Pruritus universalis

Atopic dermatitis

Outline

*Atopic dermatitis is chronic eczema/dermatitis caused by

an atopic condition (allergic asthma, rhinitis, conjunctivitis).

*Exudative eczema occurs on the face and ear pinna. It is

characterized by eruptions of dry pityriatic scales.

*The patient tests positive for white dermographism. The

IgE value is high.

*Filaggrin gene mutation is a key predisposing factor for

atopic dermatitis.

*These complications can occur: Kaposi’s varicelliform

eruption, cataract, and retinal separation.

*Topical steroids, topical immunosuppressants such as

tacrolimus and pimecrolimus, oral antihistamines, and

moisturizers are the first-line treatments.

General information

In atopic dermatitis, chronic eczematous/dermatitis lesions are

caused by various acquired stimulative factors, under conditions

in which the skin barrier function is congenitally low and IgE is

easily produced. The Japanese Dermatological Association

defines atopic dermatitis as “a disease whose main lesion is itching

eczema with recurrent remissions and exacerbations, and

most patients have some atopic condition.” Type I allergy (an

atopic condition, such as asthma, allergic rhinitis, or conjunctivitis)

and type IV allergy are involved in most cases.

Clinical features

Atopic dermatitis is classified into three age periods: infantile

(age 2 months to 4 years), childhood (early childhood to puberty),

and adolescent/adult. Different eruptions characterize each

period. Atopic dermatitis is accompanied

by intense itching in all the periods, with recurrent remissions

and exacerbations. It tends to worsen when the skin is dry and

during the summer. Although it most frequently occurs in infancy,

its incidence in patients beyond infancy, including adults, has

been increasing greatly in recent years.

Infantile atopic dermatitis

In the early stage of atopic dermatitis in infancy, erythema,

scales, and serous papules are produced on the head and face and

these gradually spread to the trunk. The condition becomes

exudative: erosions form, with crusts and scales attached to the

surface. It resembles seborrheic dermatitis. Thick crusts on the

head and ear notch, and lesions around the mouth and lower jaw

(produced by causative agents in baby food) are also observed.

The trunk and extremities become dry, and follicular papules

aggregate, appearing as goose bumps. Scaly erythematous

plaques form on these lesions and progress to childhood atopic

dermatitis.

Childhood atopic dermatitis

In childhood atopic dermatitis the skin becomes dry. Lichenified

plaques occur on the cubital fossa and popliteal fossa.

Cracks are often found in the auricle area (ear notch). Multiple

follicular papules occur on the dry skin of the trunk. This dermatitis

is accompanied by intense itching, and it progresses

quickly to eczematous crusty lesions.

Adolescent and adult atopic dermatitis

The symptoms are similar to those in childhood dermatitis, but

the lichenified plaques progress and enlarge. Rough, dry, dark

brown atopic dermatitis occurs all over the upper body. The

lesions are more severe and widely distributed than those of

childhood dermatitis. Thinning of one-third of the lateral eyebrow

is present. In serious cases, diffuse erythema occurs on the face, and a mottled

appearance is seen on the neck and upper chest (poikiloderma

lesion, dirty neck. Atopic prurigo may occur

repeatedly on the extremities.

There have been many studies on skin physiology and immune

function in atopic dermatitis; however, the pathogenesis has not

been fully clarified.

Abnormality of skin physiology: A defective skin barrier is

important for the pathogenesis of atopic dermatitis. Filaggrin

gene mutations have been shown to be a key predisposing factor

for atopic dermatitis. Abnormality in vascular response can be

tested by white dermographism (skin with atopic dermatitis

becomes white when scratched, whereas normal skin becomes

red). Dyshidrosis and decreased content (particularly

a decrease in ceramides) of lipid in the horny cell layer, facial

pallor, dry skin and multiple small follicular papules are present

(atopic skin). The atopic skin is vulnerable to extrinsic irritation;

intensely itchy eczema is easily produced by slight irritation, or

even by perspiration or contact with animal fur, wool or chemicals.

