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< Case
Discussion>
A 23-year-old man, a vegetarian, was diagnosed as having ventricular
septal defect at birth, with spontaneous closure. He
also had had a remote history of bronchial asthma, without recent
attacks. He was recruited into the navy and started the training
in Ping Tung County two months prior to admission. About
3 weeks before this admission, he began to have intermittently
periumbilical abdominal pain. The pain was dull without
radiation. There were no aggravating or relieving factors
of the pain. He did not have any fever, nausea, diarrhea,
poor appetite or weight loss. He reported no recent travel
history. Because of worsening symptoms, he went to the emergency
room of a hospital one week after the onset of abdominal
pain. He received a diagnosis of constipation; however,
symptoms were not relieved after he took medications. Laboratory
studies showed eosinophilia (white blood cell, 11250
cells/μL; eosinophil, 36%). Stool examinations showed no evidence
of eggs or larvae of parasites. An upper endoscopy and
a colonofibroscopy showed gastritis and colitis without significant
finding. Random biopsies of the colon were taken and
the pathology examination demonstrated colitis with eosinophil
infiltration. He was treated as having eosinophilic
gastroenteritis with steroids for a week. Follow-up laboratory
studies showed worsening of eosinophilia (white blood cell,
18500 cells/μL; eosinophil, 76%). He was then referred to
another hospital for further management.
At admission to the second hospital, his blood pressure was
130/70 mmHg, the pulse was 74 beats per minute, the
respiratory rate was 16 breaths per minute and the temperature
was 36.5℃. On physical examination, his consciousness was
clear. The conjunctivae were not pale, and sclerae were
anicteric. His neck was supple, and there was no jugular vein
engorgement or palpable lymphadenopathy. His chest was
symmetric expansion. The breath sounds were clear. The heart
rhythm was regular without audible murmur. The abdomen was
flat and soft. The bowel sounds were normoactive. The liver
and spleen were impalpable. There was mild epigastric
tenderness without rebound tenderness or muscle guarding.
There was no Murphy's sign or shifting dullness. The
extremities were freely movable without pitting edema or joint
deformity. There were no skin rashes, ecchymosis or
purpura.
<Course and
Treatment>
After admission, an extensive
laboratory work-up, including serology and immunology testing,
was performed to search for the causes of eosinophilia. The
serum immunoglobulin
E
was elevated and
serum electrophoresis demonstrated polyclonal gammopathy.
Other work-up showed negative findings. An enteroscopy showed
negative findings. A computed tomography of the abdomen
revealed lymphadenopathies at the mesenteric root and
para-aortic region with some local fluid collection around the
cecum (Figure 1). Three fecal specimens were collected for
stool examinations and there were ova of hookworms in the
third specimen (Figure 2). He was then treated with a 3-day
course of pyrantel 750 mg per day. The abdominal pain improved
gradually. After release from the hospital, he did not have
any abdominal discomfort. Follow-up hemograms showed no
eosinophilia and the abdominal ultrasound showed no
intra-abdominal lymphadenopathy or ascites.
<Laboratory
Studies>
1. Hemogram
| WBC |
Hb |
MCV |
Platelet |
| K/μL |
g/dL |
fL |
K/μL |
| 18.50 |
14.1 |
90.1 |
288 |
WBC differentials:
| Segment |
Eosinophil |
Basophil |
Monocyte |
Lymphocyte |
| % |
% |
% |
% |
% |
| 14.0 |
76.0 |
1.0 |
3.0 |
6.0 |
2. Blood chemistry
| BUN |
Cre |
Na |
K |
Ca |
Alb |
TP |
GOT |
GPT |
T-Bil |
ALP |
r-GT |
| mg/dL |
mg/dL |
mmol/L |
mmol/L |
mmol/L |
g/d |
g/d |
IU/L |
IU/L |
mg/dL |
IU/L |
mg/dL |
| 15.9 |
0.9 |
134 |
4.5 |
2.17 |
4.2 |
6.3 |
29 |
32 |
0.6 |
139 |
9 |
3. Autoimmune profile
| RF |
ANA |
C3 |
C4 |
Anti-SS-A |
Anti-SS-B |
Anti-Jo-1 |
| IU/ml |
|
mg/dl |
mg/dl |
AU/ml |
AU/ml |
AU/ml |
| <20.0 |
1:40 |
116.0 |
13.1 |
0.9 |
0.3 |
0.1 |
| C-ANCA |
P-ANCA |
IgG |
IgM |
IgA |
IgE |
| U/ml |
U/ml |
mg/dl |
mg/dl |
mg/dl |
mg/dl |
| 0.8 |
1.5 |
959 |
167 |
188 |
2315 |
Electrophoresis: increased alpha 1 and decreased beta
globulins (probably acute phase reaction)
4. Urinalysis
| Sp.Gr. |
pH |
Protein |
Glucose |
OB |
Bil. |
Urobi |
Ketone |
Nitrite |
| |
|
mg/dl |
g/dl |
|
|
|
|
|
| 1.024 |
6.0 |
|
|
|
|
Normal |
|
|
| RBC |
WBC |
Epithelial cell |
Cast |
Crystal |
Bacteria. |
| /HPF |
/HPF |
/HPF |
/LPF |
/LPF |
|
| 0-1 |
- |
- |
Amo-urate (2+) |
Amo-urate (2+) |
1+ |
Figure 1. Computed tomography of the abdomen showing
lymphadenopathies at the mesenteric root and para-aortic
region.
