Anemia - Sem
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ANEMIA
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Definition
According to Cawson Scully, Anemia is
not a disease in itself and may be a
feature of many diseases but the
different type of anemia have many
clinical features in common
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CLASSIFICATION
(Based on the pathogenesis)
Blood loss anemia Iron deficiency anemia; Plummer Vinsonsyndrome
Hemolytic anemia Glucose 6 Phosphate Dehydrogenase; druginduced; immune mediated
Hemoglobinopathies or disorders of hemoglobin Sickle cellanemia; Thalassemia; Cooleys anemia
Hypoproliferative anemia Vitamin B12 deficiency;
Pernicious anemia; Folic acid deficiency; Aplastic anemia
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Causes ofanemia Blood loss Menorrhagia, Any gastrointestinal lesion (e.g. ulcer
or carcinoma), lesion of the urinary tract, trauma
Impaired absorption of hematinics
Increased demands for hematinics especially pregnancy
Poor intake of Hematinics Aplastic anemia and Leukemia
Hemolytic anemias
Miscellaneous mechanisms, including drugs and chronic disease
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Clinical features of anemia
Sometimes none
General lassitude
Cardiorespiratory
DyspnoeaCongestive cardiac
failure
Murmurs
Angina pectoris
Cutaneous
Pallor
Brittle nails
Koilonychia (irondeficiency)
Oral
Sore mouth
Oral ulceration
Angular stomatitis
Glosstitis
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In general anesthetic
The main danger is when a general anesthetic is
given, as it a vital to ensure full oxygenation
Myocardium may be unable to respond to the
demands of anesthesia Whenever possible therefore the cause of the
anemia should be corrected preoperatively, but at
least the hemoglobin level must be raised, if
necessary by transfusion.
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In general anesthetic
Elective operations under general anesthesia
should not usually be carried out when the
hemoglobin is less than 10 g/dl
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In general anesthetic
In an emergency, anemia can be corrected
by whole blood transfusion, but this should
only be given to a young and otherwise fit
patient
Transfusion risks include fluid overload, and
viral infections such as hepatitis and HIV
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In general anesthetic
Packed red cells avoid the risk of fluid
overload and can be given in emergency to
the elderly patient or those with incipient
congestive cardiac failure. A diuretic given at
the same time further reduces the risk of
congestive cardiac failure.
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In general anesthetic
The patient should be stabilized at least 24
hours preoperatively and it should be noted
that hemoglobin estimation are unreliable for
12 hours post-transfusion. Nitrous oxide is
possibly contraindicated in vitamin B12,
deficiency
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Iron Deficiency Anemia
Women of child bearing age and older are
therefore mainly affected
Excessive menstrual losses or
gastrointestinal blood loss are the main
causes. Very many children are mildly iron
deficient because of the high demands for
growth, especially during adolescence.
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Iron Deficiency Anemia
By contrast, iron deficiency in an adult male
almost invariably indicates blood loss, usually
from the gastrointestinal or genitourinary
tracts. The same holds true for post-
menopausal women
Symptoms ascribed to iron deficiency do not
always respond to iron replacement
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IRONDEFICIENCY ANEMIA
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Laboratory findings during the development of iron deficiency anemia
MCVHb MCHC Serum
ferriti
n
Transferrinsaturation*
Marrow ironstores
Normal N N N N 33% N
Mild iron deficiency anaemiaq
N orq
Nq
>16%
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Treatmentofiron deficiency
The best treatment of iron deficiency is an
iron salt by mouth but the cause of the
deficiency should be found and eliminated
Ferrous gluconate 250 mg/day can be given
if ferrous sulphate is not tolerated
FeSO4200mg 3 times/ day
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Treatmentofiron deficiency
Oral iron may need to be given for 3 months
or more to replenish marrow iron stores
Parenteral iron has no advantages except,
for example, when inflammatory bowel
disease is aggravated by oral iron
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PLUMMERVINSONSYNDROME
Dysphagia; Xerostomia
Depapillated tongue
Koilonychia
Angular stomatitis
Pallor and fatigue dyspnea
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Vitamin B12 Deficiency
Pernicious (Addisonian) anemia is the most
common type of macrocytic anemia and
typically affects women in the middle age or
over particularly of Northern Europeandescent
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Pernicious anemia
It is caused by a specific defect of absorption of
Vitamin B12 not by malnutrition
Autoantibodies against gastric parietal cells and / or
intrinsic factor or both are found and the disease issometimes seen with other autoimmune diseases,
