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ALLERGIC DERMATOSIS
Allergic diseases
result from the interaction of antigen & antibodies & subsequent
release of mediators that affect various target organs.
Classification of
hypersensitivity reactions (by Gell & Coombs)
a)
Type 1 or
anaphylactic reaction,
which is mediated by Ig E, this mechanism is involved in certain
urticarias & reactions to stings.
b)
Type 2 or cytotoxic
reaction:
This reaction occurs in cases of some drug allergies.
c)
Type 3 or complex
reaction
is due to in situ complement fixation deposit caused by soluble
antigen- antibody complexes. This is the Arthus type reaction
that occurs in serum sickness & some drug allergies.
d)
Type 4 delayed
(cellular) reaction:
This occurs in allergic contact dermatitis.
ALLERGIC CONTACT
DERMATITIS
Contact dermatitis
is an acute, subacute, or chronic inflammation of the skin
caused by an external agent which comes in direct contact with
the skin. Environmental & seasonal factors play a role in the
incidence of allergic contact dermatitis. Racial factors
also play a role, as Caucasians appear to be more
susceptible than blacks to sensitization.
Approximately
two-thirds of cases of contact dermatitis occur on the hands,
are often of an occupational nature, & are of the irritant type.
Contact dermatitis
affecting other sites is most the allergic type. Allergic
contact dermatitis is due to a Type 4 cell- mediated
immune response to an allergen. It is a typical example of
the delayed type sensitivity of T cell mediated reaction.
It occurs only in individuals who have become sensitized to
substance during a previous exposure.
KEY DIAGNOSTIC
FEATURES
v
Sudden onset of
erythema, oedema, vesicle, bullae, & oozing accompanied by
pruritus & burning.
v
Eruption at a
localized site.
v
History of exposure
to a potential allergen.
v
Positive patch
test to suspected sensitizer.
The morphology of eruption may
also be helpful. Linear lesions for example are
suggestive of plant dermatitis. Allergic contact
dermatitis is usually
severely pruritic.
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Sunscreen reaction |

Watch strap reaction |
Allergy to hair
dye Contact dermatitis caused by
Nickel Severe dermatitis due to elasticized undergarment
Common sensitizers
that cause allergic contact dermatitis
|
plants |
metals |
dyes |
Rubber
compounds |
medications |
|
Phenolic
oleoresine: poison ivy, poison sumac & other
Anacardiaceae.
Rag weed
Chrysanthemum
& other compositae. |
Nickel & gold
in jewellery.
Mercury
Chromates
in shoes & cement |
Paraphenylenediamine
in hair & shoe dyes.
Azo dyes
in nail enamel & lipstick. |
Mercaptobenzothiazole
Tetramethylthiuram
|
Neomycin, benzocaine
Ethylenediamine
Antihistamines
Mercury
Lanolin
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Regional clues to
sensitizing items
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Face
|
-
Topical
medications
-
Nail polish
-
Hair dye
-
Shaving
lotion
-
Hatband
|
|
Eyelids,
periorbital area |
|
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Neck
|
|
|
Ears
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|
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Mouth, lips,
perioral area |
-
Lipstick
-
Toothpaste
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Mouth wash
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Axillae
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|
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Hands,
forearms |
-
Occupational
substances
-
Ring
-
Plants
-
Glove
-
Wrist watch
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Topical
medications
|
|
Genitals
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-
Condom
-
Pessary
-
Clothing
-
Topical
medications
|
|
Anal region |
-
Suppositories
-
Antibacterials
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Antifungals
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feet |
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TREATMENT
(homoeopathic management)
a)
HOMOEOPATHIC MEDICAL
REPERTORY BY ROBIN MURPHY
v
Skin, DERMATITIS: CHAM, HEP, MERC,
PULS, RHUST, SIL
tendency to:
CHAM
v
Diseases, DERMATITIS: CHAM, HEP,
MERC, PULS, RHUST, SIL
v
Skin, ERUPTIONS itching: ARS,
CAUST, CLEM, GRAPH, MEZ, NAT-M, NIT-AC, NUX-V, RHUST, SEP, STAPH,
SULPH
v
Skin, ITCHING
contact
from, agg:ran-b
v
Skin, POISON,
oak or ivy: ANAC, CLEM,
CROT-T, RHUS-T
b)
SYNTHESIS REPERTORY
v
Skin, ERUPTIONS
erythema:
Bell, Mez
v
Skin, ERUPTIONS itching: Ars,
Caust, Clem, Graph, Mez, Nat-m, Nit-ac, Nux-v, Rhust, Sep, Staph,
Sulph
v
Skin, ITCHING
contact
from, agg:ran-b
c)
KENT’S REPERORY
v
SKIN, ERUPTIONS
itching: Ars, Caust,
Clem, Graph, Mez, Nat-m, Nit-ac, Nux-v, Rhust, Sep, Staph, Sulph
URTICARIA
Urticaria (hives) is an acute or
chronic allergic dermatosis. It is usually a transient, mild
vascular reaction of the dermis characterized by pruritic
wheals.
