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CHAPTER I

I.I

INTRODUCTION
Urticaria describes a heterogeneous group of diseases, whose cardinal symptoms are

itching wheals. With a high life time prevalence of 25%, this disease is of major relevance.
The most common type is spontaneous Urticaria in which the wheals seem to arise without
provocation. Its subtypes are acute and chronic. The mechanism of wheal formation is the
activation and degranulation of mast cells. However, the etiology of the wheals is
multifacted. In case of acute spontaneous urticaria, the underlying cause does not have to be
verified. It is treated symptomatically by its self-limiting course of disease. The chronic
spontaneous, less frequent form of urticaria is treated curatively by identification and
elimination of underlying causes, such as autoimmune processes, intolerance to food
additives and chronic infections. The chronic subtype can persist for years and thus has an
extensive socioeconomic impact. Incidence rates for acute urticaria are similar for men and
women, chronic urticaria occurs more frequently in women (60%).Urticaria can occur in any
age group, although chronic urticaria is more common in the fourth and fifth decades. 4 Things
that trigger commonly trigger an allergic reaction, but there are other causes of urticaria, and
one of them is weather, solar exposure and cold exposure.5
The writer choose this topic because of urticaria is the most frequent dermatologic
disorder. The etiologies of urticaria are numerous, one of them is weather. As we know,
Indonesia is the tropical country that has dry and rain season. Dry season has hot weather,
and solar exposure can induce urticaria (solar urticaria). Rain season can be possible for
having cold weather that can induce cold urticaria.

Urticaria appears as raised, well-circumscribed areas of erythema and edema


involving the dermis and epidermis that are very pruritic. Because of that, before we discuss
about urticaria and its correlation with weather, firstly we must know about skin anatomy,
especially dermis and epidermis. These all will be written in chapter II and III.

CHAPTER II
II.I

ANATOMY OF SKIN

The skin covers the entire external surface of the human body and is the principal site of
interaction with the surrounding world. It serves as a protective barrier that prevents internal
tissues from exposure to trauma, ultraviolet (UV) radiation, temperature extremes, toxins, and
bacteria. Other important functions include sensory perception, immunologic surveillance,
thermoregulation, and control of insensible fluid loss.
The integument consists of two mutually dependent layers, the epidermis and dermis, which
rest on a fatty subcutaneous layer, the panniculus adiposus. The epidermis is derived
primarily from surface ectoderm but is colonized by pigment-containing melanocytes of
neural crest origin, antigen-processing Langerhans cells of bone marrow origin, and pressuresensing Merkel cells of neural crest origin. The dermis is derived primarily from mesoderm
and contains collagen, elastic fibers, blood vessels, sensory structures, and fibroblasts.6, 7

During the fourth week of embryologic development, the single cell thick ectoderm and
underlying mesoderm begin to proliferate and differentiate. The specialized structures formed
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by the skin, including teeth, hair, hair follicles, fingernails, toenails, sebaceous glands, sweat
glands, apocrine glands, and mammary glands also begin to appear during this period in
development. Teeth, hair, and hair follicles are formed by the epidermis and dermis in
concert, while fingernails and toenails are formed by the epidermis alone. Hair follicles,
sebaceous glands, sweat glands, apocrine glands, and mammary glands are considered
epidermal glands or epidermal appendages, because they develop as downgrowths or
diverticula of the epidermis into the dermis.6, 8
The definitive multi-layered skin is present at birth, but skin is a dynamic organ that
undergoes continuous changes throughout life as outer layers are shed and replaced by inner
layers. Skin also varies in thickness among anatomic location, sex, and age of the individual.
This varying thickness primarily represents a difference in dermal thickness, as epidermal
thickness is rather constant throughout life and from one anatomic location to another. Skin is
thickest on the palms and soles of the feet (1.5 mm thick), while the thinnest skin is found on
the eyelids and in the postauricular region (0.05 mm thick).
Male skin is characteristically thicker than female skin in all anatomic locations. Children
have relatively thin skin, which progressively thickens until the fourth or fifth decade of life
when it begins to thin. This thinning is also primarily a dermal change, with loss of elastic
fibers, epithelial appendages, and ground substance.9
II.I.I EPIDERMIS
The epidermis contains no blood vessels and is entirely dependent on the underlying dermis
for nutrient delivery and waste disposal via diffusion through the dermoepidermal junction.
The epidermis is a stratified, squamous epithelium that consists primarily of keratinocytes in
progressive stages of differentiation from deeper to more superficial layers. The named layers
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of the epidermis include the stratum germinativum, stratum spinosum, stratum granulosum,
and stratum corneum.
II.I.II DERMIS
The primary function of the dermis is to sustain and support the epidermis. The dermis is a
more complex structure and is composed of 2 layers, the more superficial papillary dermis
and the deeper reticular dermis. The papillary dermis is thinner, consisting of loose
connective tissue containing capillaries, elastic fibers, reticular fibers, and some collagen. The
reticular dermis consists of a thicker layer of dense connective tissue containing larger blood
vessels, closely interlaced elastic fibers, and coarse bundles of collagen fibers arranged in
layers parallel to the surface.
The reticular layer also contains fibroblasts, mast cells, nerve endings, lymphatics, and
epidermal appendages. Surrounding the components of the dermis is the gel-like ground
substance, composed of mucopolysaccharides (primarily hyaluronic acid), chondroitin
sulfates, and glycoproteins. The deep surface of the dermis is highly irregular and borders the
subcutaneous layer, the panniculus adiposus, which additionally cushions the skin.
II.II

