Anemia is one of the most commonly seen condition predominantly in women due to various causes such as some chronic infection conditions and all. There are different types of anemias are there here we discuss mainly about Iron deficiency and sickle cell anemia.

1. AMEENA KADAR K A
FIRST SEM M PHARM
PHARMACY PRACTICE
SANJO COLLEGE OF PHARMACEUTICAL STUDIES
ANEMIA

2. ANEMIA:
 It is a group of diseases characterized by a decrease in either hemoglobin (Hb)
or the volume of red blood cells (RBCs), which results in decreased oxygen-
carrying capacity of the blood.
 Anemia is defined by the World Health Organization (WHO) as Hb less
than 13 g/dL (less than 130 g/L; less than 8.07 mmol/L) in men and less
than 12 g/dL (less than 120 g/L; less than 7.45 mmol/L) in women.
 Children of both sexes below 14 years of age have lower levels, the cut-off for
anemia being 11 g/dL in those aged 6 months to 6 years and 12 g/dL in the 6–14
age group.
 Anemia is not one disease, but a condition that results from a number of
different pathologies.
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EPIDEMIOLOGY
 Anemia is possibly one of the most common conditions in the world and
results in significant morbidity and mortality, particularly in the developing
world.
 Worldwide, over 50% of pregnant women and over 40% of infants are
anemic.
 The prevalence of anemia among six groups as per the National Family Health
Survey 5 (2019-21), is 25.0 percent in men (15-49 years) and 57.0 percent in
women (15-49 years). 31.1 percent in adolescent boys (15-19 yrs), 59.1 percent
in adolescent girls, 52.2 percent in pregnant women (15-49 years) and
67.1percent in children (6-59 months).

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o A hematocrit test measures the proportion of red blood cells in your blood.
Male = <42%.
Female = <37%.

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CLASSIFICATION OF ANEMIA
 Anemia can be classified on the basis of
 Morphology of the RBCs
 Etiology
 Pathophysiology
 Physiology.

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MORPHOLOGICAL CLASSIFICATION OFANEMIA

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ETIOLOGICAL CLASSIFICATION OF ANEMIA
Etiological
classification of
Anemia
Deficiency
Iron
Vitamin B12
Folic acid
Pyridoxine
Bleeding
(hemorrhage)
Hemolysis
(hemolytic
anemia)
Peripheral
Impaired Bone
Marrow
Function
Anemia of chronic
disease
Anemia of the
elderly
Malignant bone
marrow disorders

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PATHOPHYSIOLOGICAL CLASSIFICATION OF ANEMIA
ANEMIA BASED ON
PATHOPHYSIOLOGY
EXCESSIVE
BLOOD LOSS
Recent hemorrhage
Trauma
Peptic ulcer
Gastritis
Hemorrhoids
CHRONIC
HEMORRHAGE
Vaginal bleeding
Peptic ulcer
Intestinal parasites
Aspirin and other
NSAIDs
ENHANCED RBC
DESTRUCTION
Hemolytic anemia
INADEQUATE
PRODUCTION OF
RBC
Aplastic anemia

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PHYSIOLOGIC CLASSIFICATION OFANEMIA

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ETIOLOGY
The low hemoglobin level that defines anemia results from two different
mechanisms:
• Increased hemoglobin loss due to either: – hemorrhage (red cell loss) or –
hemolysis (red cell destruction).
• Reduced hemoglobin synthesis due to either: – lack of nutrient or – bone
marrow failure.
• Host of systemic disorders such as infection, chronic renal diseases or
malignancy.

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Use of erythrocyte morphology in differential diagnosis of anemia

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MICROCYTIC ANEMIA

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IRON DEFICIENCY ANEMIA (IDA)
 Iron deficiency is a state of negative iron balance in which the daily iron intake
and stores are unable to meet the RBC and other body tissue needs.
 The body contains approximately 3.5 g of iron, of which 2.5 g are found in Hgb.
 A significant amount of iron is stored as ferritin or aggregated ferritin
(hemosiderin) in the reticulo-endothelial cells of the liver, spleen, and bone
marrow and by hepatocytes.
 Decreased level of ferritin and serum iron, as well as decreased transferrin
saturation.
 Hb and Hematocrit decrease later.
 Daily requirement of Iron 0.9mg in males, 2mg females, in pregnancy it is 3-
5mg and in infant it is 0.5mg.
 The daily recommended dietary allowance for iron is 8 mg in adult males and
postmenopausal females and 18 mg in menstruating females.