Immune function abnormality: Atopic conditions such as allergic asthma, allergic rhinitis, conjunctivitis and atopic dermatitis are

found in the family and patient’s history. Patients with atopic

dermatitis readily produce IgE antibodies. When there is a high

IgE value and positive intracutaneous reactions to various allergens,

a congenital immune abnormality of some sort is regarded

as being involved in atopic dermatitis.

Eye diseases such as cataract (in 10% of severe adult cases),

keratoconus, and retinal separation develop as complications of

atopic dermatitis. Eye-rubbing from the itch and prolonged oral

steroid use are thought to be the cause; however, this has not

been confirmed. Infectious diseases including Kaposi’s varicelliform

eruptions, molluscum contagiosum, and impetigo contagiosa

may also be caused. Patients with atopic dermatitis may be

hypersensitive to drugs and insect stings.

The serum IgE value is high; IgE RAST for mites and house

dust is positive in most cases. There is an increase in eosinophils

in the peripheral blood. Although white dermographism is highly

sensitive in detecting atopic dermatitis, it has low specificity.

When there are the clinical findings described above, atopic

dermatitis is easy to diagnose. In diagnosis, it is also important to

consider any family history of the condition. Atopic dermatitis in

adolescents and adults has been increasing in recent years. Infant

seborrheic dermatitis closely resembles infantile atopic dermatitis.

Treatment.

Topical steroid application is the primary treatment for the

intense cutaneous symptoms. The application method and dosage

of steroids are chosen according to the degree and course of the

lesion. Ointments containing immunosuppressants such as

tacrolimus and pimecrolimus have become widely used dermatological

treatments (Chapter 6). These drugs are not used for erosions

or ulcers; however, they are helpful for systemic lesions

including those on the face, and they are frequently used internationally

as first-line treatments. Moisturizer is helpful in treating

mild symptoms. Oral antihistamines are effective at preventing

the eruptions from becoming aggravated by rubbing and scratching.

Oral steroids are usually unnecessary for mild symptoms of

atopic dermatitis.

Besides these medical treatments, improvement of the living

environment (e.g., removing carpeting, keeping the temperature

and humidity low to reduce perspiration), and skin care (avoiding

contact with causative agents, keeping the skin clean) are important.

Prognosis

Atopic dermatitis tends to be chronic and recurrent. It mostly

resolves spontaneously by the time the patient reaches age 10;

however, the symptoms do not improve in some patients until

they reach adolescence or adulthood. The incidence of adolescent

and adult atopic dermatitis has been increasing in recent years.

Seborrheic dermatitis

Synonym: Seborrheic eczema

Outline

*Seborrheic dermatitis occurs on sites of skin where

sebum is actively secreted. It is characterized by erythematous

lesions accompanied by yellowish scales.

*This is one of the most common skin diseases, occurring

in infants, adolescents and adults.

*Pityrosporum fungus resident in the skin is a factor in the

occurrence.

*Skin care and application of topical steroids and antifungal

agents are the main treatments.

Clinical features

There is some controversy as to whether seborrheic dermatitis

in infants, adolescents and adults is the same disease, because

there are minor differences in the clinical courses.

Dermatitis appears as follicular eczema on seborrheic sites or

intertriginous areas in the head, face, axillary fossa, neck and

external genitals. The main features of the lesions are oleaginous

scales and erythematous plaques that may be slightly itchy.

In infants, yellowish crusts begin to form on the scalp, eyebrows

and forehead. In infants, scaly erythematous plaques may

also form 2 to 4 weeks after birth. In most cases they resolve 8 to

12 months after birth. In adolescents and adults, pityroid scales

(commonly called dandruff) increase and scaly erythematous

lesions form on the eyebrows and nasolabial groove. Seborrheic

dermatitis is chronic and recurrent.

Triglycerides in sebum are decomposed by microbes resident

in the skin to produce free acid. The free acid reacts to cause seborrheic

dermatitis. It has been reported that over-proliferation of

Pityrosporum fungi such as Malassezia furfur aggravates seborrheic

dermatitis.