especially hypothyroidism, or less often, diabetes,
mellitus, vitiligo, Addisons disease or
hypothyroidism
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Causes of vitamin B12 deficiency
Poor intake
Poverty
Strict vegetarians
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Causes of vitamin B12 deficiency
Malabsorption
Defect in intrinsic factor production Congenital
Autoimmune (pernicious anemia)
Gastrectomy
Illeal diseaseCoeliaa disease
Tropical sprue
Crohns disease
Blind loop syndrome
Resections
Fish tapeworm
Transcobalamin II deficiency
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Causes of vitamin B12 deficiency
DrugsColchicine
Neomycin
Nitrous oxide
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Causes of folate deficiency
Poor intake
Poverty
Old age Alcoholism
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Causes of folate deficiency
Malabsorption
Coeliac disease
Crohns disease Other malabsorption states
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Causes of folate deficiency
Increased demandsInfancyPregnancyChronic
hemolysisMalignant diseaseExfoliative skin
lesionsChronic dialysis
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Causes of folate deficiency
Increased demands
Infancy
Pregnancy Chronic hemolysis
Malignant disease
Exfoliative skin lesions
Chronic dialysis
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Oral aspects of the deficiency anemias
sore or burning, but otherwise normal tongue
Atrophic glossitis
Moellers glossitis and other colour changes
Candidosis
Angular stomatitis (cheilitis)
Aphthous stomatitis
PatersonK
elly syndrome (Plummer
Vinson)
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Anemia associated with systemic disease
Chronic inflammation (infections or
connective tissue disease).
Neoplasms including leukaemia. Acute
leukaemia is an important cause of
anaemia and should always be considered
when anaemia is seen in a child.
Liver disease.
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Anemia associated with systemic disease
very rarely : Hypothyroidism
Hypopituitarism Hypoadrenocorticis
Uraemia
HIV infection
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Aplastic Anemia
Bone-marrow aplasia is a rare disease
causing refractory normochromic, normocytic
anemia, leucopenia and thrombocytopenia
Drugs are an important cause but many
cases are idiopathic, though probably viral or
immunologically mediated
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Aplastic Anemia
The prognosis is poor and 50
per cent of patients die within 6
months usually fromhemorrhage or infection
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Causes of aplastic anaemia
Idiopathic
Genetic
Fanconis anaemia
Dyskeratosis congenita
Drugs
Phenylbutazone
Chloramphenicol
Sulphonamides
Gold Penicillamine
Anticonvulsants
Cytotoxic agents
Chemicals
Benzene
Toluene
Heavy metals
Glue-sniffing Viruses
Hepatitis
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Principles ofmanagement
Removal of the cause. Even when this isdecoverable, as in the case of drugs, such aschloramphenicol, marrow damage may still beirreversible
Isolation and antibiotics to control infection Androgenic steroids. (Corticosteroids are of
questionable benefit)
Bone marrow transplantation after intenseimmunosuppression. This in turn may cause graft-
versus-host disease (GVHD) which is often lethal
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Oral manifestations ofAplastic anemia
and managementare somewhat similar to those of leukemia, namely;
Anemia
Hemorrhagic tendencies
Susceptibility to infections Effects of corticosteroid therapy
Hepatitis B and other viral infections
Oral lichenoid lesions, or a Sjogren like syndrome may developif there is graft-versus-host disease if marrow transplantation hasbeen carried out to relieve the anemia. Gingival hyperplasia may
develop if cyclosporin is used.
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Fanconis anemia
a rare autosomal recessive syndrome characterized by:
skeletal defects
hyperpigmentation
pancytopenia &
other congenital anomalies
It is associated with an increased susceptability to
oral or other head and neck carcinomas at an early
age, as is dyskeratosis congenital
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Bone-marrowtransplantation
is increasingly used, particularly in
the treatment of aplastic anemia,
leukemia and some immunedeficiencies
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Bone-marrowtransplantation
Patients are usually prepared for transplantwith cyclophosphamide, with or without totalbody irradiation, such that they will accept
donor bone-marrow with minimal chance orrejection. Recipients are then, aftertransplantation, treated with methotrexate ormore usually cyclosporin for 6 months or
more to prevent or ameliorate graft-versus-host disease
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Genetherapy
Gene therapy clinical trials that could lead to
a cure for children
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Oral symptoms
are the main complaint in patients after bone-
marrow transplantation and consist of
mucositis, dry mouth, sinusitis,parotitis and otherinfections, pain orbleeding
These develop usually within the first month of the transplant and are
exacerbated by chemotherapy and immunosuppressive treatment.