URTICARIA

Hives are welts on the skin that often itch. These welts can appear on any part of the skin.
Hives vary in size from as small as a pen tip to as large as a dinner plate. They may connect
to form even larger welts.
A hive often goes away in 24 hours or less. New hives may appear as old ones fade, so hives
may last for a few days or longer. A bout of hives usually lasts less than 6 weeks. These hives
are called acute hives. If hives last more than 6 weeks, they are called chronic hives.
Acute hives often result from an allergy, but they can have many other causes.
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The medical term for hives is urticaria. When large welts occur deeper under the skin, the
medical term is angioedema. This can occur with hives, and often causes the eyelids and lips
to swell. In severe cases, the throat and airway can swell, making breathing or swallowing
difficult. If this occurs, the person needs emergency care right away.
Doctors put hives into two categories:
1. Acute hives, when the condition lasts for less than 6 weeks (also called "acute
urticaria").
2. Chronic hives, when the condition lasts for longer than 6 weeks ("chronic urticaria").
II.II.I SIGNS AND SYMPTOMS
The raised red bumps that we call hives can appear anywhere on the body. Here are some
signs to watch for:

Hives often itch or sting.

Hives can range in size from as small as a few millimeters across to as big as a dinner
plate.

Individual hives may change shape or appear in clusters. Sometimes hives join
together to form larger patches.

Hives can spread or show up on a different part of the body.

In a few rare cases, hives are part of a serious allergic reaction called anaphylaxis. Exposed to
temperature extremes, stress, infections, or illnesses. People often have a trigger (what causes
the hives). Every time they are exposed to that trigger, they get hives

The red blotches happen when cells in the bloodstream (mast cells) release the chemical
histamine. This causes tiny blood vessels under the skin to leak. The fluid pools within the
skin to form spots and larger blotches..
Your dermatologist may call this type of hives fixed, which means not moving. Fixed hives
may happen when a person takes a certain medicine (fixed drug eruption) or gets too much
sunlight (fixed solar urticaria).
II.II.II

CAUSES

An allergic reaction can trigger hives. Things that trigger commonly trigger an allergic
reaction include:

Foods: Fruits (especially citrus fruits), milk, eggs, peanuts, tree nuts, and shellfish

Medicines

Insect bites and stings

Animals

Pollen

Touching something to which you are allergic, such as latex

Allergy shots

Other causes of hives are:

Infections, including colds and infections caused by some bacteria or fungi

Some illnesses, including a type of vasculitis, lupus, and thyroid disease

Exposure to sun (solar urticaria), heat, cold, or water


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Exercise

Stress

Pressure on the skin, such as from sitting too long

Contact with chemicals

Scratching the skin

Hives can happen within minutes of exposure to the trigger. Or you can have a delayed
reaction of more than two hours.5
II.II.III