Dry seborrheic dermatitis closely resembles psoriasis vulgaris.

It is also important to differentiate seborrheic dermatitis from

pityriasis rosea and parapsoriasis en plaque. In infants, differentiation from atopic dermatitis is essential.

Proper facial cleansing with soap and hair washing with shampoo

are basic for keeping the seborrheic regions clean. Regulating

daily life is also helpful. Middle class topical steroids are

applied. Topical antifungal agents and antifungal shampoos are

effective at resolving seborrheic dermatitis accompanied by dandruff

in adolescents and older adults, which is often caused by

overproliferation of Pityrosporum fungi.

Nummular eczema (eczema nummulare)

Outline

Round, relatively large eczematous plaques are produced.

Nummular eczema may occur at any site on the body,

and it tends to progress to autosensitization dermatitis.

Topical steroids are the first choice of treatment.

Nummular eczema is frequently seen in the winter. Multiple

round eczematous lesions occur, mostly on the extremities (particularly

on the extensor surface of the lower extremities), trunk,

hips and buttocks.

At the periphery of the lesions, serous papules aggregate, in

the center of which exudative erythema is produced with scales

on the surface. Most cases are accompanied by intense itching

and multiple scars from rubbing and scratching. As the lesions

progress, they may produce dispersal eruptions (id dermatitis) to

progress into autosensitization dermatitis.

Scratched insect bites may develop urticarial lichens that,

when rubbed, progress to nummular eczema. Or nummular

eczema may result from asteatotic eczema in the elderly, or it

may appear as a symptom of atopic dermatitis.

Treatment.

Topical steroids (containing ODT) are effective. In cases in

which infiltration and exudation are intense, the application of

topical zinc ointment sheets is also effective. Oral antihistamines

are helpful in relieving the itching.

Lichen simplex chronicus

Synonyms: Lichen Vidal, Circumscribed neurodermatitis

Lichen simplex chronicus is chronic eczema in which round,

intensely itchy lichenified plaques form on the nuchal region and

extensor aspect of forearms and lower legs of middle-aged

women. Pigmentation or depigmentation is present in many

cases. Warty eruptions may proliferate (Fig. 7.14). When skin is

repeatedly stimulated by the friction of clothing or by metal allergens

and the site is rubbed and scratched for a long period of

time, it leads to the occurrence of chronic eczematous lesions.

Topical steroids and oral antihistamines are first-line treatments

for the itching.

Autosensitization dermatitis

Outline

*Multiple small papules and erythematous lesions accompanied

by itching occur systemically. They are caused by

sudden aggravation of a localized lesion.

*This dermatitis is caused by endogenous allergic reaction

(id reaction).

Clinical features

Reddening, swelling and acute aggravation of exudation occur

in the lower extremities as primary lesions of autosensitization

dermatitis (in 50% to 60% of cases). Two weeks to several weeks

after acute aggravation of reddening, swelling and exudation, dispersed

eruptions appear. In most cases, the eruptions (id dermatitis)

are erythema, papules, serous papules, or pustules of 2 to 5

mm in diameter dispersed symmetrically on the extremities,

trunk, and face. These are often accompanied by intense itching

Systemic symptoms such as fever and fatigue may

occur.

Autosensitization dermatitis arises from endogenous allergic

reaction (id reaction). Decayed proteins, bacteria, fungal components,

and toxins produced by injured tissues in a primary lesion

are considered to be the antigens. These may spread through the

entire body such in blood flow from the primary lesion, or they

Pathogenesis

Autosensitization dermatitis arises from endogenous allergic

reaction (id reaction). Decayed proteins, bacteria, fungal components,

and toxins produced by injured tissues in a primary lesion

are considered to be the antigens. These may spread through the

entire body such in blood flow from the primary lesion, or they

may spread by rubbing or by an accidental dose of the causative

substance (orally or intravenously). Autosensitization dermatitis

is caused by sensitization against the antigens. The primary

lesions can be nummular eczema, stasis dermatitis, contact dermatitis,

atopic dermatitis, tinea pedis, or eczematization of a

burn.

