested some of the
blood from the injured mucosa by means of a multienzyme cascade of
metallohemoglobinases. Each Necator worm ingests 0.03 mL of blood daily, whereas
each Ancylostoma worm ingests 0.15-0.2 mL of blood daily. 4,5
Clinical diagnosis based on history of abdominal colics, intermittent diarrhea,
vomiting, teeth grinding during sleep in children and signs of malnutrition and poor
growth for cases of chronic infestations. 8

10
 There are no specific symptoms or signs of hookworm infection, but they give
rise to a combination of intestinal inflammation and progressive iron-deficiency
anemia and protein deficiency. Coughing, chest pain, wheezing, and fever will
sometimes result from severe infection. Epigastric pains, indigestion, nausea,
vomiting, constipation, and diarrhea can occur early or in later stages as well,
although gastrointestinal symptoms tend to improve with time. Signs of advanced
severe infection are those of anemia and protein deficiency, including emaciation,
cardiac failure and abdominal distension with ascites.8,10
In these case,blood loss caused by hook warm infection could be the
reasonable explanation of big volume of hemorrhage at the beginning and heavy
grade of microcytic, hypo chromic anemia.
Diagnosis depends on finding characteristic worm eggs on microscopic
examination of the stools, although this is not possible in early infection. The
diagnosis could be established according to the positive result of hookworm ovum
and the direct finding of hookworm in the stomach. 9,11
Diagnosis is usually made by evaluation of stool for the eggs. Recently, newer
small bowel imaging modalities like capsule endoscopy and double balloon
enteroscopy has identified hookwormas a cause of obscure gastrointestinal bleed
[1,2], but it is rare to find hookworm during upper GI endoscopy (Figure 1). Multiple
worms can be identified feeding on the mucosa of the small intestine and they appear
red in color or they can be identified in the luminal cavity and appear white in
color11,14,15
However; the diagnosis may be missed due to the absence of eggs of the
parasites in single stool specimen. The eosinophilia also may not be marked.
Repeated stool examination coupled with stool concentration is easy, cheap and
reliable to establish the diagnosis. Upper gastroscopy is a very important tool for the
diagnosis of gastrointestinal problems, and there are some reports of parasitic
diagnosis during routine upper gastrointestinal gastroscopy. When a worm is found

11
during gastrointestinal gastroscopy, it is important to identify the type of the worm by
microscopic examination for appropriate treatment.11,12
In all case, we found eggs ancylostoma in the initial fecal examination After
admission,the patient received esophagogastroduodenoscopy, the location of
bleeding was identified.Therefore, there were lesions that called it ulcus gaster that
caused the blood loss and it revealed many hookworms there where active bleeding
was seen.
Management is aimed at eliminating the parasite and anemia. Albendazole
400 mg single dose resulted in recovery of 80% and a dose of 200 mg / day for 3 days
members 100% recovery. Another alternative is a single dose of 500 mg
mebendazole, pyrantel pamoate 10 mg / kg for 3 days. Treatment of anemia is the
provision of ferrous sulfate or ferrous gluconate 200 mg orally 3 times a day until
three months after the normal hemoglobin level achieved for maintaining iron
reserves. In most cases the Hb increase of 1 gram / week. Needs to be given folic acid
5 mg daily for 1 month. Another option is a parenteral iron (iron dextran or iron
sorbitol poly glutanic acid in patients who can not tolerate oral iron. 9
The specific treatment of choice for elimination of hookworms from the intestines is a
benzimidazoleanthelmintic, either albendazole (400 mg once) or mebendazole (100
mg orally twice a day for 3 days or 500 mg once). 12
In the first case we was treated patient with albendazole 1x400 mg sigle dose
and combination with pyrantel pamoate 10 mg / kg / single dose. The second and
third case we was treated the patient with mebendazole 2x100 mg for 3 days and
combination with pyrantel pamoate 10 mg / kg / single dose. All case we transfusion
PRC 1bag/daily until Hb 10 gr/dl . Both of his hemoglobin and hematocrit were
improved to normal range in a follow up.
Figure 2. result of esophagogastroduodenoscopy

12
 (a) Women, 39 yo (b) woman, 57 yo (c) man, 74 yo
With proper treatment, the prognosis is excellent. Mortality is low, though
those hookworm-related deaths that do occur are probably underrecognized as a
consequence of the insidious nature of the disease. In classic hookworm disease,
appropriate anthelmintic treatment and iron and diet therapy typically result in
complete recovery from anemia and malnutrition, though some deficits in intellectual
function may persist. In endemic areas, reinfection is very likely: Most patients
become reinfected within months unless they are relocated to an area of significantly
improved sanitation. 13
The patient has clinical improvement and allowed to outpatient on 8th (first
case), 7th (second case) and 15th (third case)days treatment
Preventive for hookworm infection are not defecate in the open, but rather in
toilets, do not use untreated human excreta or raw sewage as fertilizer in agriculture,
do not walk barefoot in known infected areas, deworm pet dogs and cats, canine and
feline hookworms rarely develop to adulthood in humans because ancylostoma
caninum, the common dog hookworm, occasionally develops into an adult to cause
eosinophilic enteritis in people, but their invasive larvae can cause an itchy rash
called cutaneous larva migrans.13
In these case we educate the patien to wear the shoes if he go to the rise field
and always washing the hand before and after lunch.

IV. Conclusion
Three cases reported, with upper gastrointestinal bleeding due to ulcus gaster
related hookworm infection. Diagnosis based on clinical features,laboratoy
examination and esofagogastroduodenoscopy. Patients receive therapy proton pump

13
inhibibitor and mucoprotecto for ulcus gaster and antihelmintic for hookworm
infection. Patients experienced clinical improvement and patients were allowed to
outpatient treatment.

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