PATHOPHYSIOLOGY

Urticaria results from the release of histamine, bradykinin, leukotriene C4, prostaglandin D2,
and other vasoactive substances from mast cells and basophils in the dermis. These
substances cause extravasation of fluid into the dermis, leading to the urticarial lesion. The
intense pruritus of urticaria is a result of histamine released into the dermis. Histamine is the
ligand for 2 membrane-bound receptors, the H1 and H2 receptors, which are present on many
cell types. The activation of the H1 histamine receptors on endothelial and smooth muscle
cells leads to increased capillary permeability. The activation of the H2 histamine receptors
leads to arteriolar and venule vasodilation.
This process is caused by several mechanisms. The type I allergic IgE response is initiated by
antigen-mediated IgE immune complexes that bind and cross-link Fc receptors on the surface
of mast cells and basophils, thus causing degranulation with histamine release. The type II
allergic response is mediated by cytotoxic T cells, causing deposits of immunoglobulins,
complement, and fibrin around blood vessels. This leads to urticarial vasculitis. The type III

immune-complex disease is associated with systemic lupus erythematosus and other


autoimmune diseases that cause urticaria.10, 11
Complement-mediated urticarias include viral and bacterial infections, serum sickness, and
transfusion reactions. Urticarial transfusion reactions occur when allergenic substances in the
plasma of the donated blood product react with preexisting IgE antibodies in the recipient.
Certain drugs (opioids, vecuronium, succinylcholine, vancomycin, and others) as well as
radiocontrast agents cause urticaria due to mast cell degranulation through a non IgEmediated mechanism. Urticaria from nonsteroidal anti-inflammatory drugs may be IgEmediated or due to mast cell degranulation, and there may be significant cross-reactivity
among the nonsteroidal anti-inflammatory drugs (NSAIDs) in causing urticaria and
anaphylaxis.10
The physical urticarias in which some physical stimulus causes urticaria include immediate
pressure urticaria, delayed pressure urticaria, cold urticaria, and cholinergic urticaria.11 For
some urticarias, especially chronic urticarias, no cause can be found, despite exhaustive
effortsthe so-called idiopathic urticarias, although most of these are chronic autoimmune
urticaria as defined by a positive autologous serum skin test (ASST).12 This test is not specific
for autoantibodies against a specific antigen or diagnostic of a specific disease state.13 To
date, no reliable test exists to identify with certainty if chronic urticaria is autoimmune or
nonautoimmune in the specific patient.14

II.II.IV EPIDEMIOLOGY
FREQUENCY
United States
Acute urticaria affects 15-20% of the general population at some time during their lifetime.
International
The frequency of urticaria internationally is similar to that in the United States.
MORTALITY/MORBIDITY
Pruritus (itching) and rash are the primary manifestations of urticaria, and permanent
hyperpigmentation or hypopigmentation are rare. Acute urticaria is usually self-limited and
commonly resolves within 24 hours but may last up to 6 weeks. Chronic urticaria lasts more
than 6 weeks. Neither acute nor chronic urticaria results in long-term consequences other than
anxiety and depression. The depression can be severe enough to lead to suicide in rare cases.
Also, many of the diseases associated with chronic urticaria may cause very significant
morbidity and mortality.
SEX
Incidence rates for acute urticaria are similar for men and women, chronic urticaria occurs
more frequently in women (60%).
AGE
Urticaria can occur in any age group, although chronic urticaria is more common in the fourth
and fifth decades.
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CHAPTER III
III.

DISCUSSION

III.I

SOLAR URTICARIA

Sun allergy is a condition in which sunlight triggers a skin reaction. For most people, sun
allergy symptoms include an itchy red rash in areas that have been exposed to sunlight. A
severe sun allergy may cause hives, blisters or other symptoms. There are several types of sun
allergy including polymorphic light eruption (PMLE), actinic prurigo, chronic actinic
dermatitis (CAD) and solar urticaria.
Solar urticaria is a form of chronic hives that is caused by exposure to sunlight. People with
this condition experience itching, redness and hives on areas of skin exposed to sunlight. At
times, symptoms can be confused with a sunburn, although solar urticaria can occur within
minutes of exposure to the sun, and goes away much quicker (less than a day) after sun
exposure has stopped.
The appearance of the hives is no different from other forms of urticaria, although these hives
only occur on skin that is directly exposed to the sun. Hives may also occur under thin
clothing. Skin that is frequently exposed to sunlight, such as the skin on the face, is typically
unklikely to develop hives as opposed to skin that is less frequently exposed to the sun.
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It appears that people with solar urticaria make allergic antibodies against various proteins
found in their own skin. These proteins' structure changes with sunlight, allowing the allergic
reaction to occur, causing hives. It is possible for a person with solar urticaria to experience
anaphylaxis is enough skin is exposed to sunlight.
III.I.I

