Acne, . Etiopathogenesis, Clinical History, Modern Methods of Treatment

Содержание

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PAPULAR AND PUSTULAR ERUPTION ON THE FACE WITH SCARRING . CASE

PAPULAR AND PUSTULAR ERUPTION ON THE FACE WITH SCARRING .
CASE 1


A 25-year-old woman presents to the dermatology clinic with a long history of a facial eruption that has been getting worse progressively over the past few years. Some of the lesions on her face are painful at times and sometimes heal with scarring. The rest of her skin is unaffected. Her GP(general practitioner) had prescribed several prolonged courses of tetracycline antibiotics with little benefit, and she was unable to tolerate erythromycin due to its gastrointestinal side effects. She took Dianette (oral contraceptive pill) for several months
but this had to be stopped as it was significantly lowering her mood.
skin
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Examination There are numerous comedomes, particularly on her forehead, pustules, papules,

Examination
There are numerous comedomes, particularly on her forehead, pustules, papules, inflammatory

lesions, cysts and atrophic scars (Fig.). There is sparing of the periorbital
Questions
What is the likely diagnosis?
What is the underlying pathophysiology?
What treatment would you suggest?
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Diagnosis This patient had been suffering from acne vulgaris on her

Diagnosis
This patient had been suffering from acne vulgaris on her

face for many years. This is a common condition, which usually starts around puberty but can persist into the third or fourth decades.
Acne lesions develop from sebaceous glands that produce lipid material called sebum .
The role of the sebaceous gland in the pathogenesis of acne .
The role of hormones in controlling of sebum secretion, in the development of acne .
What causes the appearance of comedones , pustules and papules in this case .
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Sebaceous glands are exocrine glands that release sebum. These glands are

Sebaceous glands are exocrine glands that release sebum. These glands are connected

with the hair follicles, and, in most cases, sebum is released through the same pore through which hair grows.
Sebaceous glands are located on every surface of your skin, with the exception of your palms, bottom lip, and the soles of your feet.

Sebaceous Glands

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In the average adult up to 20 g sebum is secreted

In the average adult up to 20 g sebum is secreted

per day;
Between 400 and 900 sebaceous glands per 1 square centimeter are located in seborrheic areas;
Maximum activity of sebaceous glands in a healthy person begins at puberty and lasts up to 24-25 years.

Sebaceous Glands

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Varying Density of Sebacious Glands Distribution Scalp, face - 400-900 cm2;

Varying Density of Sebacious Glands Distribution


Scalp, face - 400-900 cm2;
Upper

third of chest and back - 300-500 cm2;
Extremities - 50 cm2.
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Sebaceous Glands Sebaceous Gland Composition Triglycerides 41% Wax ester 25% Fatty

Sebaceous Glands

Sebaceous Gland Composition
Triglycerides 41%
Wax ester 25%
Fatty acids 16%
Squalene 12%
Diglycerides2%
Cholesterol

ester 2%
Cholesterol 1-2%

Sebaceous glands function by producing and releasing sebum in order to help protect and lubricate the surface of the skin. Sebum is composed of fat, cellular debris, and keratin.

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Sebaceous Glands Functions: Softens epidermis giving it water-proofing properties; Regulates water

Sebaceous Glands Functions:

Softens epidermis giving it water-proofing properties;
Regulates water evaporation;
Blocks

penetration of certain substances from the environment;
Imparts antifungal and antibacterial effect.
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Sebacious Glands Regulation Androgens increase sebum production, and estrogen reduce it.

Sebacious Glands Regulation

Androgens increase sebum production, and estrogen reduce it.