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EPIDEMIOLOGY
 Iron deficiency anemia is the commonest form of anemia worldwide and may
be present in up to 20% of the world's population.
 A diet deficient in iron, parasitic infestations, for example, hookworm (causing
blood loss), and multiple pregnancies contribute to its high prevalence in
underdeveloped countries.
 Even in Western societies, it has been reported that as many as 20% of
menstruating females show a rise in hemoglobin levels on iron therapy

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 Causes of Iron Deficiency Anemia
 Blood Loss
• Menstruation
• Gastrointestinal (e.g., Peptic ulcer)
• Trauma
 Decreased Absorption
• Medications
• Gastrectomy
• Regional enteritis
 Increased requirement
• Infancy
• Pregnant/lactating women
 Hereditary
 Impaired Iron use

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PATHOPHYSIOLOGY OF IDA
 Diminished total body iron content, developing in stages over a period of
negative iron balance.
Iron depletion – Stage One
Iron deficient erythropoiesis – Stage Two
Iron deficiency anemia – Stage Three
 Stage One
Iron storage is exhausted - indicated by decrease in serum ferritin levels, no
anemia – RBC morphology is normal.
 Stage Two
Insufficient iron to insert into protoporphyrin ring to form heme – Protoporphyrin
accumulates in cell and complexes with zinc to form ZPP, no anemia, no
hypochromia, but slight microcytosis may be decreased.

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 Stage Three
All laboratory tests for iron status become abnormal, most significant finding is
microcytic, hypochromic anemia and there is hyperplasia of erythroids.
 Erythroid hyperplasia is a condition of excessive count of erythroid precursor
cells (in layman words, immature red blood cells) in the bone marrow.

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ANEMIA
Decrease synthesis of hemoglobin, myoglobin and other iron containing
proteins
Decrease in serum iron and decrease in serum transferrin
Decline in serum ferritin and absence of stainable iron in bone marrow
Iron stocks deplete
Iron deficiency develops insidiously

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 Pale skin and mucous membranes
 Painless glossitis (Inflammation of the tongue)
 Angular stomatitis (Red, swollen patches in the both corners of mouth)
 Koilonychia (spoon shaped nails)
 Dysphagia (difficulty in swallowing)
 Pica (unusual cravings)
 Atrophic gastritis
 Poikilocytes
SIGNS OF IDA
Chronic Iron deficiency

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Atrophic gastritis: Chronic
inflammation of gastric mucosa
with loss of gastric glandular cells.
Poikilocytes: Increase
in abnormal shape of
RBCs

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Plummer-Vinson syndrome (PVS)
 It is a rare condition characterized by the classic triad of dysphagia, iron-
deficiency anemia, and esophageal webbing.
 Plummer-Vinson syndrome is more common in middle-aged women and is
associated with an increased risk of developing squamous cell carcinoma of the
pharynx and proximal esophagus.
 A disorder marked by anemia caused by iron deficiency, and a web-like
growth of membranes in the throat that makes swallowing difficult.

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SYMPTOMS OF IDA
1) Faintness
2) Fatigue
3) Dizziness
4) Irritability
5) Malaise
6) Palpitation
7) Headache
8) Shortness of breath
9) Angina
10) Ankle edema

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LABORATORY DIAGNOSIS OF ANEMIA

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MANAGEMENT OF IDA
Treatment Goals
 To Decrease Signs And Symptoms
 Correct The Underlying Etiology
 Prevent Recurrence Of Anemia.