The common mechanism
of urticaria is considered to be the release of histamine
from mast cells, which causes an increased capillary
permeability & vasodilatation leading to the formation of dermal
swellings. Most urticarias represent a Type 1 (Ig E)
mediated reaction. Acute urticaria is often caused by insect
bites or stings, medications, foods like shellfish, pork etc.
CLINICAL FEATURES
The onset is usually
sudden with development of blotchy spots which rapidly become
white or pinkish wheal or plaques, often surrounded by an
erythematous halo. The eruption tends to appear on covered
areas, mostly the trunk & buttocks. Acute urticaria is often
self limited. Chronic urticaria lasts several weeks to many
months.
Clinical varieties:
·
Angioedema
This affects the
subcutaneous tissues rather than the dermis & mostly involves
the lips, eyelids & genitals.
·
Cholinergic urticria
(heat or stress induced)
The lesions are
associated with perspiration.
·
Cold urticaria
It is due to cold
exposure. Symptoms subside quickly when the affected areas are
rewarmed.
·
Contact uticaria
It is due to contact
with an external substance.
·
Dermographism
It is a physically
induced variety which results from firm stroking of the skin.
TREATMENT
(homoeopathic management)
a)
SYNTHESIS REPERTORY
v
Skin, ERUPTIONS
urticaria: (→angioedema): Apis, Ars, Astac, Calc, Calc-s, Carbn-s,
Caust, Chlol, Cop, Dulc, Hep, Nat-m, Rhust, Sulph, Urt-u
d)
KENT’S REPERTORY
v
SKIN, ERUPTIONS
urticaria.
e)
MURPHY’S REPERTORY
v
Skin, URTICARIA,
hives: APIS, ARS, ASTAC, CALC, CALC-S, CARBN-S, CAUST, CHLOL,
COP, DULC, HEP, NAT-M, RHUST, SULPH, URT-U
v
Diseases, HIVES,
urticaria
f)
BOENNINGHAUSEN’S THERAPEUTIC
POCKET BOOK
v
SKIN
Eruptions Nettle-rash: APIS, CALC-C, CAUST, DULC, HEP, RHUS.
v
SKIN
Eruptions, Nodular (Wheals and Hives): APIS, CALC-C, CAUST, DULC,
LACH, MEZ, RHUS.
g)
BOGER BOENNINGHAUSEN’S REPERTORY
v
SKIN & EXTERIOR BODY
Eruptions urticarious
(nettle-rash):
APIS, CALC-C, CAUST, DULC, HEP, RHUS
ATOPIC DERMATITIS
Atopic dermatitis (atopic eczema)
is a genetically determined disease in which there is a high
personal or familial incidence of allergic conditions.
Clinically the disease is characterized by an acute eczematous
dermatitis in early life & a chronic lichenified eruption in
adolescence.
Various factors such
as altered immune defenses, abnormal beta adrenergic receptors &
food allergies are the possible causes. Atopic individuals tend
to produce high levels of circulating Ig E.
CLINICAL FEATURES
Atopic dermatitis s divided into
3 stages:
·
Infantile
·
Childhood
·
Adolescent/ adult
The infantile
stage affect infants aged 2 months to 2 years. It involves
mainly the scalp & face sparing the perioral region. The
childhood forms are usually less vesicular, drier&
more popular. The flexural aspects of elbows & knees are
frequently involved. Pruritus is always present &
scratching cause lichenification. In the adult form, the
eruption is frequently dry & often lichenified. The
antecubital & popliteal spaces are usually involved. The
cardinal symptom is pruritus.
ALLERGIC DRUG
ERUPTIONS
These are
hypersensitivity reactions that result from allergic
sensitization to systematically administered drug. Children &
the aged appear to be less prone to drug sensitization than
adults.
CLINICAL FEATURES
A drug may be
tolerated for weeks or even years without ill effects. But once
an individual become sensitized, the reaction usually occurs
within minutes to 24 hours. In Steven- Johnson’s syndrome, a
severe form of erythema multiforme, there are also mucoal
lesions & involvement of internal organs with significant
constitutional symptoms.
Some drug eruptions
have the appearance of various dermatoses,
but with atypical presentation:
Frequently due to arenicals & barbiturates.
May be
caused by hydralzine & isoniazid.
Often due to beta blockers & gold.
Commonly
due to rifampicin.
Course is usually
brief if the drug is identified & discontinued.
HOMOEOPATHIC
MANAGEMENT
a)
SYNTHESIS REPERTORY
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