The

embryologic development of the human sebaceous gland is closely related to the differentiation of the hair follicle and the epidermis. The number of sebaceous glands remains approximately the same throughout life, whereas their size tends to increase with age.
The activity of the sebaceous glands increases during puberty because of heightened levels of androgens.
Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands .
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The glands (skin sebocytes ) contain an enzyme called 5á-reductase, which

The glands (skin sebocytes ) contain an enzyme called
5á-reductase, which

converts less potent testosterone into more potent dihydrotestosterone, which is directly responsible for sebaceous gland activity.
This stimulates the sebaceous glands, causing an increase in sebum production, which can lead to an oily skin. (Are involved in skin problems such as acne)

Sebacious Glands Regulation

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Acne is one of the commonest skin disorders – if not

Acne is one of the commonest skin disorders – if not

the commonest. It has been estimated that 70 per cent of the population have some clinically evident acne at some stage during adolescence!
Acne vulgaris is a chronic disorder of the pilosebaceous apparatus caused by abnormal desquamation of follicular epithelium leading to obstruction of the pilosebaceous canal, resulting in inflammation and subsequent formation of papules, pustules, nodules, comedones, and scarring with varying extent and severity.
While the course of acne may be self-limiting, the sequelae can be lifelong, with pitted or hypertrophic scar formation.

Acne vulgaris

Acne means eruption and Vulgaris means common so

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Etiology of Acne Genetic factors. If both parents suffer from such

Etiology of Acne

Genetic factors. If both parents suffer from such

disease likelihood of its development in children is 50%. The number, size and sensitivity of receptors of the sebaceous glands is genetically determined.
Hormonal disorders:
Absolute hyperandrogenism (at androgen-productivity of ovarian and adrenal glands tumors, PCOS, adrenal hyperplasia);
Relative hyperandrogenism (elevated activity of 5-alpha-reductase);
Iatrogenic hyperandrogenism (anabolic steroids, androgens, progestins , etc. intake ).
The effects of stress.
Pathology of the immune system.
Gastrointestinal diseases.
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Acne Pathophysiology

Acne Pathophysiology

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1 - Androgens stimulate sebum production and proliferation of keratinocytes in

1 - Androgens stimulate sebum production and proliferation of keratinocytes in

hair follicles.
2 - Sheets of desquamated keratin obstruct the follicle opening, which forms the precursor to acne
3 - This results in sebum accumulation and swelling of the follicle.
4 - P. acnes colonize and proliferate in the plugged follicle
5 - This causes the hydrolyzation of sebum triglycerides into free fatty acids. This further plugs the follicle and pro-inflammatory mediators causes inflammation of the follicle and surrounding dermis.

Acne Pathophysiology

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Changes in Follicular Keratinization In the lower portion of the follicular

Changes in Follicular Keratinization In the lower portion of the follicular
infundibulum,

the normal process of keratinization occurs in the same way
that it occurs on the skin’s surface.
This maturing of keratinocytes and subsequent exfoliation into the follicle marks the beginning of the formation of comedones.
In acne patients, these keratinocytes tend to stick together because of the effects of positive and negative charges, the actions of transglutaminase, and the stickiness of sebum.

Follicular Hyperkeratosis

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The clumped keratinocytes block hair follicle (pore) , creating a blackhead

The clumped keratinocytes block hair follicle (pore) , creating a blackhead if

the pore is open (“open comedone”) or a whitehead if it is closed (“closed comedone”).
The clogged pore is a great nutritional source for bacteria so
Propionibacterium acnes gravitate to the blocked pores.
The immune system recognizes the presence of bacteria and mounts an immune response resulting in redness, pus, as well as inflammation, and the typical “pimple” results.
Most of the inflammation, however, is likely due to inflammatory mediators that are released when bacteria digest sebum

Follicular Hyperkeratosis

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Comedone formation Acne Pathogenesis Increased sebum secretion Sebaceous gland activity Sebaceous

Comedone formation

Acne Pathogenesis

Increased sebum secretion
Sebaceous gland activity

Sebaceous Gland Hyperactivity

This

imbalance between sebum production and the secretion capacity leads to a blockage of sebum in the hair follicle followed by inflammation.
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Occlusion of the follicular canal Acne Pathogenesis (to be continued) Follicular

Occlusion of the follicular canal

Acne Pathogenesis (to be continued)

Follicular hyperkeratosis;

Abnormal follicular

keratinization
• ↑ Corneocyte cohesiveness and proliferation.
Pilosebaceous orifice in acne is occluded by a keratinous plug induced by: Chemicals (present as ingredients of cosmetics).
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Microbial colonization The bacterium Propionibacterium acnes is considered a key player

Microbial colonization

The bacterium Propionibacterium acnes is considered a key player in

acne development. Studies have shown that P. acnes use sebum as a source of energy, and its presence in the pores initiates an immune response that triggers inflammation.

