Treatment  of  Anemia  

Antihistamines,  Glucocorticoids  and  
Epinephrine    
Antihistamines,  Glucocorticoids  and  
Epinephrine  
 
 
 
 
This  document  was  done  by    
Pharmacology  Scientific  Committee,    
and  Designed  by  Dr.  Seba  Rammal  
 
    1  
4/26/2011  
 
  

  2  
  

                                       Lectures  index    

 
T r e a tm e n t o f A n e m ia p.  4  

 
T r e a tm e n t o f H y p e r s e n s itiv ity  
A n ti-H is ta m in ic D r u g s , G lu c o c o r tic o id s p.  16    
a n d A d r e n a lin e

 
Im m u n o s u p p r e s s iv e d r u g s p.  26  

  3  
 T r e a t m e n t o f A n e m ia
 

FFiirrsstt::    PPhhyyssiioollooggyy    IInnttrroodduuccttiioonn::    

 Hemopoiesis (The Formation of Blood) occurs mainly in:

 Bone Marrow: where RBCs, Platelets and Granulocytes
(Neutrophils, Eosinophils & Basophils) are formed.
 Lymphatic Tissue: where Lymphocytes and Monocytes are
formed.

 Factors influencing Erythropoiesis (Formation of Red

Blood Cells):

 Iron Deficiency Anemia (Hypochromic-microcytic) due to:

• Chronic Nutritional Deficiency of Iron
• Post Hemorrhagic

 Folic Acid Deficiency Anemia (Macrocytic), which occurs

sometimes in:
• Pregnancy
• Using of Antiepileptic Drugs

  4  
  Aplastic Anemia, which is due to aplasia or hypoplasia of
bone marrow. It may be:
• Primary (Idiopathic)
• Secondary, Due to:
 Exposure to X-Rays or Radioactive material
 Some drugs (e.g. Chloramphenicol)
 Hemolytic Anemia (Excessive blood destruction),
which may be due to:
 Congenital Abnormalities or RBC
 Infective or toxic factors
 Hemolytic Disease of Newborn

 
SSeeccoonndd::    PPhhaarrm
maaccoollooggyy::    
   

T rea tm en t o f I ro n d eficien cy a n em ia

Ir o n
 In the Body
 Absorption of Iron takes place in the form of inorganic
Ferrous Iron
 In the intestinal mucosa, the Ferrous Iron Fe++ reoxidized
to Fe+++ where it is bound to the protein Apoferritin to form
Ferritin

  5  
 Normal daily requirement for an adult man is 5-10mg in
food (of which, 10% is absorbed for the actual body needs)

 Ferrous Sulphate is required to correct the deficiency,

especially in the case of MILD MICROCYTIC ANEMIA associated
with pregnancy
 

 Administration

 Orally: in the form of:

• Ferrous SO4
• Ferrous Gluconate
• Ferrous Fumarate
 Parenteral (Does not make contact with the GIT), in the
form:
• Iron Dexteran (Imeferon), either I.M. or I.V.
• Iron-Sorbitol-Citric Acid Complex, given I.M.

 Side Effects
(Not all of the following occurs, it depends on Inter-Patient Variability)

 If given orally:
• Gastric Distress (e.g. Necrotizing Gastroenteritis,
Diarrhea or Constipation)

  6  
  If given Parentral:
• Locally:
 Pain at site of injection
 Skin discoloration
 Local inflammation
• Systemically:
 Headache
 Malaise (Vague feeling of being unwell)
 Muscle and joint pain
 Bronchospasm
 Chills, Rash or Convulsions

 Treatment of toxicity:
 If given orally:
• Gastric Lavage (Stomach Pump) with 1% Na
Bicarbonate
• Iron Chelating Agent (Desferrioxamine) by:
 Stomach Tube (5-10g in 100ml Saline)
 I.V. (2g/12hours)
 If given Parentral:
• I.V. Fluid (Saline) to treat collapse and dehydration
• NaHCO3 for Metabolic Acidosis
• Barbiturate to counteract Convulsions

  7  
 T rea tm en t o f P ern icio u s A n em ia a n d o th er
M e g a l o b l a s t i c A n e m i a ’s

 Cause of Pernicious Anemia (Addisonian Pernicious

Anemia):

Failure of stomach to secrete the intrinsic factor, which is

required for the absorption of Cyanocoblamine (Vitamin B12)

 Intrinsic Factor:

Is a glycoprotein secreted from parietal cells of the stomach,

which binds to B12 and aids it’s absorption from the ileum

 The condition is characterized by the following

manifestation:

 Hematological Manifestation:
• Macrocytic Hyperchromic Anemia
• Megaloplastic Bone Marrow (Bone marrow is full of
Large nucleated red cells (megaloblasts), which are
the precursors)
 GI Manifestation:
• Histamine Fast Achlorhydria (Achylia Gastrica):
which is a condition where the secretion of HCL is
lowered, leading to decrease in intrinsic factor 
low absorption of B12
• Glossitis (Inflammation of the tongue)
• Diarrhea
  8  
  Neurological Manifestations:
• Peripheral Neuritis
• Subacute combined degeneration of posterior and
anterior columns of spinal cord.

Cyanocoblamine (B1122):
 Sources
 Extrinsic:
• Meat, Liver, Fish and Egg Yolk
 Intrinsic:
• Synthesized by intestinal bacteria in man, but isn’t
sufficient because it is produced in the colon from
which site is not well absorbed

 In the body:
 Has an important role in nucleoprotein synthesis
 Required for normal maturation of Epithelial Cells
 Required for normal Hemopoiesis
 Essential for proper function of nerve tissue and the
formation of the myelin sheath
 Has a lipotropic action (Prevents accumulation of fat in
the liver)

 Its absence

Causes accumulation of Megaloblasts in the Bone Marrow

 Macrocystic (Pernicious) Anemia

  9  
 Body Requirement

2 µg daily

 Drugs that impair it’s absorption:

 Paraminosalicylic Acid (for treating TB)
 Neomycin
 Colchicines
 Metformin (for Treating Diabetes)
 Slow Release KCl preparations

 Excretion

Via Bile and Kidney

 Therapeutic Uses

Used as treatment for pernicious anemia

 Administration

 Orally: (not used anymore)

• Combined with Intrinsic Factor in the form of
capsules of tablets
 Injection:
• Vitamin B12, given I.M.
• Liver Extract is also administered I.M.
• Hydroxycoblamine, also given I.M., and is retained
in the body for a long time due to its protein binding
properties

  10  
F o lic A c id :
 Sources

Liver, Fresh Green vegetables and Fruits

 In the body:
 Is not active by itself, and must be enzymatically
reduced in the mucosa of duodenum and jejunum to H4
Folic Acid by dihydrofolate Reductase.
 H4 Folic Acid = THFA (Tetrahydrofolate Acid) =
Citrovonum Factor = Leucovorin

 Functions

 Both Folic Acid and B12 promote erythropoiesis

 THFA is a coenzyme in the synthesis of nucleoprotein

 Therapeutic Uses: In Cases of:

 Inadequate dietary intake
 Abnormally increased requirement (e.g. Pregnancy)
 Defective Absorption in malabsorption syndrome, e.g.
Tropical and Tropical Sprue
Tropical Sprue: Absorption Deficiency due to change of
the climate from cold to warm, and usually accompanied by
Diarrhea and Cramps

  11  
  Also used as an adjuvant (complement) to anticonvulsant
Therapy (Prolonged use to Barbiturates and Hydantoin
leads to developing of Macrocytic Anemia, which respond
well to Folic Acid)
 Folic Acid should never be used alone in the therapy of
pernicious anemia, because it only corrects the
hematological manifestations, and the neurological
ones proceed uncontrolled

H e m o p o ie tic G r o w th F a c to r s :

Erythropoietin:
 Glycoprotein produced by the kidney
 Its action is to stimulate the proliferation and
differentiation of erythrocyte precursors
 Recombinant derived human erythropoietin (Epoietin),
is used in management of patients with anemia
associated with chronic renal failure

 Administered
S.C. Or I.V.

  12  
 Side effects include

 Hypertension, due to rise of red blood cells mass

 Iron Deficiency, because more iron is required for
enhanced erythropoiesis (Give Iron Supplement to
counteract this effect)

Colony-Stimulating Factors (CSF):

 Natural occurring glycoprotein

 Stimulates proliferation, differentiation and activity of
Neutrophils, Monocytes and Macrophages (Used in
severe leucopenia)

 Preparations

 Granulocyte-Macrophage CSF (GMCSF), e.g.

