What is the treatment for eczema?

The goals for the treatment of eczema are to prevent itching, inflammation, oozing and worsening of the condition. Oozing is controlled by condy’s compress( potassium permanganate). The commonly used drugs to control itching, inflammation is corticosteroid & antihistamine. For the acute and sub acute eczema lotion, and cream are used. Ointments are used for chronic eczemas,which requires occlusion. Our experience shows lesions having lichenification and induration often needs oral steroid and needs long treatment as the disease last for a long. Rarely the cytotoxic drugs are used for treating eczema. If used its used as the steroid spearing agent. Our experience is with Methotrexate, Azathioprine, Cyclophospamide, and Cyclosporine in treating eczemas with chronic recurrence as a steroid sparing agents.

Recently U.S. FDA has approved topical tacrolimus and pimecrolimus for the treatment of eczema. Photochemotherapy has been used in case of hyper keratotic and dry discoid eczema with variable success.

For Scientific english editing and Medical Writing Services visit www.manuscriptedit.com

How to diagnose eczema?

Diagnose eczema is mostly clinical. It includes history, physical examination of the skin lesion .In particular, presence of erythema, edema, papule, vesicle & oozing at the site is characteristic. Biopsy is indicated only in few cases where there is no definite clinical feature of eczema. Findings like spongiosis in the epidermis in histology is suggestive of eczema. Patch test is indicated in allergic contact dermatitis to find out /identify the allergen. Depending upon the suspected allergen either patch or photo patch test is carried out. There are no laboratory or blood tests present, that can be used to establish the diagnosis of eczema.

For Scientific english editing and Medical Writing Services visit www.manuscriptedit.com

Types of eczema

Contact eczema

Contact eczema (contact dermatitis) is broadly used term for irritant contact dermatitis and allergic contact dermatitis. The contact dermatitis is a localized reaction on the skin due to the direct contact with the allergen. Type of reaction depends on the nature of the allergen, like alkali/acid induces toxic effects on the skin and produces irritant contact dermatitis, when allergen induces sensitization (produces memory cells) in the boy and produces allergic reaction in the subsequent contact, it is regarded as allergic contact dermatiti .

Irritant contact dermatitis is characterized by erythema, edema, redness, itching, burning sensation , papules , vesicles & oozing at the site of contact . Irritant contact eczema (irritant contact dermatitis) are due to direct toxic effect of the allergen on the skin . The common irritant allergens are poison ivy and poison sumac.

Allergic contact eczema (allergic contact dermatitis) occurs in an individual who has previously sensitized, following an exposure to the allergen. It takes about 5-7 days for a individual to develop sensitivity, however it may take months and years to develop sensitivity in some. After the individual has developed sensitivity to the allergen, in the subsequent exposure to the allergen, skin reaction develops in the form of erythema, edema, itching and papules. Allergic contact eczema is commonly cause by laundry detergents, nickel (present in jewelry), cosmetics, fabrics, clothing, and perfume.

Atopic dermatitis

Atopic dermatitis is a chronic form of eczema characterized by itchy, edema, population , vesicle formation. It is believed to be due to abnormal function of the body's immune system. Like all eczema, it has remission and relapsing course. This disease starts as early as 3-4 months of life. However the disease can start at any age. In infancy it may confine to cheeks and extensors of the leg(shine), in childhood(by 18-24months)it remains to both flexures and extensors. In adult it remains confine to the flexures. In a rare occasion it becomes so extensive that it covers the entire body. And it tends to run in families, either as asthma or hay fever. Eczema may resolve spontaneously in majority of cases in few months and years. In some it tends to recur throughout life.

Seborrheic eczema

Seborrheic eczema (seborrheic dermatitis) is an inflammatory condition of skin, cause is unknown, but it is possibly believed to be due to Pityrosporum ovale. The signs and symptoms of seborrheic eczema are yellowish, & greasy, scales present in patches on the scalp, nasolabial fold, post auricular area, inter scapular area, and “V” area of the chest, and rarely on the other parts of the body. In infants it presents as "cradle cap" which is due to passively transmitted hormone from mother to baby before birth, it subsides spontaneously over 12-16 weeks. In adult it may present as Dandruff, which is due to excessive secretion of sebum from the sebaceous gland, which is responsible for producing suitable environment for the skin commensal Pityrosporum ovale to colonize. In the immunocompromized individual there is increased colonization of the p.ovale and often its regarded as the cutaneous marker of AIDS.