Treatment.

Topical steroids are applied and oral antihistamines are administered,

in addition to whatever treatment is given for the underlying

lesion. In severe cases, oral steroids are also administered.

Stasis dermatitis.

Outline

*Edematous erythema or eczematous plaques form on

the lower thighs as a result of varicose veins or congestion

in the lower extremities.

*This disease tends to affect those who work standing,

the elderly, and obese women.

*It may progress to autosensitization dermatitis.

Elastic bandages and varicose vein phlebectomy are

effective in reducing congestion.

Clinical features.

Edematous erythema occurs on the lower third of the leg, particularly

at the upper ankles. The site gradually presents a dark

red, scaly, eczematous plaque, pigmentation or whitish atrophie

blanche. Minor trauma may induce ulceration. Treatments

for stasis dermatitis may induce allergic contact dermatitis

as a complication, from the application of an antiseptic or a topical

agent (lanoline, antibiotic agent, preservative). Aggregated

serous papules often progress to autosensitization dermatitis.

Epidemiology.

Stasis dermatitis is frequently found in those who work standing

for long periods of time. Pregnancy may trigger stasis dermatitis

as a complication of varicose veins.

Pathogenesis.

Congestion in the cutaneous blood vessels is caused by impairment

of venous outflow, which leads to bleeding from the capillary

vessel loop in the dermal upper layer. Hemosiderins deposit

in tissues, and the skin takes on a blackish-brown appearance.

The keratinocytes are injured by further impairment of blood

flow. Atrophy and scaling occur in the epidermis and there is tendency

of ulceration. The skin looses its function as a barrier and

becomes more reactive to extrinsic irritation, leading to eczematous

lesions in many cases.

Laboratory findings, Diagnosis.

Stasis dermatitis is easy to diagnose from the varicose veins

and the characteristics and distribution of the eruption. A Doppler

test and angiography are performed on the varicosity to examine

the physical potential of patients for surgical treatment. A patch

test is performed if allergic contact dermatitis is suspected.

Treatment.

Topical steroids are effective in treating eczematous lesions.

When there is ulceration, it is cleansed and dressed. Induced

allergic contact dermatitis is carefully avoided during treatment.

Intravenous circulatory impairment is treated to prevent stasis

dermatitis from progressing. Pressure that is greater than that of

elastic bandages and socks should not be given to the patients.

They should take bed rest and keep the lower extremities elevated.

Surgery such as sclerotherapy, ligation, and removal of varicose

blood may be necessary for cases with severe varicosity.

Asteatotic eczema.

Skin dryness (asteatosis, xerosis) occurs when sebum decreases

as a result of aging or excess washing. When the horny cell

layer is destroyed, the skin is vulnerable to extrinsic irritation.

When asteatosis becomes inflamed and eczematous, the condition

is called asteatotic eczema. This mostly affects

the lower extremities of elderly in dry seasons, especially winter.

For those who have a habit of excessively washing or rubbing the

body with a towel, lifestyle guidance to avoid such behavior has

therapeutic effects. Use of moisturizer prevents skin dryness.

Eczema is treated with topical steroids. Skin care with moisturizer

is helpful afterwards.

Wiskott-Aldrich syndrome.

Outline.

*The three major characteristics of this disorder are

immunological deficiency (T-cell dysfunction), thrombocytopenia,

and intractable eczema.

*It is hereditary (X-linked recessive).

*There are decreased levels of immunoglobulins.

*Bone marrow transplantation may be performed.

Clinical features.

Wiskott-Aldrich syndrome is characterized by eczema or purpura

that occurs in newborn babies within 6 months after birth.

The eczema that occurs on the head, face, buttocks and extremities

appears similar to atopic dermatitis and seborrheic dermatitis

(Fig. 7.18). Purpura is caused by thrombocytopenia. Immunedeficiency-

derived infections occur repeatedly as the patient

grows. Infections are caused by various factors including bacteria,

viruses, fungi and protozoa. Impetigo contagiosa (Staphylococcal

infection), pseudomonas infection, herpes simplex, varicella (herpes

virus infection), and candidiasis are particularly likely to

accompany this syndrome, and they tend to become aggravated

and persistent. Systemic symptoms such as bloody diarrheic

stool, internal organ hemorrhage, infection (e.g., tympanitis,

paranasal sinusitis, pneumonia) are seen recurrently.

