Drugs Affecting the Immune

System
CORTICOSTEROIDS

Mechanisms of action. After passage through the cell membrane corticosteroids react with
receptor proteins in the cytoplasm to form a steroid-receptor complex. This complex moves
into the nucleus, where it binds to DNA. The binding process then changes the transcription
of messenger RNA (mRNA).

Pharmacotherapeutic/Indication

 Endocrine – adrenocortical insufficiency and thyroiditis.

 Dermatologic – Stevens-Johnson syndrome, psoriasis, dermatomyositis

 Respiratory – chronic asthma, chronic obstructive pulmonary disease, sarcoidosis

 Hemotologic – idiopathic thrombocytopenic purpura, hemolytic anemia, systemic lupus

erythematosus

 Neuro – exacerbation of multiple sclerosis, tuberculosis, meningitis, acute spinal injury

 GI – ulcerative colitis, regional enteritis

 Ophthalmic - acute or chronic allergic inflammatory process involving the eye (corneal
marginal ulcers, herpes zoster ophthalmicus, choriditis, optic neuritis

 Allergic states – allergies asthma, contact dermatitis, drug sensitivity reactions.

 Collagen diseases – lupus erythematosus, sarcoidosis, rheumatoid arthritis

 Suppression of inflammatory responses during organ transplantation.

 Neoplastic disease

Pharmacokinetics

 Preparations are well absorbed through the GI tract and are widely distributed.

 They are metabolized in the liver and excreted through the kidneys.
Pharmacokinetics

 Route Onset Peak Duration

 PO Varies 1- 2 hours 1 -1.5 Hours

Common Corticosteroids

1. PO and parenteral agents:

a. prednisone (Deltasone)

b. Triamcinolone (Aristocort)

c. Dexamethasone(Decadron)

d. Methylprednisolone(Depo-Medrol, Medrol, Solu- Medrol)

e. Prednisolone (Delta- Cortef)

f. Hydrocortisone (Cortef)

g. Cortisone (Cortone)

h. Betamethasone (Celestone)

2. Inahaled agents:

a. Triamcinolone (Azmacort)

b. Beclomethosone (Beclovent, Beconase, Vancenase, Vanceril)

c. Flunisolide (Nasalide)

d. Dexamethasone (Decadron)

3. Ophthalmic solution and ointment

a. Dexamethasone(Decadron)

b. Fluorometholone (Flarex)

c. Medrysone (HMS)
4. Topical steroid creams

a. Alclometasone (Aclovate)

b. Betamethasonebenzoate (Uticort)

c. Betamethasone Dipropioante (Diprolene)

d. Clobetasol (Temovate)

e. Desoximetasone (Topicort)

f. Fluocinonide (Lidex)

g. Mometasone(Elocon)

h. Hydrocortisone (Hytone, Cort-Dome)

i. Triamcinolone(Kenalog)

Antihistamine

 Chemical mediator found in the body’s entire cell.

 Released into the blood stream by the mast cells in response to the presence of several
different stimuli such as drugs, trauma, or antigens to which an individual may be
allergic

 These agents block the effects of histamine, bringing relief to patients suffering from
itchy eyes, swelling, congestion, and drippy nose.

Pharmacodynamics/action

1. Antihistamine does not change the secretion or production of histamine, but block the
action of histamine by competing with histamine for cell receptor sites.

2. When the cell receptor site is occupied with the antihistamine, the histamine cannot
enter the cell and exert its detrimental effect

Pharmacotherapeutics/indication

 Prevention or treatment of symptoms of allergic disorders that are either seasonal of

acute (due to ingestion of food or inhalation or contact with an allergen)

 Motion sickness
  Used as hypnotics in the elderly (sedating antihistamine)

Pharmacokinetics

 These agents are well absorbed 15 to 30 minutes after ingestion, widely distributed, and
excreted in the urine.

 Onset is within 15 to 30 minutes, nonsedating antihistamine have an onset of 30

minutes to 2 hours.

 Peak varies with the preparation ( eg, sustained-release preparations tend to peak 8 to
12 hours after ingestion

 Duration is usually 3 to 4 hours, but varies with the drug used; nonsedating
antihistamines have a duration of 12 to 24 hours.