However, P. acnes is highly abundant in the pores of individuals with and without acne, which indicates that it is not simply the presence of this bacterium that drives the skin condition.

Propionibacterium acnes ( P. acnes ) in sebum
• Gram + anaerobic rod, resident flora in follicle but acne patients with higher concentration

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Inflammation development Acne Pathogenesis (to be continued) Release of inflammatory mediators

Inflammation development

Acne Pathogenesis
(to be continued)

Release of inflammatory mediators
Distended follicle ruptures, releasing

inflammatory
chemicals into the dermis, stimulating intense inflammation.
Ductal epithelium also produces cytokines, triggering
an inflammatory cascade.
Microbes also produce extracellular enzymes,
which attract inflammatory cells.
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KERATINIZATION IN EPIDERMIS

KERATINIZATION IN EPIDERMIS

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How Acne or Pimple Forms Under Skin

How Acne or Pimple Forms Under Skin

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The greatest number of sebaceous glands follicles is located on the

The greatest number of sebaceous glands follicles is located on the face,

chest, neck and upper back. These are the areas of acne localization.

Acne Localization

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Individual lesions are centred on the pilosebaceous unit, ie the hair

Individual lesions are centred on the pilosebaceous unit, ie the hair

follicle and its associated oil gland.

Superficial lesions
Open and closed comedones (blackheads and whiteheads)
Papules
Pustules
Deeper lesions
Nodules (large painful red lumps)
Pseudocysts (cyst-like fluctuant swellings)
Secondary lesions
Excoriations (picked or scratched spots)
Erythematous macules
Pigmented macules
Scars or various types

clinical features

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Comedones Comedones are non-inflammatory elements resulting from blockage of the mouths

Comedones

Comedones are non-inflammatory elements resulting from blockage of the mouths of

hair follicles.
Closed" comedones
open" comedones
Submarine comedones respond poorly to medical treatment.
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Clinical History of Acne Comedones (comedo sou acne comedonica); Acne papulosa

Clinical History of Acne

Comedones (comedo sou acne comedonica);
Acne papulosa and acne

pustulosa (acne papulosa et papulopustulosa);
Acne indurata (acne indurativa);
(acne phlegmonosa);
Acne conglobata;
Acne fulminans (also known as "Acute febrile ulcerative acne" ;
Acne inversa or hidradenitis suppurativa.
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Acne can be classified by the type of lesion (comedonal, papulo

Acne can be classified by the type of lesion (comedonal, papulo

pustular, and nodulocystic).
The American Academy of Dermatology classification scheme for acne denotes the following three levels:
1. Mild acne: characterized by the presence of comedomes (noninflammatory lesions), few papules and pustules (generally _10), but no nodules.
2. Moderate acne: presence of several to many papules and pustules (10-40)
along with comedomes (10-40). The presence of more than 40 papules and
pustules along with larger, deeper nodular inflamed lesions (up to 5) denotes moderately severe acne.
3. Severe acne: presence of numerous or extensive papules and pustules as well as many nodular lesions.
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Blackheads vs. Whiteheads

Blackheads vs. Whiteheads

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Acne indurativa is characterized by the formation of deep infiltrates with

Acne indurativa is characterized by the formation of deep infiltrates with

the formation of scars and is prone to merge cystic cavities filled with pus - phlegmonous types. Indurative and phlegmonous acnes are called nodulocystic ones. Nodulocystic acne is a sign of fairly severe course of acne.