Pathogenesis.

Wiskott-Aldrich syndrome is caused by abnormality of a

WASP gene at Xp11.22-11.23. The function of the WASP protein

is unknown; however, it is thought to be associated with the

cell viability and functional activation of T cells and platelets.

Treatment, Prognosis.

Born marrow transplantation may be conducted as a treatment.

Treatments for atopic dermatitis are given for skin lesions produced

by Wiskott-Aldrich syndrome. Patients with the syndrome

may not survive, because of bleeding and infection in infancy

(until about age 10); nevertheless, long-term survival is possible

if the patient survives this period. In long-term survival cases,

autoimmune disease and malignant lymphoma may arise as complications.

Eczema and Dermatitis.

Eczema and dermatitis are synonyms for a disease that is the most commonly seen in dermatology practice.

Eczema/dermatitis has the symptoms of itching, reddening, scaling, and edematous papules, and the condition

progresses in a specific inflammatory reaction pattern. Eczema/dermatitis is histopathologically characterized by

intercellular edema called spongiosis, which can be caused by extrinsic factors, such as irritants or allergens, or

by intrinsic factors, such as atopic diathesis. These factors interact in complex ways, and extrinsic and intrinsic

factors are seen together in many cases. There is no international agreement on the subcategories of eczema.

If the cause is not identified, eczema may be called acute, subacute or chronic, depending on the clinical and

pathological features.

Outline.

*Eczema and dermatitis are synonymous.

*Pathologically, eczema is accompanied by itching, reddening,

scaling, and edematous or serous papules.

*Histopathologically, it is characterized by intercellular

edema (also called spongiosis).

*It accounts for one-third of all dermatology cases.

*Extrinsic and intrinsic factors are simultaneously involved

in its onset.

*The first-line treatment is topical steroid application.

Clinical features.

Itchy edematous erythema forms, on which papules and serous

papules are produced. After the formation of vesicles, pustules,

erosions, crusts and scales, the condition begins to subside.

The progress of eczema is illustrated in the chart.

In the acute stage, these symptoms are present singly or together.

In the chronic stage, acanthosis, lichenification, pigmentation and

depigmentation are found, in addition to the symptoms of the

acute stage.

Pathogenesis.

Both extrinsic and intrinsic factors are involved in eczema. When an extrinsic agent such as a drug, pollen, house

dust, or bacteria invades the skin, an inflammatory reaction is

induced to eliminate the foreign substance. The severity and type

of reaction vary according to intrinsic factors such as seborrhea,

dyshidrosis, atopic diathesis, and the health condition of the patient.

Pathology

Eczema is characterized by intercellular edema (spongiosis). In the acute stage, it is accompanied by exocytosis of lymphocytes

and spongiotic bulla. In the chronic stage, hyperkeratosis, parakeratosis, irregular acanthosis, and elongation of rete ridges

are observed. Spongiosis and spongiotic bulla are less severe in

chronic eczema than in acute eczema.

Classification.

Eczemas are generally classified by cause. These

causes interact in complex ways and are not always clearly identifiable.

The name of the disease may differ from country to

country.

Contact dermatitis

Housewives hand eczema

Keratodermia tylodes palamaris progressiva

Diaper dermatitis

Atopic dermatitis

Seborrheic dermatitis

Nummular eczema

Lichen simplex chronicus􀉼lichen Vidal

Autosensitization dermatitis

Stasis dermatitis

Other

Pompholyx, dyshidrotic eczema

Pityriasis simplex faciei

Perioral dermatitis

A. Eczema with unidentified cause

When the cause is not identified, eczema is simply called

acute, subacute or chronic, according to the clinical findings, the

course of the eruption, and the pathological findings. There is no

clear definition of eczema. Lesions in various stages often exist

together on the same individual. Eczema with unidentified cause

is usually considered contact dermatitis with the involvement of

an extrinsic substance. Topical steroids and oral antihistamines

are applied as the first line of treatment for eczema at all stages.