Common Antihistamines

1. First Generation Drug

a. azelastin (Astelin)

b. brompheniramine (Bidhist)

c. buclizine (Bucladin – S)

d. cetirizine (Zyrtic)

e. chlorpheniramine (Aller – Chlor, others)

f. clemastin (Tavist)

g. cyclizine (Marezine)

h. cypropheptadine (generic)

i. dexchlorpheniramine ( generic)

J.dimenhydrinate ( Dimentabs)

k. diphenhydramine ( Benadryl)

L. hydroxyzine (Vistaril, others)

m. meclizine ( Antivert)

n. promethazine (phenergan)
2. Second Generation (Nonsedating)

a. desloratadine (clarinex)

b. fexofenadine (Allergra)

c. loratidine (Claritin)

Salicylates

 Are popular anti-inflammatory agents, not only because of their ability to block the
inflammatory response, but also because of their antipyretic and analgesic properties.

 They are generally available without prescription and are relatively nontoxic when used
as directed.

 They were extracted from a willow bark, poplar trees, and other plants by ancient
peoples to treat fever, pain, and what we now call inflammation.

Pharmacodynamic/Actions

 Salicylates inhibit the synthesis of prostaglandin, an important mediator of the

inflammatory reaction. The antipyretic effect of salicylates may be related to blocking of
prostaglandin mediator of pyrogens (chemical that cause an increase in body
temperature and that are released by active white blood cells)at the thermoregulatory
center of the hypothalamus.

Drug Indications

 are indicated for the treatment of mild to moderate pain, fever, and numerous
inflammatory condition, including rheumatoid arthritis and osteoarthritis.

 Indicated in the prevention of transient ischemic attack (TIA) and stroke in adults with
history of emboli. It also is indicated to reduce the risk of death and myocardial
infarction (MI) in patients with a history of MI or unstable angina.

Pharmacokinetics

Route Onset Peak Duration

Oral 5-30 min 0.25-2hrs 3 – 6 hrs

Rectal 1-2 hrs 4-5 hrs 6-8 hrs

Common Salicylates Drugs

 aspirin(Bayer, Empirin)

 balsalazide (Colasal)

 choline magnesium trisalicylate (Tricosal)

 choline salicylate (Arthropan)

 mesalamine (Pentasa, others)

 olsalazine (Dipentum)

 salasalate (Argesic, others)

 sodium thiosalicylates (Rexolate)

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Therapeutic Actions and Indications:

 The anti-inflammatory,analgesic,and antipyretic effects of the NSAIDs are largely related

to inhibition of prostaglandin synthesis.

 The NSAIDs block two enzymes, known as cyclooxygenase-1(COX-1) and

cyclooxygenase-2 (COX-2). COX-1 is present in all tissues and seems to be involved in
many body function, including blood clotting protecting the stomach lining and
maintaining sodium and water balance in the kidney. COX-1 turns arachidonic acid into
prostaglandins as needed in a variety of tissues. COX-2 is active at sites of trauma or
injury when more prostaglandins are needed, but it does not seem to be involved in the
other tissue functions. By interfering with this part of the inflammatory reaction, NSAIDs
block inflammation before all of the signs and symptoms can develop. COX-2 inhibitors
are thought to act only at sites of trauma and injury to more specifically block the
inflammatory reaction.

Pharmacokinetics

 The NSAIDs are rapidly absorbed from the GI tract, reaching peak levels in 1 to 3 hours.
They are metabolized in the liver and excreted in the urine

Common NSAIDs

 Aspirin(Acetylsalicylic acid)
  Diflunisal (Dolobid)

 Ibuprofen(Advil, Motrin, Nuprin)

 Ketorolac tromethamine(Toradol)

 Naproxen (Naprosyn)

 Diclofenac(Voltaren)

 Indomethacin(Indocin)

 Ketoprofen (Orudis)

 Nabumetone(Relafen)

 Naproxen Sodium (Aleve, Anaprox)

 Oxaprozin (Daypro)

 Sulindac (Clinoril)

Immunosuppressants

 Are used to block the normal effects if the immune system in cases of organ
transplantation(in which nonself-cells are transplanted into the body and destroyed by
the reaction) and in autoimmune disorders(in which the body’s defenses recognize self-
cells as foreign and work to destroy them).