Cyclosporin may induce gingival hyperplasia
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Management problems caninclude
Oral complications of cytotoxic treatment and
radiotherapy, particularly oral herpetic and
fungal infections which are now recognized
as the main causes of death
Immunosuppressive therapy
Graft-vesus-host disease
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Anaemia caused bymarrowinfiltration
Replacement of haemopoietic marrow by abnormal cells
(metastases, leukaemias, myeloma or myelofibrosis) causes
normocytic anaemia and often leucopenia or thrombocytopenia
with a leucoerythroblastic peripheral blood picture. There may be
extramedullary haemopoiesis in other organs
Dental care may be complicated by
susceptibility to infections, haemorrhage
(as in aplastic anaemia) or the
underlying disease
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Hemolytic anemias
Worldwide, malaria is the most common
cause of hemolytic anemia
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Hemolytic anemia mayalsoresultfrom
manyothercauses
Abnormal hemoglobin (the
hemoblobinopathies)
Abnormal structure or function of the
erythrocyte
Damage to erythrocytes (autoimmune or
infective)
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Congenital Hemolytic Anemias
Hemoglobinopathies
sickling disorders
Thalassaemias
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Sickling disorders include
Heterozygoous sickle cell trait (HbAS)
Homozygous sickle cell anaemia or disease
(HbSS)
Heterozygous sickling trait associated with
another hemoglobinopathy
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Disorder Haemoglobin typeOrigins of predominant racial groups
affectedClinical features
Sickle cell trait S A Africa, West Indices, Mediterranean, India Usually asympotomatic
Sickle cell anaemia S-S Africa, West Indices, Mediterranean, India Severe anaemiaJaundice
Impaired growthCrises
InfarctsInfections
Sickle cell HbC disease S-C West Africa, South East Asia Variable anaemia
Sickle cell HbD disease S-D Africa, India, Pakistan Moderately severe anaemia
Sickle cell HbE disease S-E South East Asia Moderately severe anaemia
Sickle cell thalassaemia S-A-F Mediterranean, Africa, West Indices Moderately severe anaemia
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Sickle cell trait (HbAS)
The sickling trait is frequently
asymptomatic, but sickle cell crises can be
caused by reduced oxygen tension (general
anesthesia, high altitudes or unpresurizedaircraft). At times such patients may have
renal complications causing hematuria or
splenic infarcts
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Features of sickle cell anemia
Anemia
Jaundice
Impaired growth
Dactylitis
Skeletal deformities Painful crises
Aplastic crises
Susceptability to infections
Infarcts of CNS, lungs, kidney, spleen
Skin ulcer
Gall stone
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Painful crises
Infection
Dehydration
hypoxia
acidosis or
cold and cause severe bone pain and pyrexia
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Hematological crises
These are often causes by parvovirus
infections and can be of three types, namely :
Hemolytic
Aplastic
Sequestration crises
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main cause of death in sicklecell anemia is infection,
particularly by pneumococci,meningococci and salmonellae,because of an associated
immune defect mainly as aresult of splenic dysfunction.
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Laboratoryinvestigations in sickling
disorders
In sickle cell disease there is anemia and
reticulocytosis; sickled erythrocytes are
sometimes seen in a stained blood film
By contrast, hematological findings are often
normal in sickle cell trait
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Laboratoryinvestigations in sickling
disorders
Sickling may be demonstrated in both sickle cell
anemia and trait, by tests relying on the decreased
solubility of HbS (Sickledex) or by the additionof a reducing agent (such as 10 per cent sodiummetabisulphate or dithionite) to a blood sample
Hemoglobin electrophoresis shows HbS and upto 15
per cent HbF, but no HbA in sickle cell anemia
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Nowadays an increasing number of patientswith sickle cell disease survive into latemiddle age; infections and thromboses are
the main cause of death If the sickle cell test is positive, hemoglobin
electrophoresis is required to establish thediagnosis, but if the hemoglobin is less than
11 g/dl sickle cell anemia is probable
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Sickle cell trait (HbAS)
Patients with the common sickle cell trait
cause few problems in management but if
general anesthesia is necessary full
oxygenation must be maintained throughout.Respiratory infections must be treated
vigorously as they can cause a crisis
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Sickle cell anemia (HbSS)
oral mucosa may be pale or jaundiced and
there may be a susceptability to dental
infection
Hard tissue changes are conspicuous:hypercementosis may develop and there is
bone-marrow hyperplasia with apparent
osteoporosis of the jaw. Skeletal but notdental maturation is delayed
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The lamina dura is distinct and dense and the
permanent teeth may be hypomineralized,
though neither caries nor periodontal disease
is more severe
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The skull is thickened but osteoporotic with a