Acut eczema.

Acute eczema is accompanied by exudative erythema, edema,

and sometimes vesicles. It is newly produced eczema

only several days after its onset. Intercellular edema (spongiosis),

intense dermal edema, and inflammation occur. Acanthosis usually

does not.

Subacute eczema.

Subacute eczema has a severity between that of acute and that

of chronic. Such eczema is accompanied by erythema and edema,

and it is slightly lichenoid. Mild edema is produced in the epidermis.

Acanthosis and parakeratosis are observed.

Chronic eczema.

Chronic eczema is characterized clinically by lichenification.

When acute eczema continues for more than one week after

onset, it is likely to appear lichenified, and the diagnosis is chronic

eczema. Acanthosis and parakeratosis are noticeable

histopathologically; however, there is less infiltration

of inflammatory cells into the epidermis than with acute and subacute

eczema.

B. Eczemas with more specific names

According to their distinguishing

Features.

Contact dermatitis.

Outline

*Contact dermatitis is localized to the site of extrinsic stimulation

by foreign substance or allergic reaction.

*Eczema reactions such as reddening and blistering

occur at the contact site.

*There are specific types of contact dermatitis, such as

diaper dermatitis and housewive’s hand eczema.

*The causative substances include certain plants, chemical

agents, and nickel, mercury and other metals.

*Patch testing is useful for diagnosis. Topical steroid

application is the first-line treatment. The causative agent

should be eliminated.

Prurigo.

Outline.

*Prurigo is a condition in which there are independent

itchy papules or small nodular eruptions.

*It is induced by insect bite, allergy, or atopic condition.

*It may be aggravated by rubbing, whereby small

intractable nodules form.

Clinical features, Classification.

In prurigo, papules or small urticarial nodules are accompanied

by intense itching that becomes chronic. These nodules are called

pruritic papules. There are various etiologies and clinical

features; however, the condition is thought to be a specific

inflammatory reaction. Prurigo is characterized by exudative

inflammatory lesions and by its failure to develop into

the other types of eruptions that are seen with eczematous and

dermatitis lesions. Prurigo remains as chronic papules and nodules.

It is often categorized as acute or chronic.

Pathogenesis

Prurigo is exudative inflammation that occurs in the dermal

upper layer. It is accompanied by lymphocytic or neutrophilic

infiltration. It is thought to be induced by specific inflammatory

reaction (pruritic reaction); however, the causative agent is

unknown in many cases. Insect bites, mechanical or electrical

stimulation, certain kinds of foods, and chemical stimulation

such as by histamines are thought to be causative factors. Prurigo

may also accompany malignant tumor, leukemia or Hodgkin’s

disease. Atopic dermatitis can also cause prurigo.

Acute prurigo.

Synonym: Strophulus infantum.

Clinical features

Urticarial erythema or wheals appear and become exudative

papules, usually in small children. Secondary infection may be

caused by rubbing and scratching brought on by intense itching.

Although acute prurigo tends to last only several weeks, it tends

to recur. Symptoms do not appear after the patient reaches a certain

age.

Pathogenesis.

Atopic condition and hypersensitive reaction to insect bite or

certain foods (e.g., eggs, soybeans, pork) are known to be associated

with the occurrence of prurigo. Children under age 5 are

mostly affected in the summer, when insect stings are common.

Treatment.

Topical steroids and oral antihistamines are the first-line treatment.

Insect bites and intake of causative foods should be avoided.

Subacute prurigo.

Synonym: Prurigo simplex subacuta.

An urticarial papule accompanied by intense itching occurs on

the extensor surface of the extremities or the trunk. When it is

rubbed and scratched, erosion or crust forms. Subacute prurigo is

intractable and may become chronic.