SYMPTOMS

Sun allergy symptoms depend on the particular type of sun allergy you have. Solar urticaria
symptoms start within minutes of exposure to sunlight and can include hives, itching and
blisters. Solar urticaria can affect both exposed areas and areas covered by clothes. It occurs
most often in older adults. Symptoms usually improve within an hour after covering exposed
skin.

III.I.II CAUSES
Solar urticaria is possibly caused by an antigen-antibody reaction. Solar irradiation may
induce an antigen in the serum or plasma of affected individuals. Intradermal injection of
serum from a solar urticaria patient passively, but not consistently, transfers the condition to a
healthy individual.
The following types of solar urticaria have been proposed:
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Type I - This type is characterized by an immunoglobulin E (IgE)mediated


hypersensitivity to specific photoallergens generated only in solar urticaria patients

Type II - This type is characterized by an IgE-mediated hypersensitivity to


nonspecific photoallergens found in solar urticaria patients and in healthy individuals

Passive-transfer test findings are positive in patients with type II solar urticaria, but they may
be positive or negative in those with type I.
The wide action spectrum (290-800 nm) implicated for solar urticaria may be related to the
specific photoallergen and its molecular weight. Diversity in the reported action spectra for
the disease may be due to differences in photoallergens. In addition, spectra believed to be
responsible for either inhibition or augmentation of the reaction have been detected.15
Complex interactions occur between the various wavelengths and the photoallergen.
The result of these interactions is mast cell degranulation with subsequent histamine release.
Mediators other than histamines may also be involved.
Inhibition of solar urticaria with light suppresses the wheal-flare response following
intradermal injection of photoactivated autologous serum but does not suppress the wheal and
flare associated with compound 48/80.16
III.I.III

TESTS AND DIAGNOSIS

Your doctor will want to make sure your skin reaction isn't due to something other than a sun
allergy. A number of conditions can cause similar symptoms. In some cases, a skin allergy
can be diagnosed by answering questions or by having your doctor examine the affected areas
when symptoms are present. However, if the diagnosis isn't clear-cut, you may need tests to

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help identify what's going on. If this is the case, you'll most likely need to see a
dermatologist.
Tests to diagnose skin reactions caused by sun exposure can include:

UV light testing. Also called phototesting, this exam is used to see how your skin
reacts to different wavelengths of ultraviolet light from a special type of lamp.
Determining which particular kind of UV light causes a reaction can help pinpoint
which sun allergy you have.

Photopatch testing. This type of test is used if your doctor suspects something you've
come in contact with makes your skin react to sunlight. To do the test, your doctor
will apply two identical patches of a substance that may be causing a reaction to your
skin. After 24 hours, your doctor will expose one area to UV light, but not the other. If
a reaction occurs only on the exposed area, it's likely your reaction is linked to the
substance in question. Light testing and photopatch testing are generally available
only at specialized clinics.

Blood tests and skin samples. These tests usually aren't needed. However, your doctor
may order one of these tests if he or she suspects your symptoms might be caused by
an underlying condition such as lupus instead of a sun allergy. With these tests, a
blood sample or a skin sample (biopsy) is taken for further examination in a
laboratory.17, 18

III.I.IV TREATMENTS AND DRUGS


Treatment depends on the particular type of sun allergy you have. It may include:

Corticosteroid creams. These creams are available over-the-counter and in stronger,


prescription form. For example, hydrocortisone medications (Cortaid, others) are
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available over-the-counter and triamcinolone medications (Kenalog, others) require a


prescription.