Sargramostin
 Granulocyte CSF (GCSF), e.g. Filgrastim (not used in
case of renal failure)

Both preparations are used clinically to:

• Accelerate the rate of granulocyte recovery

(Following bone marrow transplantation)
• Reduce Neutropenia induced by cytotoxic drugs
(Chemotherapy)
• Increase the numbers of Neutrophils and Decrease
the risk of infection (in patients with aplastic
anemia (bone marrow depressed)
  13  
 T rea tm en t o f A p la stic A n em ia

 Cause

Bone Marrow Depression

 Treatment (In such cases are only supportive)

 Immediate withdrawal of causative agent (if any existed)
 Blood Transfusion
 Antibiotics (to decrease the risk of infection)
 Vitamin B12, Liver Extract, Vitamin C and Folic Acid
(Stimulate Erythropoiesis)
 Corticosteroids
 Testosterone or Anabolic Steroids

  14  
 T rea tm en t o f H em o ly tic A n em ia
 Cause

 Drugs having direct toxic effects on RBCs, e.g.

Phenacetin, Nitrobenzene
 Drugs in certain patients with G-6-P Dehydrogenase
Deficiency, e.g. Primaquine, Aspirin and Sulphonamide

 Treatment

 Immediate withdrawal of causative agent (if any existed)

 Blood Transfusion
 Corticosteroids (inhibits the production of hemolysin <<<
causes hemolysis)
 Spleenectomy may be needed in cases of hereditary
spherocytsis (presence of abnormal spherical shape of
RBCs in blood)

T rea tm en t o f A g ra n u lo cy tsis (M a rk ed
L eu k o p en ia a n d N eu tro p en ia )
 Cause:

 Hypersensitivity to some:
• Anti-thyroid Drugs
• Anti-Rheumatic Drugs (e.g., Phenylbutazone)
• Arthritis Treatment (e.g. Gold preparations)
• Anti-Epileptic Drugs
 Appearance of sore throat and Pyrexia (Fever), should
raise suspicion of the condition
 Treatment:

As Aplastic Anemia
  15  
 T r e a t m e n t o f H y p e r s e n s it iv it y
A n t i- H is t a m in ic D r u g s ,
G l u c o c o r t ic o id s a n d A d r e n a l in e
   

FFiirrsstt::    PPhhyyssiioollooggyy    IInnttrroodduuccttiioonn::    

Types of Hypersensitivity:

 T y p e I r e a c tio n
 Definition:
IgE-mediated noncytotoxic mediator release from basophiles
and mast cells.

 Mechanism:
 Drug or metabolite enters the body
 Tissue sensitizing IgE antibodies from and are fixed to Mast
cells or leukocytes
 2nd presentation of antigen  Ag-Ab Complex activates the
release of active substances (histamine, leukotrines &
Prostaglandins)

 Examples:
1. Anaphylactic shock (can be caused by penicillin and is
usually treated with epinephrine)
2. Urticaria
3. Extrinsic asthma
4. Allergic rhinitis
5. Aspirin drugs may cause an asthmatic attack with some
people

  16  
 T y p e II r e a c tio n

 Definition:
Complement-mediated injury involving antibodies (IgM and
IgG).

 Mechanism:
 The drug or metabolite combines with a protein in the body
(the size increases)
 The body treat it as a foreign protein  forms (IgM and IgG)
 IgM and IgG combine with antigen and activate complement
which damage cells

 Examples :
1. RH hemolytic disease of the newborn
2. Thrombocytopenia: may occur after exposure to heparin.
3. Aplastic anemia: may be caused by chloramphenicol or
sulphonamide

  17  
 T y p e III r e a c tio n
 Definition:
Immune complex initiated by soluble Ag-Ab (mainly IgE)
Complex

 Mechanism:
 Ag-Ab Complex form
 Leukocytes are attracted to site of reaction  engulf the
complex
 Release of active substances (e.g. Lysosomal Enzymes) 
inflammation

 Exa mples :
1. Serum Sickness
2. Lupus Nephritis
3. Glomerulonephritis

 T y p e IV :
 Definition:
Lymphocyte mediated cellular (delayed) hypersensitivity

 Mechanism:
 Ag Receptors develop on T-lymphocytes
 2nd exposure to Ag  local or tissue allergic reaction

 Examples :
1. Contact Dermatitis
2. Tuberculin Hypersensitivity
3. Allograft Rejection

  18  
SSeeccoonndd::    PPhhaarrm
maaccoollooggyy::    

D ru g U sed fo r trea tm en t o f h y p ersen sitiv ity rea ctio n s:

A n t ih is t a m in ic s
(block histamine
receptors)  

A d ren ocep tor

agonists e.g. eeppiinneepphhrriinnee
(Or Adrenaline, which is
the Physiological
Antagonist for histamine)
 

C o r t ic o s t e r o id s
(Or Glucocorticoids,
which prevent Ab-Ag
reaction)  

  19  
H ista m in e

H is t a m in o p e x ia :

The ability of the plasma to bind histamine to specific

plasma protein (making it inactive)
Which is reduced in some allergic reactions

 Histamine Release:
Agents that can release histamine include:
1. Proteolytic Enzymes (Trypsin), which may be associated with
gross cell damage
2. Histamine Liberators (Morphine, D-Tubocurarine), which
displace the histamine from its binding sites in tissues without
producing visible tissue damage
3. Hypersensitivity phenomenon (Allergy and Anaphylaxis)
4. Mechanical, Thermal or Radiation Energies
5. Venoms and Toxins

  20  
 Histamine Receptors:
 H1Receptors: These receptors mediate the contraction of
smooth muscles of the bronchi and intestines, and are blocked
by Antihistamines H1 Receptors blockers (Mepyramine)

 H2 Receptors: These receptors are responsible for

stimulation of gastric acid secretion, and are blocked by
antihistamines H2 receptor blockers only (Cimetidine)

 H3 Receptors: These receptors are found mainly on

presynaptic neuronal sites, they are responsible for
presynaptic regulation of release of histamine and other
mediators, and are blocked by H3 Blockers (Acetylcholine,
Dopamine and Epinephrine)

Adverse Effects Due to Blocking of Other Receptors:

when blocking:
1. Cholinergic Receptors: (by Diphenhydramine or
Promethazine), Atropine-like effects occur (dry mouth,
urine retention and sinus tachycardia)

2. α-Adrenergic Receptors: (By Promethazine), hypotension

develops and leads to reflex tachycardia

3. Serotonin: (Periactin = Cyproheptadine), which leads to

increases appetite

  21  
Types of Anti-Histaminic Drugs:

1. First Generation Drugs: (Less Specific)

1. Cyclizine U
Usseedd    ffoorr    ttrreeaattiinngg    
2. Diphenhydramine (Sedative) mmoottiioonn    ssiicckknneessss    
3. Dimenhydrinate

2. Second Generation Drugs: (More Specific)

The “-dine” group:
1. Loratadine N
Noonn-­-­SSeeddaattiinngg    
2. Desloratadine
3. Fexofenadine

 Therapeutic Uses:
1. Allergic Reactions: H1 Blockers are useful in treating
allergies caused by Ag acting on Ab IgE sensitized mast cell
(E.g. Rhinitis and Urticaria), but It can’t be used alone
in Bronchial Asthma (because histamine is not the
only mediator)
2. Motion Sickness and Nausea: Dimenhydrinate,
Cyclizine and Meclizine, which are all used to prevent
motion sickness
3. Somnifacients: Diphenhydramine, which is used for
treating Insomnia

 Pharmacokinetics:

Well be absorbed after oral administration and have long half-life

  22  
 Adverse Effects:
1. Sedation
2. Tremors
3. Tinnitus
4. Dry Mouth (Result from blocking the cholinergic receptors)
5. Fatigue
6. Blurred Vision
7. Lassitude (Lack of energy and fatigue)

 Drug Interactions:
 With Alcohol: CNS Depression
 MAO Inhibitor (Anti-Depressants): Increase the anti-
cholinergic effects of antihistamines
 Erythromycin and Clarithromycin: interfere with the
metabolism of Terfenadine and Astimazole, causing Cardiac
Arrhythmias

  23  
C o r tic o ste r o id s:

 Glucocorticosteriods show GREATER anti-inflammatory

effects than anti-histamines
 Used for treating symptoms of bronchial asthma, allergic
rhinitis, and drug/serum/transfusion allergic reactions
 They are NOT CURATIVE
 Their Mechanism is Interfering in mast cell degranulation
(mast cell stabilizer), which means that they work by
inhibiting the formation of the Ag-Ab complex, preventing its
reaction
 DECREASE histamine release and capillary permeability
 Can be applied topically or systemically

 Some of the adverse effects include:

1. Osteoporosis (most common side effect when used for long
term. Supplement of Vit. D and Ca++ are used to counter
this effect)
2. Cushing syndrome when high doses of corticosteroids are
used
3. Diabetes, Hypertension, Salt and Water Retention and
Hypokalemia are also possible
4. Cataract, Glaucoma and Euphoria may occur (Treatment
should be stopped immediately)
5. They also increase acid and enzyme secretion
(Contraindicated in Peptic Ulcer)

  24  
A d r e n e r g ic A g o n ists:

 Epinephrine ( = Adrenaline ), is the drug of choice in

TREATING SYSTEMIC ANAPHYLAXIS and other
type I allergy conditions

 Because these conditions involve massive release of

histamine, they usually respond to rapidly to parenteral
administration of epinephrine (because it activates α, β1 and
β2 receptors  reversal of pathophysiological process
underlying anaphylaxis)

 Glucocorticoids and Anti-Histamines may be useful as

secondary therapy in anaphylaxis, however, epinephrine is
the initial treatment

  25  
 Im m u n o s u p p r e s s iv e D r u g s

FFiirrsstt::    PPhhyyssiioollooggyy    IInnttrroodduuccttiioonn::    

Types of Lymphocytes:
 B-Cells: Derived from bone marrow and responsible for
antibody production and for the humoral immune response
 T-Cells: Derived from thymus and responsible for the cell-
mediated immune response

The innate immune system:

First line of defense against an antigen insult, and include
these components:

 Physical (Skin)
 Biochemical (Complement and Lysosomes)
 Cellular (Macrophage, Neutrophiles)

SSeeccoonndd::    PPhhaarrm
mccaaoollooggyy::    

Immunosuppressants:
 Earlier drugs were unselective and suppressed both active T
Cells and Ab formation
 They Include Anticancer Drugs, such as:
 Methotrexate
 Cyclophospamide
 Azathioprine
 Glucocorticoid Prodrug Prednisone
  26  
 Types of Immunosuppressants:
A. Non-selective Immunosuppressants:
1. Azathioprine:
 Corner stone of Immunosuppressants
 It has 6-MP nucleus (Mercaptopurine), a purine antagonist
 The 6-MP nucleus is attached to a nitroimdazolyl side chain
 This molecule is converted non-enzymatically to 6-MP by
Glutathione

6-MP ----------> Thioinosinic Acid (Thio-IMP) --------->

Dehydrogentaion -----> Thio-GMP Feedback  inhibition  of  purine  synthesis  
Phosphorylation  
HGPRT  

Di  and  Triphosphate  
incorporate  in  RNA  
HydroxyGlutrylPhosphoRibosyl  
Transferase  

 Resistance to drug may occur, and it's due to:

1. Decrease of HGPRT levels  Decrease in Thio-
IMP levels, in:
o Lesch-Nyahn Syndrome
o Severe Gout
o Mental Retardation
2. Increased Dephosphorylation
3. Increased Metoabolism of drug into thiouric Acid
 Side effects
 may include Bone Marrow Depression

  27  
 2. Mycophenolate Mofetil:

 It is rapidly hydrolyzed in GIT to mycophenolic Acid, which

is quickly and almost completely absorbed
 It reversibly inhibit IMP Dehydrogenase
 Leading to decrease in GMP  decrease in nucleic acid of T
and B Cells

 Side Effects
1. Pain
2. Diarrhea
3. Leucopenia
4. Sepsis
5. Lymphoma
6. When given with Antacid (Anti-hyperacidity drugs),
containing Mg or Aluminum, or with Cholestyramine
(Antihyperlipidemic Drugs) leads to decrease
absorption of drug

  28  
 3. Antibodies:
 Antilymphocyte and Antithymocyte Globulin:

Prepared by 2 methods:

1. Immunization of large animals with human lymphoid cells

(Polyclonal)
2. Hybridoma Technique (Monoclonal)
 It's Mechanism is:

1. Ab-bound cells are opsonized and phagocytosed in liver and

spleen  Lymphopenia and Impaired T-Cell response

2. They are primarily employed to treat Acute Phase

Allograft Rejection (by impairing T cell response)

 Administration
2. is I.M. or I.V., and the half-life is 3-9 days

 Side Effect include:

1. Chills & Fever
2. Leucopenia
3. Thrombocytopenia
4. Skin Rashes
5. Formation of Ab against foreign proteins

  29  
  Muromonab-CD3 (CK T3):
1. A murine (Dimerich) monoclonal Ab directed against
glycoprotein CD3 Antigen of human cells
2. It binds to CD3 protein leading to disruption of T
Lymphocytes function  decrease T-Cell participation in
I.R.
3. CK-T3 is used to treat Acute Rejection of Renal Allograft
4. Also used as steroid resistant acute allograft rejection in
Cardiac and Hepatic Transplantations

 Administered

I.V.