Acne Indurata

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Excoriated Acne This clinical type may be associated with obsessive neurosis

Excoriated Acne

This clinical type may be associated with obsessive neurosis or

indicate more severe psychiatric pathology. Therefore, patients with excoriated acne should be advised to consult a psychotherapist or neuropsychiatrist

Excoriated acne. These are the acnes that occur predominantly in patients prone to excoriate even minor eruptions. Thus excoriations may be at the background of initially existing acnes and without them.

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Acne Conglobata Acne conglobata is nodulocystic elements connecting with each other,

Acne Conglobata

Acne conglobata is nodulocystic elements connecting with each other, as

well as with large comedones. Lesions can be located everywhere. They are resolved into keloids. They relapse until the age of 40 and sometimes lasts even  lifelong.
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Acne Fulminans Acne fulminans ,also known as "Acute febrile ulcerative acne“,

Acne Fulminans

Acne fulminans ,also known as "Acute febrile ulcerative acne“, is a

rare severe type of acne. The disease occurs more frequently in men aged 13-18 years with mild papulopustular, rarely nodulocystic type of acne, and is characterized by sudden onset, appearance of necrotizing ulcerative elements (mainly on the trunk)  and general symptoms of intoxication on the background of  chronic severe diseases.
Associated with fever, myalgia, and arthralgia.
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Acne Inversa Acne inversa is associated with secondary lesions of apocrine

Acne Inversa

Acne inversa is associated with secondary lesions of apocrine sweat

glands. Initially, there is occlusion of the hair follicle, and apocrine sweat glands are involved in the process again. The disease develops after puberty and is combined with a high body mass. Localization - armpits, perineal region, navel, nipple areola. As a result, fistulae are formed with the formation of inverted scars. The course is chronic with relapses.
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Post-acne. Consequences and Complications of Acne. At a resolution of inflammatory

Post-acne. Consequences and Complications of Acne.

At a resolution of inflammatory elements

(papules, pustules and nodules) secondary changes, post-acnes, are formed on the skin of patients.
These are the persistent changes on the skin resulting from a long-term acne and seborrhea and manipulations performed to treat these diseases.
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Post-acne Uneven skin texture; Permanent scars; Stagnant spots; Secondary hyperpigmentation; Persistent

Post-acne

Uneven skin texture;
Permanent scars;
Stagnant spots;
Secondary hyperpigmentation;
Persistent erythema;
Dilation of the capillaries;
Hyper and

/ or hypopigmentation;
Psychological problems;
Depression, anxiety, social isolation.
Intensity of post-acne is associated with age and duration of exacerbations.
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Treatment Be sure to recommend: Daily cleansing of the skin. When

Treatment

Be sure to recommend:
Daily cleansing of the skin.
When caring for

skin one should avoid fatty creams and ointments, causing hair follicles occlusion.

The choice of treatment should be based on:
Anamnesis;
Adequate clinical assessment of disease;
Assessment of psychosocial status of the patient with acne.

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General measures Local hygiene Regular gentle cleansing (not overzealous) with soap

General measures
Local hygiene
Regular gentle cleansing (not overzealous) with soap and

water should be encouraged.
Application of oil-based cosmetics should be avoided as they may aggravate acne, but water-based cosmetics can be used.
Diet
Stress
Acne induces stress and this needs to be handled.
Some patients with mild acne may be more distressed than those with severe acne.
Stress itself may induce acne.
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The success of acne treatment is possible only if it affects

The success of acne treatment is possible only if it affects

all factors of pathogenesis.
Treatment is multipronged, attacking the four mechanisms which lead to acne.
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Principles of Acne Treatment

Principles of Acne Treatment

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Benzoyl peroxide (BP) Benzoyl peroxide (BP) Mode of action: Is a

Benzoyl peroxide (BP)

Benzoyl peroxide (BP)
Mode of action: Is a powerful antimicrobial,

decreasing population of P. acnes.
Also has anti-inflammatory effect.
Indications:
Mild acne, as stand-alone therapy, especially if few inflammatory lesions also present.
Always to antibiotic therapy, to reduce resistance.
Moderate-severe acne as topical adjunct to systemic therapy
Used in both inflammatory and noninflammatory acne.
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Topical antibiotics Most frequently used topical antibiotics are clindamycin (1–2%) and

