ANTILEPROSY DRUGS

PATEL KETAN A.
THIRD YEAR B.Pharm,
Roll No-25
Gitanjali Pharmacy College,
Talod
 What is Leprosy?
 It is chronic infectious
granulomatous disease caused by
Mycobacterium leprae
 Develop in two forms
-Non Lepromatous (Tubercluloid)
-Lepromatous
 FIRST STAGE
-Patient’s skin sensation is dulled and
small patches of anesthesia develop

 SECOND STAGE
-Skin becomes thick and wrinkled
-Ear become swollen
-Nodules are formed in skin of nose
and throat
 THIRD STAGE
-Bacteria burst out of the nerve cells
and go to peripheral tissues and
begin to proliferate there
Lepromatous vs. Tuberculoid Leprosy
Lepromatous Leprosy (Early/Late Stages)
 Drugs Use In The Treatment
Of Leprosy

 Depsone
 Rifampicin
 Clofazimine
 DEPSONE
 Depsone is chemically related to the
sulfonamides and
 because it's action is antagonised by
PABA.
 Probably acts through inhibition of
bacterial folate synthesis.
 Resistance to the drug is increasing,
and treatment with combination of
drugs is now recommended.
 Depsone is given orally; it is well absorbed
and widely distributed through the body
water and in all tissues.
 The plasma half-life is 24-48 hours,
 but some depsone persists in certain
tissues (Liver, Kidney and to some extent
Skin and Muscle) for much longer periods.
 There is enterohepatic recycling of the
drug, but some is acetylated and excreted
in the urine.
 Depsone is also used to at dermatitis
herpetiformis
 UNWANTED EFFECTS OF
DEPSONE
 Haemolysis of red cells
-methaemoglobinaemia
-anorexia -nausea
-vommiting -fever
-allergic dermatitis -neuropathy

 Lepra reaction is occurs

 RIFAMPICIN
 Acts by binding to, and inhibiting DNA-
dependent RNA polymerase.
 One of the most active antituberculosis
agent known
 Also active against most Gram positive
bacteria and many Gram negative species
 It enters phagocytic cell and kill
intracellular micro-organisms including
Tubercle bacillus
 PHARMACOKINETIC ASPECTS
 Orally given
 Widely distributed in the tissues and body fluid
 Gives orange tinge to saliva, sputum, tears and
sweat
 In the CSF it reaches 10-40% of its serum
conncentration
 It is excreted in urine and bile
 Enterohepatic hepatic cycling
 Half-life is 1-5 hours
 Become shorter during treatment owing to
induction of hepatic microsomal enzymes
 UNWANTED EFFECTS OF
RIFAMPICIN

 Relatively infrequent
 Skin eruptions
 Fever
 Gastrointestinal disturbance
 Liver damage with Jaundice
 Liver function should be assessed
before treatment is started
 Cause induction of hepatic metabolisic
enzmes
 Result in degredation of warfarin,
glucocorticoids, narcotic analgesics,
oral antidiabetic drugs, depsone,
estrogens
 Failure of oral contraceptives
 CLOFAZIMINE
 Clofazimine is a dye of complex
structure.
 It is having action on DNA.

 It also has anti-iflammatory activity

and is useful in patients in whom
depsone causes inflammatory side
effects.
 Clofazimine is given orally and
accumulated in the body, being
sequerstered in the mononuclear
phagocyte system.
 The plasma half life may be as long as
8 weeks.
 The antileprotic effect is delayed and is
usually not evident for 6-7 weeks.
UNWANTED EFFECTS OF CLOFAZIMINE

 The skin and urine can develop a

reddish colour
 the lesions a blue black discoloration.
 Dose-related
-nausea
-giddiness
-headache and
-gastrointestinal disturbances
Thank you!!