Oral antihistamines. These medications block histamines, symptom-causing


chemicals released during an allergic reaction. Your doctor may recommend you use
over-the-counter antihistamine pills, or he or she may write you a prescription.
Examples of over-the-counter antihistamines include loratadine (Claritin, Alavert) and
cetirizine (Zyrtec). Older over-the-counter antihistamines such as diphenhydramine
(Benadryl) and clemastine (Tavist) work as well as newer ones, but can make you
drowsy. Prescription antihistamines include desloratadine (Clarinex), fexofenadine
(Allegra), hydroxyzine (Vistaril) and levocetirizine (Xyzal).

Oral corticosteroids. For a severe allergic skin reaction, you may benefit from a short
course of these powerful anti-inflammatory medications. In some cases, an oral
corticosteroid such as prednisone is given prior to a period of sunlight exposure, such
as before a summer vacation. Oral corticosteroids can cause serious side effects when
used long term, so they're used to prevent and relieve severe sun allergy symptoms
only on a short-term basis.

Other medications. In some cases, drugs usually used to treat other conditions are
used to treat sun allergies. For example, the malaria medication hydroxychloroquine
may ease symptoms of polymorphic light eruption and other sun allergies. In some
cases, antibiotics generally used to treat infections are used for chronic actinic
dermatitis.

Ultraviolet light therapy. This treatment is also called phototherapy. A special lamp is
used to shine ultraviolet light on areas of your body that are often exposed to the sun.
It's generally done a few times a week over a period of several weeks each spring.
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During the course of treatments, your doctor will gradually increase the dose of UV
radiation. Your skin becomes accustomed to UV light, reducing symptoms caused by
sun exposure. This treatment is generally available only at specialized clinics.17, 18
III.I.V PREVENTION
If you have a sun allergy or an increased sensitivity to the sun, you can help prevent a
reaction by taking these steps:

Limit your time in the sun. Stay out of the sun between 10 a.m. and 3 p.m. when the
sun is brightest.

Avoid sudden exposure to lots of sunlight. Many people have sun allergy symptoms
when they are exposed to more sunlight in the spring or summer. Gradually increase
the amount of time you spend outdoors so that your skin cells have time to adapt to
sunlight.

Wear sunglasses and protective clothing. Long-sleeved shirts and wide-brimmed hats
can help protect your skin from sun exposure. Avoid fabrics that are thin or have a
loose weave UV rays can pass through them. You may want to consider wearing
clothes specifically designed to block UV rays, which can be found at sporting goods
stores.

Apply sunscreen frequently. Use broad-spectrum sunscreen with a sun protection


factor (SPF) of 30 or higher on exposed skin. Reapply sunscreen every two hours.19

III.II

COLD URTICARIA

Cold urticaria is an allergy to cold temperatures. With cold urticaria, exposure to cold
temperatures causes redness, itching, swelling and hives on the skin that has been in contact
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with the cold. As much as possible, people with cold urticaria should avoid exposure to cold
air and cold water. For example, swimming in cold water is the most common cause of a
severe, whole-body reaction leading to fainting, shock and even death.
If you think you have cold urticaria, also called cold allergy or cold hives, consult your
doctor. Treatment for cold urticaria may include antihistamines taken before cold exposure.

III.II.I

SYMPTOMS

Cold urticaria symptoms begin soon after the skin is exposed to a sudden drop in air
temperature or to cold water. Although symptoms may begin during the cold exposure,
symptoms of cold urticaria are often worse during rewarming of the exposed skin. The
majority of cold urticaria reactions occur when skin is exposed to temperatures lower
than 40 F (4.4 C), but some people can have reactions to warmer temperatures. Damp
and windy conditions may make cold urticaria more likely.
Cold urticaria signs and symptoms may include:

Reddish, itchy hives (wheals) on the area of skin that was exposed to cold. Wheals
generally last for about half an hour.

Swelling of hands when holding cold objects.

Swelling of lips when eating cold foods.

In rare cases, severe swelling of the tongue and throat that can block breathing
(pharyngeal edema).