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A. NON- PHARMACOLOGICAL MANAGEMENT OF IDA
 Iron rich diet
 Blood Transfusion

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B. PHARMACOLOGICAL MANAGEMENT OF IDA
IRON
ORAL IRON
Ferrous sulphate
Ferrous gluconate
Ferrous fumarate
Ferrous succinate
PARENTERAL
IRON
Iron-dextran
Iron-sorbitol-citric acid
Ferrous sucrose
Ferric carboxymaltose

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 ORAL IRON THERAPY
 Iron Salts
o Ferrous Sulphate
o Ferrous Fumarate
o Ferrous Gluconate
 200 mg elemental iron per day for 3-6 months.
 2-3 divided doses to maximize tolerability.
 Administration should be 1 hour before meals or on empty stomach.
 Daily requirement of iron
• Male 0.5-1mg
• Female 1-2mg
• Pregnancy 3-5mg.

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Characteristics of various iron formulations

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ORAL IRON DOSING
 Ferrous sulphate given as oral dose, the usual dose for an adult is 325mg (one
tablet), administered 2-3 times a day
 However, due to limited absorption of iron by the intestinal walls, its preferred
to administer lower doses of iron as its shown to be more effective with less
side effects and improved compliance.
 The required daily dose may be calculated using the formula given, with
assumption that 0.25g/dL/day is the maximal rate of Hgb regeneration.
 Elemental iron(mg/day)= 0.25g Hgb/100mL blood/day
(5000mL blood)(3.4mg Fe/1g Hgb)
=40mg Fe/day/20% absorption (approximate absorption rate in
iron-deficient states)
=200mg Fe/day
=1000mg ferrous sulphate/day
=325mg TID ferrous sulphate

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ADR OF ORAL IRON
 Epigastric pain
 Heart burn
 Nausea
 Vomiting
 Bloating
 Staining of teeth
 Metallic taste
 Constipation (More common- believed to be astringent action of iron)
 Abdominal pain.
 Patients should be warned that their faeces may become darker.
 Food interfere with iron absorption but sometimes administration with food
is recommended incase of GI symptoms.

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DRUG INTERACTIONS

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PARENTERAL IRON THERAPY
Indications of therapy
o Intolerance to oral route
o Malabsorption
o Long term non adherence
o Patient with significant blood loss who refuse transfusion and are
intolerant to oral therapy
o Chronic kidney disease (CKD).
 Examples:
Iron dextran
Iron sucrose
Iron carboxymaltose

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1. Iron-dextran
 High Mol.wt colloidal solution containing 50 mg elemental iron/ml.
 It is the only preparation that can be injected I.M. as well as I.V.
 The total dose of iron dextran to be administered can be determined using the
following equation:
Iron (mg) = [Weight (pounds) × 0.3]
[100 − {100(Hgb)/14.8}]
where Hgb is the patient’s measured hemoglobin (g/dL).
 ADR:
a. Local: Pain at site of I.M. inj, pigmentation of skin, sterile abscess-especially
in old and debilitated patient.
b. Systemic: Fever, headache, joint pains, flushing, palpitation, chest pain,
dyspnea, lymph node enlargement.
c. Anaphylactoid reaction resulting in vascular collapse & death.

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Parenteral Iron Preparations

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Hemochromatosis (Iron overload)
 Iron overload is defined as excess stores of iron in the body.
 Excess iron is deposited in organs throughout the body.
 The most notable organs with iron deposition are the liver, heart, and endocrine
glands.
 The resulting symptoms and disease are related to specific organ damage.
 The treatment for iron overload is reduction therapy. This is most commonly
achieved through therapeutic phlebotomy.
 In patients with hemoglobin levels that do not tolerate therapeutic phlebotomy,
iron chelation therapy becomes an option.
 Desferoxamine (IV/SC) is an iron chelation therapy currently in use.
 It binds free iron and iron bound to ferritin.
 An oral deferiprone is also beneficial but it causes reversible neutropenia
in some patients and weekly neutrophil count are required.

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TREATMENT ALGORITHM

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SICKLE CELLANEMIA
 An inherited disease in which the red blood cells have an abnormal crescent
shape, block small blood vessels, and do not last as long as normal red blood
cells.
 Sickle cell anemia is caused by a mutation (change) in one of the genes for
hemoglobin (the substance inside red blood cells that binds to oxygen and
carries it from the lungs to the tissues).
 It is most common in people of West and Central African descent.