hair on end pattern to the trabeculae.The dipole are thickened, especially in the
parietal regions giving a tower skull form Lesions suggestive of bone infarction
dense radio-opacities may be seen in the
skull and / or jaws
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Patients with sickle cell anemia must bemanaged with the help of a hemotologist
Pulpal symptoms are common in the absence
of any obvious dental disease Acute infections should be treated
immediately, since they may precipitate asickling crisis
Surgical procedures should have antibioticcover
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Alpha thalassaemias
Beta thalassaemias
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Cooleys anemia most serious type and is characterized by failure to
thrive, increasingly severe anemia,hepatosplenomegaly and skeletal abnormalities
Affected children are susceptible to folate deficienc(as in other chronic hemolytic states) and also to
infection
Discolouration of teeth
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Patients with homozygous beta-
thalassaemia become overloaded with iron
and hemosiderosis damages the heart, liver,
pancreas, skin and sometimes the salivary
glands, causing a sicca syndrome
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major oral changes in thalassaemia are
enlargement of the maxilla caused by bone
marrow expansion (chipmunk facies) Alveolar bone rarefaction produces a chicken
wire appearance on radiography Pneumatization of the sinuses may be delayed
Expansion of the dipole of the skull causes a
hair-on-end appearance that is frequentlyconspicuous on lateral skull radiographs
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Less common oral complications include
painful swelling of the parotids and
xerostomia caused by iron deposition, and a
sore of burning tongue related to the folatedeficiency
difficulties in intubation
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G6PDDEFICIENCY
Icteric sclera skin, soft palate
and floor of the mouth
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G6PDDEFICIENCY
Apart from the problems of anemia it is vital to avoid
oxidant drugs such as the sulphonamids (including
co-trimoxazole) or menadiol (water soluble vitamin K)
which can precipitate hemolysis
Aspirin can be safely used in G6PD deficiency
Metabolic acidosis also causes hemolysis and must
be avoided during general anesthesia
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Acquired hemolytic anemia
Intravascular destruction of erythrocytes can
caused by factors such as gross trauma,
complement mediated lysis, toxins and
malaria These diseases are rare but may
occasionally have dental relevance because
of anemia, corticosteriod treatment orhemorrhagic tendencies
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Ch l l P
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Chronic Renal FailurePatients
Administration of PROCRIT is an increasein the reticulocyte count within 10 days,followed by increases in the red cell count,
hemoglobin, and hematocrit, usually within 2to 6 weeks
PROCRIT, at a dose of100 Units/kg TIW,
is effective in decreasing the transfusionrequirement and increasing the red bloodcell level of anemic
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CONCLUSION
The existence of anemia in surgical patients
has implications that are brief consideration.
Anemia has a number of pathophysiological
consequences of decreased oxygen carryingcapacity of the blood.
CONC S ON
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CONCLUSION
Cardiorespiratory problems
Impaired wound healing
Precipitation of hemolysis
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CONCLUSION
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CONCLUSION
Wound healing:
Relative hypoxia impairs tissue
healing and increases the risk of infection.
CONCLUSION
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CONCLUSION
Precipitation of Hemolysis:
Hypoxia of anesthesia can induced
hemolysis crises in certain hereditary
hemolytic anemias such as sickle celldisease. Preoperative planning with or
without transfusion and careful anesthesia
aim to prevent this
CONCLUSION
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CONCLUSION
Operating on a background of anemia will
result in the patient having fewer reserves to
compensate for operative blood loss. There
might be associated depletion of other bloodcells, including WBC, which increases
susceptibility to infection and platelets which
increases the bleeding tendency.
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CONCLUSION
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CONCLUSION
Oxygen carrying capacity of the transfused
blood is lowered by the presence of high
concentration of2,3 Di Phosho Glycerate
(DPG) and H+ ions which sift the oxygen hemoglobin dissociation curve to the
right.(known as Bohr effect)
CONCLUSION
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CONCLUSION
According to the principles of radiation
oncology, a patient with significant anemia
has been suggested to adversely effect the
efficacy of radiation therapy in patients withhead and neck cancer and therefore patients
being treated with curative intent should have
a hematocrit more than 30%
REFERENCE
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REFERENCE
CAWSON & SCULLY
DAVIDSON
DAVID WRAY JATIN SHAH
OOO/FEB2003/SCOTT
NCCN
ROSSERT www.goggle.com
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