The etiology is unknown. A primary disease such as atopic

dermatitis, diabetes, liver dysfunction, lymphoma, leukemia,

Hodgkin’s disease, internal malignancy, polycythemia, gout, uremia

or pregnancy is often involved. Mental stress has also been

pointed out as associated with onset. The clinical features are

intermediate between those of acute and chronic urticarias. However,

acute and chronic urticarias may be found simultaneously

in the same patient.

In addition to treatments for the primary disease, topical

steroids and antihistamines are administered as needed.

Chronic prurigo.

Classification.

Chronic prurigo is subdivided into prurigo chronica multiformis,

with aggregated individual papules that tend to form a

lichenoid lesion; and prurigo nodularis, with large nodular

papules that form sparsely and individually.

Clinical features

Prurigo chronica multiformis occurs most frequently in the

trunk and legs of the elderly. Exudative or solid

papules aggregate to form invasive plaques. The lesions are

rubbed as a result of intense itching, and exudate and crusts form

to present intermingled pruritic papules and lichenoid lesions.

The condition is often chronic, with recurrences and remissions.

Prurigo nodularis most commonly affects adolescents and

older women. Papules and nodules occur in the extremities,

accompanied by intense itching. When rubbed they develop

erosion and bloody crusts, resulting in dark brown solid papules

or nodules. These are isolated and do not coalesce to form

plaques. They persist for several years.

Treatment

Topical steroids or ODT is applied as a local therapy. Application

of a zinc ointment sheet over topical steroids is effective.

Oral antihistamines are helpful in relieving itching. Oral steroids

and cyclosporines may be applied for a short period of time in

severe cases. Local injection of steroids and phototherapy are

also conducted.

Prurigo gestationis.

Prurigo gestationis appears on the extremities or trunk of

women in their 3rd or 4th month of pregnancy and subsides after

delivery. It is increasingly likely to occur with each successive

pregnancy. Differentiation between prurigo gestationis and

PUPPP (pruritic urticarial papules and plaques of pregnancy) is

controversial; however, the former occurs in the early stages of

pregnancy, whereas the latter occurs in the later stages of pregnancy.

Prurigo pigmentosa (Nagashima).

Prurigo pigmentosa (Nagashima) is urticarial erythema accompanied

by intense itching. Pruritic erythematous papules recur

and heal with reticular pigmentation. It

most frequently occurs on the back, neck and upper chest of adolescent

women. The pathogenesis is unknown. Minocycline and

DDS (dapsone) are extremely effective treatments.

Pruritis cutaneously.

Outline.

*In pruritus cutaneous there is no obvious eruption; only

itching is present.

*It is often accompanied by dry skin (xerosis).

* Eruptions, lichenification and pigmentation may be produced secondarily by rubbing and scratching.

*Oral antihistamines and psychological counseling are

helpful.

Clinical features, Classification

The disease is classified by distribution into pruritus universalis

and pruritus localis.

Pathogenesis

Pruritus cutaneous occurs secondarily to various underlying

diseases, including liver dysfunction and renal failure. Scarring, thickening of the skin, lichenification and pigmentation

often develop secondarily by rubbing and scratching. The

disease is accompanied by dry skin (xerosis). It tends to occur

when the skin is sensitive to external stimulation, especially in

winter and at bedtime.

Differential diagnosis

Systemic examinations such as blood test and renal function

test are necessary for diagnosis. When the genitalia are affected,

pruritus cutaneous should be differentiated from scabies and candidiasis.

Treatment focuses on the underlying disease, if detected.

Treatment.

Application of antihistamines and moisturizer, and UV irradiation

are conducted as symptomatic therapies. It is also important

to eliminate pruritus-inducing factors such as alcohol, coffee and

spices. Bathing to keep the body clean, wearing cotton clothes,

avoiding dryness, and eliminating emotional stress are also helpful.

Topical steroid application is effective against secondary

eruptions; however, it is ineffective against pruritus itself.

Pruritus universalis

Itching is present on the whole body surface. As shown in

Table 8.1, it usually accompanies other diseases. In the elderly,

pruritus may be present without a disease because of dry skin and

age-related processes; this is called senile pruritus.

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