 Used to

Pretreat patients with: diphydramine (Antihistaminic),

Acetaminophen (Paracetamol) or Methyl Predniosolone to
prevent cytokine release syndrome due to:

Binding of CK T3 Ab to Ag, causing activation of T-Cells 

release of cytokines

 Metabolism

Of Ab is extensive and Eliminated predominantly in bile

 Side Effects include:

1. Anaphylactic Shock
2. Cytokines Release Syndrome
3. Shock-like Reaction & High Fever

  30  
 Contraindicated in:

1. Patients with history of seizures

2. Patients with Uncompensated Heart Failure

3. Pregnant or Breast Feeding Women

B. Selective Immunosuppressant’s:
1. Cyclosporine:
 Suppresses Cell-Mediated I.R.
 Humoral Immunity is affected to a far lesser extent
 Drug monitoring is essential to sustain the drug in
within a therapeutic responsive dose (100-400mg,
>400 Toxicity, <100 not effective)

 Mechanism:
1. Physiological Pathway (normal I.R.):
1. Activation of T Cell Receptor  +
intracellular Ca++
2. Activation of Calcineurin (Ca++ Dependent
phosphatase responsible for
Dephosphorylation)

  31  
 3. Dephosphorylation NFATc moves to
CCyyttoossoolliicc    N Nuucclleeaarr    
FFaaccttoorr    ooff    A
Accttiivvaatteedd     nucleus
T
T    CCeellllss    

4. NFATc associates with other nuclear

X components
5. Activation of genes controlling cytokines
6. Release of cytokines
7. Cell-Mediated Immune Response

 Effect of Cyclosporine:
1. Binds with Cyclophilin
2. Cyclosporine-Cyclophilin Complex
inhibit the activation of Calcinurine,
preventing all following steps
3. End result of Cyclosporine is to DECREASE
IL-2 (main stimulus for increase of T Cells)

 Used to

prevent rejection of Kidney, Liver and Cardiac

allogenic Transplantation

 Using Steroids with Cyclosporine decrease the

rate of mortality

  32  
 Administered

Orally or by I.V. Infusion

 Oral Absorption depend on inter-patient

variability (Due to metabolism by cytochrome P450
present in GIT)
 Grapefruit lowers the level of P450  increased
Absorption of cyclosporine (may lead to toxicity)

 Side Effects
1. Nephrotoxicity (most common) & Liver
Toxicity
2. Anaphylactic Shock (on Parenteral
Administration)

  33  
 2. Tacrolimus (FK 506):
 Macrolide isolated from a soil fungus
 It's Mechanism differs from Cyclosporine that it
binds to a different immunonophilin FKBP (FK Binding
Protein)

 Administration

Is similar to Cyclosporine (also the oral Absorption)

 It's 10-100 times more potent than Cyclosporine

 It's Metabolites are more toxic than
Cyclosporine

 Side Effects

more Severe CNS and Nephro Toxicity

3. Sirolimus:
 Recently approved Macrolide
 Equipotent to CsA (same potency as Cyclosporine)
 Used in renal transplantation, along with CsA and
Glucocorticoids
 Due to its Anti-Proliferative Effect, it is now
used in cardiology, SRL-coated Stents are inserted into
cardiac vasculature inhibiting re-stenosis of blood
vessels (By reducing proliferation of Endothelial Cells)
 Side Effects include Hyperlipidemia

  34  
 4. IL-2 Receptor Antagonist:
 Basilixamab, which Chimerized (from 2 origins)
from 25% Murine(rodent, e.g. Rats) and 75% Human
Protein
 Daclizumab (90% Human)
 Both of them are used in Renal Transplantation
along with CsA and Glucocorticoids
 Mechanism

Since both of them are Anti-CD25 Ab, they bind to

Alpha chain of IL-2 receptor on activated T-Cells

Basilixamab is more potent (about 10 times)

 Administration

Both are I.V.

5. Glucocorticoids:
Such as Prednisone and Metyhlprednisone

 Side Effects

Of long-term therapy include:

1. Hypertension
2. Diabetes
3. Infection
4. Osteoporosis
5. Peptic Ulcer

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