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Severe reactions
For people who have cold urticaria, exposure to cold can be dangerous. In some people,
reactions affect the whole body. This is known as a systemic reaction. Signs and symptoms of
a severe reaction include:

Fainting

Chills

Fast heartbeat

Swelling of limbs or trunk

The worst reactions generally occur with full skin exposure, such as swimming in cold water.
A massive release of histamine and other immune system chemicals causes a sudden drop in
blood pressure that can lead to fainting, shock and, in rare cases, death. In the case of coldwater swimming, drowning can be caused by loss of consciousness.
The severity of cold urticaria symptoms varies widely. Some people have minor reactions to
cold, while others have severe reactions. It's also impossible to say whether it will get better
over time. In some cases, cold urticaria goes away on its own after several months. In other
cases, it lasts many years.
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III.II.II

CAUSES

The cause of cold urticaria isn't clear. Certain people appear to have overly sensitive skin
cells, either due to an inherited trait or caused by a virus or other illness. Exposure to cold
triggers the release of histamine and other immune system chemicals into the skin. These
chemicals cause redness, itching and other symptoms.
III.II.III

RISK FACTORS

Cold urticaria can occur in any age group, whether female or male. You're more likely to have
cold urticaria if:

You're a child or young adult. A type of urticaria called primary acquired urticaria
occurs in children and young adults. This is the most common type of urticaria, and it
usually improves on its own within two to three years.

You recently had a viral infection. Mycoplasma pneumonia and mononucleosis have
been linked to cold urticaria.

You have an underlying health condition. Known as secondary acquired urticaria, this
less common type of cold urticaria can be caused by an underlying health problem,
such as rheumatoid arthritis, hepatitis or cancer.

You have certain inherited traits. Rarely, cold urticaria is associated with an inherited
condition called familial cold autoinflammatory syndrome. This condition causes
painful wheals and flu-like symptoms after exposure to cold.

III.II.IV TESTS AND DIAGNOSIS

19

Cold urticaria can be diagnosed by placing an ice cube on exposed skin for several minutes.
If you have cold urticaria, a raised, red bump (hive) will form after the ice cube is removed.
Most cases of urticaria occur in children and young adults and don't have an apparent
underlying cause. This type of urticaria usually gets better on its own after a few weeks to
months, but sometimes it can last for years.
In some cases, cold urticaria is caused by an underlying condition that affects the immune
system. Some conditions that can cause cold urticaria include hepatitis, rheumatoid arthritis,
certain cancers or an infection such as mononucleosis. If your doctor suspects you have an
underlying condition, you may need blood tests or other tests.20
III.II.V TREATMENTS AND DRUGS
There is no cure for cold urticaria, but treatment can help. Treatment includes avoiding cold
temperatures and exposure to sudden changes in temperature. Medications can help prevent
and reduce symptoms.
Medications used to treat cold urticaria include:

Antihistamines. These medications block the symptom-producing release of


histamine. Some of these medications are available over-the-counter, whereas others
require a prescription. Examples include loratadine (Claritin), fexofenadine (Allegra),
cetirizine (Zyrtec), levocetirizine (Xyzal) and desloratadine (Clarinex).

Cyproheptadine. This medication is an antihistamine that also affects nerve impulses


that lead to symptoms.

Doxepin (Silenor). Normally used to treat anxiety and depression, this medication can
also reduce cold urticaria symptoms.
20

These medications won't cure cold urticaria they'll only ease symptoms. If you have cold
urticaria because of an underlying health problem, you may need medications or other
treatment for that condition as well.

III.II.VI

PREVENTION

There's no way to avoid getting cold urticaria in the first place, but you can help prevent
symptoms by taking medications as prescribed and avoiding cold temperatures, especially
cold exposure to unprotected skin.21, 22

21

CHAPTER IV
IV.I

CONCLUSION
Urticaria, commonly referred to as hives, is the most frequent dermatologic disorder.

It appears as raised, well-circumscribed areas of erythema and edema involving the dermis
and epidermis that are very pruritic. Urticaria may be acute (lasting less than 6 weeks) or
chronic (lasting more than 6 weeks). The etiologies of urticaria are numerous, one of them is
weather. As we know, Indonesia is the tropical country that has dry and rain season. Dry
season has hot weather, and solar exposure can induce urticaria (solar urticaria). Rain season
can be possible for having cold weather that can induce cold urticaria.

22

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