Topical antibiotics

Most frequently used topical antibiotics are clindamycin (1–2%) and

erythromycin (2–4%).
Mode of action: Suppress P. acnes and its mediators of inflammation and so are more effective against inflammatory acne.
Clinical use: Useful in inflammatory acne but must always be combined with topical retinoic acid or benzoyl peroxide .
Side effects: Resistance of microorganisms to antibiotic is a major problem, so should be combined with topical retinoids or benzoyl peroxide.
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Topical retinoids Topical retinoids are comedolytic and work by normalizing follicular


Topical retinoids
Topical retinoids are comedolytic and work by normalizing follicular

keratinization.
comedones are treated with topical tretinoin cream, what are the side effects.
at the beginning of therapy the acne may appear worse but after three to four weeks it improves.
The side effects can appearance photosensitivity and skin irritation, which therefore requires protective clothing and sunscreen.
It should be avoided during pregnancy, since there is risk of birth defects.
for those who cannot tolerate topical tretinoin, we can use peeling agents like salicylic acid and gluconic acid creams.
we can use other creams but with fewer side effects, such as skin irritation and photosensitivity adapalene and tazarotene, both are effective, like tretinoin .

adapalene (0.1% gel or cream, applied once or twice daily).
Tazarotene (0.1% cream or gel applied daily) .
Azelaic acid (Skinoren

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Topical retinoids Tretinoin is inactivated by UV light and oxidized by

Topical retinoids

Tretinoin is inactivated by UV light and oxidized by

benzoyl peroxide; therefore, it should only be applied at night and not used concomitantly with benzoyl peroxide
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Systemic treatment Antibiotics Drugs used: Doxycycline and minocycline are most commonly

Systemic treatment

Antibiotics
Drugs used: Doxycycline and minocycline are most commonly used.

Less frequently, erythromycin and azithromycin.
Mode of action:
Inhibit growth of P. acnes and its metabolism.
Direct anti-inflammatory effect.
Indications:
Moderately severe acne (being the most frequently used systemic therapy).
Mild acne, if acne is affecting patient’s quality of life.
Severe acne, if oral retinoids cannot be used.
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Severe Degree of Acne. Therapy A combination of standard topical and

Severe Degree of Acne. Therapy

A combination of standard topical and

general treatment is necessary to treat severe degree of acne.
Severe inflammatory acne is when we can see more than 100 commodones or more than five cysts , here it's not enough to you antibiotics or topical tretinoin , here we have to use our strongest drug, namely oral is so tretinoin, which is a retinoid that is related to vitamin A the therapy should be between 16 and 20 weeks .
Before beginning the therapy we need to check some lab values of the patients like fasting glucose, triglycerides, cholesterol, complete blood count and liver function.
Other side effects are redness, dryness, irritation, and peeling of the skin.
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The woman should not take this drug if they are pregnant

The woman should not take this drug if they are pregnant

because birth defects can happen to the baby because this is a very this is very serious, pregnancy tests should also be done before the beginning the therapy and monthly until one month of the therapy stops.
so the woman should use two methods of contraception for one month before the treatment during the treatment and for at least one month after the treatment.
In women with severe manifestations of acne with the ineffectiveness of antibiotics therapy combined oral contraceptives with estrogen profile or anti-androgenic drugs are administered after examination by gynecologist-endocrinologist.
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Isotretinoin is a powerful medication used to treat severe inflammatory acne.

Isotretinoin is a powerful medication used to treat severe inflammatory acne.

It is an oral medication that is taken once or twice daily. This medication is probably best known by the now-defunct brand name Accutane.
Isotretinoin (not to be confused with tretinoin) is classified as a retinoid, made from a synthetic form of vitamin A. It is taken orally, in pill form, once or twice daily.
It's considered the most effective prescription treatment available for severe acne. Isotretinoin can successfully treat, and completely clear up acne, even acne that has not improved with other treatments.
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Methods of Cosmetic Correction Cleaning of face (manual, vacuum, ultrasound); Cosmetic

Methods of Cosmetic Correction


Cleaning of face (manual, vacuum, ultrasound);
Cosmetic anti-inflammatory

treatment;
Jacquet massage;
Cryotherapy;
Chemical peelings;
Phonophoresis;
Phototherapy;
D'arsonvalization;
Laser Therapy.
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Thanks for your attention!!