Nummular eczema

Nummular eczema (nummular dermatitis) is characterized by coin-shaped patches of eczema on the skin located on the arms, back, buttocks, and lower leg. It is characterized by papule, vesicle, oozing, crusting , scaling, and itching. Nummular eczema is usually a chronic condition. And it’s associated with personal or family history of atopic dermatitis, asthma, or hay fever.

Neurodermatitis/Lichen simplex chronicus

Neurodermatitis is also known as lichen simplex chronicus, a chronic skin inflammatory condition, characterized by the changes due to constant scratching, like thickening, pigmentation and increased skin marking. Women are more commonly affected than men, and the condition is most frequent in people aged 20-50years.

Stasis dermatitis

Stasis dermatitis is related to the circulatory problem known as venous insufficiency, in which the function of the valves within the veins has been compromised, because of this there is constant stasis & local changes on the skin. It occurs almost exclusively in middle-aged and elderly people. The risk of developing stasis dermatitis increases with advancing age and prolonged standing. Symptoms include itching and/or reddish-brown discoloration of the skin on one or both legs, later the condition can lead to the edema, vesiculation, oozing and ulceration at the site. Stasis dermatitis has also been referred to as varicose eczema as veins are tortuous and dilated .

For Scientific english editing and Medical Writing Services visit www.manuscriptedit.com

What is eczema?

What is eczema?

Eczema is an inflammatory response of skin to foreign or inside stimulus. It is also often regarded as dermatitis by many dermatologists casualy. The common form of eczema are atopic dermatitis, seborrheic dermatitis, nummular eczema, pompholix, stasis dermatitis, and asteatotic eczema. These eczema occurs due to disturbens in the functioning of T cells. However, there are eczemas which occurs from the out side source like air born contact dermatitis(ABCD), photodermatitis (due to sun) phytophotodermatitis( due to contact with light and plant), infective eczematoid dermatitid( due to infection), dematitis medicamentosa( due to drug) and allergic conntact dermatitis ( due to ornaments, cosmetics, daily use things etc.).

Eczema is caused by abnormal functioning of the immune system but some forms of eczema occurs due to contact of skin with irritant and allergic allergens like soaps, cosmetics, clothing, detergents, or jewelry. Environmental allergens causes two type of reaction one is due to direct toxic affect on the skin and other is following the sensitization of skin to the particular allergen..

How to recognize eczema?

Eczema is characterized by itching, papule, vesiculation & oozing from the skin. The appearance of eczema varies according to its stage like acute eczema presents as erythema, edema, micropapules, vesicles, oozing , crusting, pain and burning sensation. subacute eczema presents as itching erythema, edema, thickening with crusting, on removal of the crust, it leaves a moist area, chronic eczema has features like thickening , dis-colouration , severe itching and increased skin marking. Beside the common form of eczema there is a dry discoid form, where the skin is thickened, scaly and fissured.

For Scientific english editing and Medical Writing Services visit www.manuscriptedit.com

Leishmaniasis - Manuscriptedit.com's Analysis

Leishmaniasis is a disease caused by protozoa species, which is transmitted by the bite of a female sandfly. It is classified as cutaneous, mucocutaneous, and visceral leishmaniasis.

The typical lesions of cutaneous leishmaniasis were described as early as 900 BC and have been referred to as the "Balkan sore" in the Balkans, the "Delhi boil" in India, the "Baghdad boil" in Iraq, and "saldana" in Afghanistan.

These protoza spend part of their life cycle in the gut of the sandfly, during feeding it ingest about 1000 parasites per bite into the host skin at the site of bite, from where they pass into the blood and tissues. These promastigotes are phagocytosed by macrophages at the reticuloendothelial system, where they shed their flagella and become amastigotes and multiply by binary fission. Once the infected macrophages rupture, the infection spreads to other macrophages and other parts of the body. Temperature is an important factor that determine the localization of the lesions. Species causing visceral leishmaniasis are able to grow at core temperatures, while those responsible for cutaneous leishmaniasis grow best at lower temperatures.