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ETIOLOGY
 In Haemoglobin,
Alpha chain = 141 Amino acids
Beta chain = 146 Amino acids
When the 6th Amino acid (Glutamic acid) in the Beta chain of Haemoglobin
replaced by Valine leads to sickle cell Anemia.
 Mutant haemoglobin polymerises which sticks together and form bundle of
long rods.
 They tends to block the blood flow in the blood vessels of organs and limbs
and it cause pain and organ damage.
 The sickle shaped cell break apart easily causing Anemia.

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 Normal RBC Live for 120 days but sickle cell RBC live only 9-10 days

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PATHOPHYSIOLOGY
 The membrane of red cells containing hemoglobin S is damaged, which leads
to intracellular dehydration.
 In addition, when the patient's blood is deoxygenated, polymerization of
hemoglobin S occurs, forming a semisolid gel.
 These two processes lead to the formation of crescent-shaped cells known as
sickle cells.
 Sickle cells are less flexible than normal cells (flexibility allows normal cells to
pass through the microcirculation).
 The inflexibility leads to impaired blood flow through the microcirculation,
resulting in local tissue hypoxia.
 Anemia results from an increased destruction (hemolysis) of red cells in the
spleen.

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 Some red cells in patients with sickle cell disease contain fetal hemoglobin (Hb F).
 These cells do not become sickle cells.
 Drugs that may increase fetal hemoglobin production:
• 5-Azacytidine
• Cytarabine
• Vinblastine
• Hydroxycarbamide
• Erythropoietin
• Short chain fatty acids (butyrates, valproate).

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INHERITANCE OF SICKLECELL DISEASE
• AA – Normal
• AS – Sickle cell trait (heterozygous)
• SS – Sickle cell disease (homozygous)

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CLINICAL MANIFESTATION
 Chronic Anaemia
 Arthralgia – Pain in joints
 Anorexia – less appetite
 Fatigue
 Splenomegaly
 Fever
 Frequent infection
 Episodes of pain in chest, abdomen and joints
 Vision problems
 Weakness and Pallor
 Dehydration

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COMPLICATIONS
 Acute Complications
 Fever and Infection
 Acute chest syndrome (ACS), defined as a new pulmonary infiltrate
associated with fever and/or respiratory symptoms, is the second most
common cause of hospitalization and leading cause of deaths among
individuals with SCD.
 Priapism- prolonged erection of the penis.
 Sickle Cell Pain
 Splenic sequestration is the sudden massive enlargement of the spleen
resulting from the sequestration of sickled RBCs in the splenic parenchyma.
 Venous Thromboembolism

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 Chronic Complications
 Pulmonary hypertension
 Airway inflammation
 Hyper-responsiveness
 Skeletal and Skin Diseases
 Ocular Manifestations
 Hepatobiliary Diseases
 Cardiac Diseases
 Cardiac Diseases

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DIAGNOSIS
COMPLETE BLOOD COUNT:
 Hb- Low level of Hb ( 6-8g/dl)
 RBC Count- Decreased
 Hematocrit value- Decreased
 Reticulocyte count – Increased
 Presence of Auto Antibodies

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HAEMOGLOBIN ELECTROPHORESIS
(SICKLE CELL SCREENING)
• Used to confirm the Diagnosis

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1. Routine Health Maintenance
 SCD is a complex chronic disease involving multiple organs.
 In addition to the preventive care recommended for the general population,
individuals with SCD also need health maintenance and screenings that
focus on minimizing complications.
2. Immunizations
 Administration of routine immunizations is crucial preventive care in
managing SCD. Children 6 months and older and adults with SCD should
receive influenza vaccine annually.
 Two different pneumococcal vaccines are available.
 The 13-valent pneumococcal conjugate vaccine (PCV13; Prevnar®)
induces good antibody responses in infants and children less than 2 years of
age.