5. Stool
examinations
Specimen 1: Fecal occult blood
test: 2+; no pus; no parasite ovum
Specimen 2: Fecal occult
blood test: 3+; no pus; no parasite ovum
Figure 2. A hookworm ovum was identified in the third stool
sample.
<Discussion>
Eosinophilia is defined as a peripheral blood eosinophil
count >450 cells/μL. Acquired eosinophilia can be divided
into categtgories of primary or secondary eosinophilia,
depending on whether eosinophils are considered integral to
the underlying diseases. Causes of primary eosinophilia can be
classified into (1) clonal eosinophilia: usually occurs in the
context of hematologic malignancies (e.g., acute leukemia or
chronic myeloid disorders), or (2) hypereosinophilic syndrome:
persistent eosinophilia (absolute eosinophil count >=1,500
cells/μL for >=6 months) and target organ damage (e.g., skin,
heart, lung, nerve tissue), as well as lack of other known
causes of secondary hypereosinophilia. The causes of secondary
eosinophilia include infectious and non-infectious diseases.
Non-infectious causes of secondary eosinophilia include drugs,
allergic disorders (e.g., asthma, atopic dermatitis, allergic
bronchopulmonary aspergillosis), autoimmune inflammatory
diseases (e.g., granulomatous or systemic vasculitis,
Churg-Strauss syndrome, Wegener's granulomatosis, cutaneous
disorders, scleroderma, polyarteritis, sarcoidosis,
inflammatory bowel disease), malignancies (in which
eosinophils are not considered part of the neoplastic clone)
and endocrinopathies. Secondary eosinophilia can be caused by
a variety of infections, among which parasitic infection is the
most common one.
The most common cause of secondary eosinophilia is
parasitic infection, including hookworms. Hookworm infection
in humans is caused by an infection with the helminth nematode
parasites, and is one of the most common chronic infections.
Hookworm is one of the most common parasites in the world. The
majority of human hookworm infections are caused by
Ancylostoma duodenale and Necator americanus. A. duodenale and
N. americanus hookworm eggs hatch in the soil. On contact with
the skin, infectious third-stage larvae penetrate the human's
skin and enter subcutaneous venules and lymphatic vessels. The
larvae are trapped in pulmonary capillaries, enter the lungs,
pass over the epiglottis, and migrate into the
gastrointestinal tract. Once the hookworms mature in the small
intestine, eggs may be found in stool. The time from skin
penetration to development of egg-laying adults needs about 5
to 9 weeks. A. duodenale larvae are also orally infective.
Repeated exposure to third-stage larvae of A. duodenale or
N. americanus results in a local erythematous and papular rash
accompanied by pruritus, known as “ground itch”, which appears
most frequently on the hands and feet. If third-stage larvae
of zoonotic hookworms, typically A. braziliense, enter the
skin, they produce cutaneous larva migrans, known as “creeping
eruption”, which was characterized by serpiginous tracks on
the feet, buttocks and abdomen. The major clinical
manifestations of hookworm infection are the consequences of
chronic intestinal blood loss, including iron deficiency
anemia and hypoalbuminemia. In addition, the most prominent
laboratory finding is eosinophilia, which peaks at 5 to 9
weeks after the onset of hookworm infection. A total number of
40 to 160 adult hookworms in the small intestine are estimated
to be sufficient to reduce the host's hemoglobin below 11
g/dL. Patients with a light hookworm burden are usually
asymptomatic. A moderate or heavy hookworm burden results in
recurrent stomachache, nausea, dyspnea, pain in the lower
extremities, palpitations, headache and fatigue. Other
manifestations include skin itching, cough and sore
throat.
The diagnosis of hookworm infection is usually made by the
characteristic clinical findings (e.g., eosinophilia and egg
shape appearance on fecal examinations). Because many hookworm
infections present without specific symptoms and signs, the
physicians need some index of suspicion (e.g., local
epidemiology or travel history) to request a fecal
examination. However, stool examinations for the eggs of A.
duodenale and N. americanus are not helpful during the early
phase of infection (larval migration phase) because eggs begin
to appear in the stool approximately 6 to 8 weeks after dermal
acquisition of N. americanus infection and up to 38 weeks for
A. duodenale. It is recommended that at least three stool
specimens be examined to detect the presence of intestinal
hookworms. However, misdiagnosis still can occur due to the
absence of eggs of the parasites in stools or eosinophilia. In
addition, endoscopy can be helpful in diagnosing hookworm
infection in patients with abdominal pain or other
gastrointestinal symptoms. If present, these parasites usually
live in the upper part of the small intestine. Reliable
serologic tests are not available.
The specific treatment of choice for the removal of
hookworms from the intestines include (1) albendazole 400 mg
once; (2) mebendazole 100 mg twice daily for 3 days; (3)
pyrantel pamoate 11 mg/kg (maximum dose 1 g) for 3 days; or
(4) levamisole 2-5 mg/kg once (repeat after 7 days in heavy
infection).
<References>
- Bethony
J, Brooker S, Albonico M, et al. Soil-transmitted helminth
infections: ascariasis, trichuriasis, and hookworm. Lancet.
2006;367:1521-1532.
- Bungiro
R, Cappello M. Hookworm infection: new developments and
prospects for control. Curr Opin Infect Dis 2004;
17:421-426.
- Hotez
PJ, Brooker S, Bethony JM, et al. Hookworm infection. N Engl
J Med. 2004;351:799-807.
- Tefferi
A. Blood eosinophilia: a new paradigm in disease
classification, diagnosis, and treatment. Mayo Clin Proc.
2005;80:75-83.
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Case Discussion
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