.

In cutaneous leishmaniasis, the hallmark of the disease is skin lesions, which can spontaneously heal in 2-10 months. Untreated cutaneous leishmaniasis have tendency to progress to cause disseminated mucocutaneous leishmaniasis and can cause death.

In mucocutaneous leishmaniasis, mucosal ulcerations usually develop by metastasis from disseminated protozoa rather than by local spread. Secondary infection plays a prominent role in the persistence of ulcers. Ulcer progression is slow and steady.

Visceral leishmaniasis become clinically apparent after weeks to months of infection. The disease can be acute, subacute, or chronic. The disease manifest in patients who loses immunity after they have left the endemic regions. Visceral leishmaniasis is progressive and mortality rates in untreated cases range from 75-95% or as high as 100% within 2 years in the developing countries

It is estimated by Centers for Disease Control and Prevention (CDC) that approximately 1.5 million new cases of cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur worldwide every year. Mucocutaneous leishmaniasis is less common. Current prevalence of the disease is about 12 million worldwide. The incidence is highest in tropical and subtropical regions where conditions are favorable for sandflies. Most cases of cutaneous leishmaniasis are seen in Afghanistan, Brazil, Iran, Iraq, Peru, and Saudi Arabia, while visceral leishmaniasis is most common in Bangladesh, Brazil, India, Nepal, and Sudan. Males are more commonly infected than females, most likely because of their increased exposure to sandflies. Visceral leishmaniasis has been shown to be common in males than in females.

Lyme disease

Lyme disease became apparent in 1975. This is a bacterial illness caused by Borrelia burgdorferi & Borrelia afzelii. There are certain ticks found on deer which harbor these bacteria in their stomachs and transmit the disease to the human by bite. Lyme disease does not transmit from person to person. It causes disease of the skin, joints, heart, and nervous system.The bacteria enter at the site of the tick bites on the skin and spread in the skin by inducing peripherally spreading reddish rash, often associated with "flu-like" symptoms. In the late stage, it can affect joints, heart, and nervous system.
Lyme disease passes through three phases as: (1) early localized disease on the skin ; (2) early disseminated disease affecting heart and nervous system.(3) late stage disease characterized by motor and sensory nerve damage and inflammation of joint.
The early phase of illness occurs within days to weeks of the tick bite, the skin around the bite develops an expanding ring of un-raised redness. The outer ring of lesion is brighter when a central area has faint erythema called "erythema migrans" (formerly called erythema chronicum migrans). Majority of patients often can't recall the tick bite. The skin rash is often accompanied by generalized fatigue, muscle and joint pain, stiffness, swollen lymph nodes and headache resembling symptoms of a virus infection. The redness resolves, without treatment, in about a month. Weeks to months after the skin lesion , the bacteria effects joints, heart, and nervous system.
The late phase of Lyme disease causes inflammation of the heart muscle resulting in arrhythmia and heart failur. Facial muscle paralysis (Bell's palsy), abnormal sensation of extremities due to peripheral nerve involvement (peripheral neuropathy),brain involvement as meningitis, and confusion , inflammation of joints with swelling, stiffness, and pain.
Diagnosis of early Lyme disease is clinical by finding the classical red rash on the skin. Blood testing for antibody to Lyme disease is generally not necessary or helpful in early stage disease, but it can be of help in the diagnosis of late stage disease. The antibody is detected by enzyme-linked immunosorbent assay [ELISA].) But he confirmatory test is by Western Blot Assay
Most cases of Lyme disease are cured with antibiotics. The antibiotics used in the disease are doxycycline, amoxicillin, or cefuroxime axetil. Use of antibiotic resolves the rash within one or two weeks, with no long-term consequences. Later stage illness involving nervous-system, cardiac and joint might require intravenous ceftriaxone and penicillin G. www.manuscriptedit.com

Tinea Versicolor

Tinea versicolor is a common skin infection caused by Malassezia furfur. It is characterized by multiple circular small patches, often coalesce to form large patches. The patches are asymptomatic, covered with powdery scales, varying in color from white to brown.