Thanks for your attention!!

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UV Radiation in the Treatment of Acne. Pros and Cons. The

UV Radiation in the Treatment of Acne. Pros and Cons.

The

question of administration of ultraviolet radiation (UVR) to a patient with acne should be solved individually without doubt:
Many patients notice improvement in the acne course in summer, after insolation;
UVR causes surface exfoliation and in small doses;
It may stimulate an immune response in the skin on the other hand;
UVR enhances comedogenic properties of squalene, a component of sebum;
UVR in high erythema doses causes a sharp decrease in local immune defense and worsening of acne disease course.
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A 59-year-old man attends the dermatology clinic for a skin review

A 59-year-old man attends the dermatology clinic for a skin review

following renal transplantation for hypertensive nephropathy. He is immunosuppressed with sirolimus
and mycophenolate mofetil. He has a few viral warts on his hands but his main complaint is a 6-month history of facial redness and painful ‘spots’. The erythema is exacerbated by heat. He has applied a bland emollient cream and topical antibacterials to the affected areas with little benefit. At the initial consultation he is noted to have a florid facial erythema
with multiple papules and pustules over his forehead and cheeks. He is commenced on oral minocycline 100 mg daily and is asked to come back in 3 months.
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Rosacea Rosacea (acne rosacea, gutta rosacea, teleangiectasiasis faciei, cuperose) is a

Rosacea

Rosacea (acne rosacea, gutta rosacea, teleangiectasiasis faciei, cuperose) is a chronic,

relapsing disease, usually of facial skin having polietiologic nature and characterized by phases of its course. Rosacea manifests itself primarily by arising hyperemia (redness) of face, telangiectasia (dilation of small blood vessels) on the face as well as hyperplasia of the sebaceous glands and connective tissue. The basis of the disease there are changes in the tone of the surface of blood vessels of the skin caused by the action of various external and internal factors.
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Rosacea is a very common disease - among dermatological diagnoses, it

Rosacea is a very common disease - among dermatological
diagnoses, it

is about 5%, occurs in all races, but mainly in fair-skinned inhabitants of Scandinavia and Ireland. British represent rosacea as "Celtic Tides."
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Rosacea begins in most cases at the third and fourth decade

Rosacea begins in most cases at the third and fourth

decade of life flourishes between 40 and 50 years. Often affects women. The disease should be called rosacea (from the Latin rosaceus - pink) as used previously terms "rosacea" or «acne rosacea» are untrue morphology essence of rosacea. Rosacea is a very common disease in Caucasians, known since ancient times. So, a man with a red face and a bulbous nose was described in the "Canterbury Tales", written by D. Chaucer (1340-1400). Later rosacea patients appeared in the works of Shakespeare. The famous Italian painter of the early Renaissance D. Ghirlandaio first depicted a man suffering from rosacea, to be strict  rather a form of rosacea - rhinophyma in the picture "An Old Man and His Grandson", done in 1480 (Louvre).
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Rosacea Etiology Endogenous factors: Genetic predisposition (presence of more large and

Rosacea Etiology

Endogenous factors:
Genetic predisposition (presence of more large and superficial

blood vessels on the face).
Disruption of digestive tract (gastritis, gastric ulcer, spastic colitis, gallbladder disease).
Neurovegetative and endocrine disorders (steroid hormones imbalance, menopause, hypertension).
Exogenous factors (climate, eating habits, wrong outer care, emotional peculiarities, intake of certain medications).
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Rosacea Pathogenesis - Increased vascular permeability of the skin; - Accumulation