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 Immunization with the PCV13 is recommended for all children, regardless of
SCD status, younger than 24 months of age.
 Infants should receive the first dose after 6 weeks of age.
 Two additional doses should be given at 2-month intervals, followed by a
fourth dose at age 12 to 15 months.
 The 23-valent pneumococcal polysaccharide vaccine (PPSV23;
Pneumovax®23) is recommended for all children with functional or acquired
asplenia but must be given after 2 years of age because of poor antibody
response.
 A booster dose of PPSV23 is recommended 5 years after the first dose. Both
pneumococcal vaccines are recommended for adults with certain medical
conditions, including SCD.

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 The risk of meningococcal disease is also higher in SCD and vaccination is
recommended for individuals with functional or acquired asplenia.
 Two types of meningococcal vaccines are available:
(1) Quadrivalent
(2) Meningococcal group B vaccine.
3. Penicillin
 Penicillin prophylaxis until at least 5 years of age is recommended in children
with SCD, even if they have received PCV13 or PPSV23 immunization, as
prophylaxis against invasive pneumococcal infections.
 An effective regimen that reduces the risk of pneumococcal infections by 84%
is penicillin V potassium at a dosage of 125 mg orally twice daily until the
age of 3 years, followed by 250 mg twice daily until the age of 5 years.

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 Individuals who are allergic to penicillin can be given erythromycin 20
mg/kg/day.
4. Hydroxyurea

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 The starting dose for adult is 15 mg/kg/day rounded to the nearest 500 mg
as a single daily dose.
 A lower dose of 5 to 10 mg/kg/day is used for patients with chronic disease.
 The recommended dose for children is 20 mg/kg.
 Dosage can be increased by 5 mg/kg up to a maximum of 35 mg/kg in 8-
week intervals if the patient does not demonstrate significant adverse effects
and blood counts are stable.
 Patients receiving HU should be closely monitored for toxicity.
 Blood counts should be checked every 4 weeks during dose titration and
every 8 weeks thereafter.

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 Treatment should be interrupted if hematologic indices fall below the
following values:
 Absolute neutrophil count, 2,000 cells/mm3 (2 × 10 9 /L)
 Platelet count, 80,000 cells/mm3 (80 × 10 9 /L)
 Hemoglobin, 5 g/dl (50 g/L; 3.1 mmol/L)
 Reticulocytes, 80,000 cells/mm3 (80 × 10 9 /L)
 If the hemoglobin concentration is less than 9 g/dl (90 g/L; 5.59
mmol/L)

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5. Glutamine
 Sickled RBCs are susceptible to oxidative damage leading to hemolysis and
vasoocclusion.
 Glutamine, an essential amino acid, is a precursor for nicotinamide adenine
dinucleotide (NAD+ ) synthesis.

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 Early studies have shown increased uptake of glutamine by sickle RBCs,
mainly to produce NAD+.
 Children with SCD have lower glutamine levels; an increase of NAD+ can
potentially restore the redox balance in oxidative stressed cells.
 L-glutamine (Endari®) was FDA-approved in July 2017, becoming the first
product approved for pediatric patients with SCD and the first new treatment for
adults in almost 20 years.
 It is indicated for SCD patients age 5 and older to reduce the acute
complications of SCD.
 The product is available in 5-g packets and should be mixed with 8 ounces of
liquid (~240 mL) or 4 to 6 ounces (~110- 170 g) of food.
 The recommended dose is based on weight: 5 g twice a day for less than 30 kg;
10 g twice a day for 30 to 65 kg and 15 g twice a day for greater than 65 kg.
The most common gastrointestinal side effects are constipation, abdominal pain,
and nausea.

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6. Iron chelators
 Patients who require RBC transfusion become Iron overloaded and leads to
toxicity to several vital organs.
 Iron can be removed using Iron chelators.
 Desferrioxamine (IV/SC for 5-7 days in a week)
 Deferasirox
 Deferiprone

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REFERENCES
1. Pharmacotherapy: A Pathophysiologic approach, Joseph T Dipiro,
Thomas D Nolin.., 11th edition. Page No: 4942- 4972, 5054-5100.
2. Clinical Pharmacy and Therapeutics by Roger Walker. Page No: 784-
790.
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