Pharmacokinetics

Route Onset Peak

Oral Varies 3.5 hrs

IV Rapid 1-2 Hrs

It is rapidly absorbed from the GI tract, reaching peak levels in 1.5 to 3.5 hours. It is metabolized
by the liver and excreted in the urine

Common Immunosuppresors

 Alefacept(Amevive)

 Azathioprine (Imuran)

 Cyclosporine (Sendimmune, Neoral)

  Glatiramer acetate(Copaxone)

 Mycophenolate(Cellcept)

 Pimecrolimus(Elidel)

 Sirolimus (Rapamunet)

 Tacrolimus (Prograf)

 Tacrolimus (Protopic)

Vaccines and Sera

 Vaccines comes from a latin word for smallfox, vaccinia. Vaccines are immunizations
containing weakened or altered protein antigens that stimulate formation of antibodies
against specific disease.

 They are used to promote active immunity.

 Vaccines can be made from chemically inactivated microorganism or from live,

weakened viruses or bacteria.

 Vaccines stimulate active immunity in people who are at high risk for development of a
particular disease.

 Vaccines needed for a patient depends on the exposure that a person will have to the
pathogen. Exposure is usually determined by where the person lives, travel plans, and
work or family environment exposures. Vaccines are brought to provide lifelong
immunity to the disease against which the patient is being immunized

Pharmacokinetics

Route Onset Peak

IM Rapid 3-12 Hrs

Metabolized in the tissues, excretion is unknown

Common Vaccines

 Bacterial Vaccines

BCG (TICE BCG)

Haemophilus influenza b conjugates vaccine (HibTiter, Liquid PedvaxHIB)

 Haemophilus influenza b conjugate vaccine and hepatitis B surface antigen (Comvax)

meningococcal polysaccharide vaccine (Menomune-A/C//Y/W-135)

meningococcal polysaccharide diptheria toxoid conjugate vaccine (Menactra)

pneumococcal vaccine, polyvalent (Pneumovax 23)

 Bacterial Vaccines

pneumococcal 7-valent conjugate vaccine (Prevnar)

typhoid vaccine (Vivotif Berna TyphimVI)

Immune Sera

 The term Immune Sera, is usually used to refer to sera that contain antibodies to
specific bacteria or viruses. The term antitoxin and antivenin are used to refer to
immune sera that have antibodies to very specific toxins that might be released by
invading pathogens or to venom that might be injected through spider, snake bites

Indications

 Immune sera are used to provide passive immunity to a specific antigen or disease.

 They may also be used as prophylaxis against specific diseases after exposure in patients
who are immunosuppressed. In addition, immune sera may be used to lessen the
severity of a disease after known or suspected exposure.

 Prophylaxis against hepatitis A, measles, varicella, rubella; prophylaxis for patients with
immunoglobulin deficiency

Pharmacokinetics

Route Onset Peak

IM Slow 2-5 days

Metabolized in the tissues, excretion is unknown

Common Immune Sera

 Anti-thymocyte immune globulin(Thymoglobulin)

 Cytomegalovirus immune globulin (CytoGam)

  Hepatitis B immune globulin (BayHep B Nabi-HB)

 Immune globulin, intramuscular(BayGam)

 Immune globulin, intravenous(Gamimune N, Gammagard, and others)

 Lymphocyte immune globulin(Atgam)

 Rabies immune globulin(BayRab, Imogam Rabies)

 Respiratory syncytial virus immune globulin (RespiGam)

 RHO immune globulin(BayRho-D full dose, Rhogam)

 RHO immune globulin(BayRho-D mini dose, MICRhoGam)

 Tetanus immune globulin (Bay Tet)

 Vaccinia immune globulin IV(VIGIV)

 Varicella zoster immune globulin(Varicella Zoster Immune Globulin)

Antitoxins and Antivenins

 Antivenin(crotalidae polyvalent)generic

 Antivenin(micrurus fulvivus)generix

 Black widow spider antivenin (Antivenin)

 Crotalidae polyvalent immune fab(Crofab)