Rosacea Pathogenesis

- Increased vascular permeability of the skin;
- Accumulation of mediators

of inflammation and metabolic products (serotonin, bradykinin, prostaglandins, opioid peptides and gastrin);
-Degeneration of  dermis matrix and vascular endothelial damage.
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Classification of Rosacea G. Plewig and et al have proposed clinical

Classification of Rosacea

G. Plewig and et al have proposed clinical classification

based on the sequence of stages:
Rosacea-diathesis is occasional hot flashes.
. Rosacea proper:
Stage 1: Erythematous-telangiektatic,
Stage 2: Pustulopapular (persistent erythema, telangiectasia, papules, pustules),
Stage 3: Pustulonodular (persistent erythema, numerous telangiectasia, papules, pustules and swollen nodes).
III. Special forms of rosacea: rosacea-steroid, granulomatous, Gram-negative, conglobate, fulminant, rosacea with a solid persistent facial edema, ophthalmic rosacea, rhinophyma and "Phyma" of other localizations.
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Rosacea proper is characterized by persistent erythema predominantly of the nose

Rosacea proper is characterized by persistent erythema predominantly of the

nose skin, usually with the presence of telangiektasia with periodic rush of blood to the face as a result of endogenous, psychogenic and external stimuli. Demodex mites thus are completely absent or are detected as single samples on the skin, especially in the follicles of the nose. Antiparasitic treatment has no effect in this case.
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Rosacea Proper

Rosacea Proper

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Rosacea ComplicatedWith Demodicosis In this form, besides the usual phenomena of

Rosacea ComplicatedWith Demodicosis
In this form, besides the usual phenomena

of rosacea, there are scattered micropapules and follicular micropustules, in which demodicids are found. At anti-parasitic treatment pustules and papules disappear, but persistent erythema and telangiectasia remain.
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Rosacea-like form of demodicosis in which there is a large number

Rosacea-like form of demodicosis in which there is a large number

of mites and which may resemble a  rosacea proper, but it responds well to anti-parasitic treatment.
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Ophthalmic Rosacea Blepharitis (erythema, desquamation and crusts on the edges of

Ophthalmic Rosacea

Blepharitis (erythema, desquamation and crusts on the edges of

the eyelids):
Conjunctivitis
Iritis
Scleritis
Keratitis

Frequent symptom of rosacea, severity of the eye damage does not correspond to the severity of the skin process, in severe cases it can lead to blindness.

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Hypertrophic Rosacea Rhinophyma; Gnatophyma; Metophyma; Otophyma; Blefarophyma. It develops as a

Hypertrophic Rosacea

Rhinophyma;
Gnatophyma;
Metophyma;
Otophyma;
Blefarophyma.

It develops as a consequence of tissue hyperplasia of

subcutaneous fat and sebaceous glands. The skin thickens, takes on a lumpy appearance, reminds orange peel. It is observed more frequently in men.
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Rosacea Treatment Elimination of etiological and precipitating factors; Treatment of comorbidity;

Rosacea Treatment

Elimination of etiological and precipitating factors;
Treatment of comorbidity;
Diet;
Antibiotic treatment (imidazoles-

противогрибковые);
Synthetic retinoids;
Antihistamines;
Venotonics and angioprotectors (Ascorutinum and Detralex).
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Topical Therapy Topical anti-inflammatory drugs: cold lotions with 1-2% solution of

Topical Therapy
Topical anti-inflammatory drugs: cold lotions with 1-2% solution of resorcinol,

boric acid, decoction of herbs, thermal water in the form of aerosol.
Topical antibiotics and anti-parasitic (acaricidal) means prescribed for rosacea papulopustular (Metronidazole, Erythromycin and Clindamycin).
Azelaic acid.
Synthetic retinoids.
Cryotherapy.
For the destruction of telangiectasia laser therapy (argon, CO2 laser) is used.
Photoprotection.
Appropriate care (cosmetic Bioderma, Avene etc.).
  Calcineurin inhibitors (Tacrolimus, Pimecrolimus).
- Предыдущая
Маленькие органы большого значения. Интегрированный урок-исследование
Следующая -
Нетрадиційні техніки зображувальної діяльності, що використовую в роботі з дітьми

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