Malassezia furfur is a dimorphic fungus , present on skin as a normal skin flora but in some people it causes infection called tinea versicolor. The prevalence of Tinea versicolor is high in young adults suggesting link to increased secretion of sebum; other risk factors includes heat and humid climate, increase sweat and immunosuppression either due to corticosteroids, HIV and other diseases.

Symptoms and Signs

Tinea versicolor is usually asymptomatic, rarely causes mild irritation following sweating. Classically, it appears as multiple tan, brown or white scaling lesions at the hair follicle, on the trunk, neck, abdomen, and occasionally face. The lesions coalesce and form large patches. It is commonly encountered in the summer months .

Diagnosis

Appearance of the lesion
Potassium hydroxide(KOH) wet mount
Wood's light examination

Treatment
Topical antifungals ( Ketoconazole)
Oral antifungals

www.manuscriptedit.com

Pemphigus Vulgaris

Background
Pemphigus is derived from the Greek word pemphix meaning bubble or blister. Pemphigus describes a group of chronic bullous diseases, originally named by Wichman in 1791. The term pemphigus once included most bullous eruptions of the skin, but diagnostic tests have improved, and bullous diseases have been reclassified.
The term pemphigus refers to a group of autoimmune blistering diseases of the skin and mucous membranes characterized histologically by intraepidermal blister and immunopathologically by the finding of in vivo bound and circulating immunoglobulin G (IgG) antibody directed against the cell surface of keratinocytes. The 3 primary subsets of pemphigus include pemphigus vulgaris (PV), pemphigus foliaceus, and paraneoplastic pemphigus. Each type of pemphigus has distinct clinical and immunopathologic features. PV accounts for approximately 70% of pemphigus cases.

Pathophysiology
PV is an autoimmune, intraepithelial, blistering disease affecting the skin and mucous membranes and is mediated by circulating autoantibodies directed against keratinocyte cell surfaces. In 1964, autoantibodies against keratinocyte surfaces were described in patients with pemphigus. Clinical and experimental observations indicate that the circulating autoantibodies are pathogenic. An immunogenetic predisposition is well established.
Blisters in PV are associated with the binding of IgG autoantibodies to keratinocyte cell surface molecules. These intercellular or PV antibodies bind to keratinocyte desmosomes and to desmosome-free areas of the keratinocyte cell membrane. The binding of autoantibodies results in a loss of cell-cell adhesion, a process termed acantholysis. The antibody alone is capable of causing blistering without complement or inflammatory cells.
PV antigen: Intercellular adhesion in the epidermis involves several keratinocyte cell surface molecules. Pemphigus antibody binds to keratinocyte cell surface molecules desmoglein 1 and desmoglein 3. The binding of antibody to desmoglein may have a direct effect on desmosomal adherens or may trigger a cellular process that results in acantholysis. Antibodies specific for nondesmosomal antigens also have been described in the sera of patients with PV; however, the role of these antigens in the pathogenesis of disease is not known.
Antibodies: Patients with active disease have circulating and tissue-bound autoantibodies of both the immunoglobulin G1 (IgG1) and immunoglobulin G4 (IgG4) subclasses.1 Disease activity correlates with antibody titer in most patients.2
Complement: Pemphigus antibody fixes components of complement to the surface of epidermal cells. Antibody binding may activate complement with the release of inflammatory mediators and recruitment of activated T cells.

Frequency
United States
PV is uncommon, and the exact incidence and prevalence depends on the population studied.
International
PV has been reported to occur worldwide. PV incidence varies from 0.5-3.2 cases per 100,000. PV incidence is increased in patients of Ashkenazi Jewish descent and those of Mediterranean origin.
Mortality/Morbidity
PV is a potentially life-threatening autoimmune mucocutaneous disease with a mortality rate of approximately 5-15%. Complications secondary to the use of high-dose corticosteroids contribute to the mortality rate. Morbidity and mortality are related to the extent of disease, the maximum dose of systemic steroids required to induce remission, and the presence of other diseases. Prognosis is worse in patients with extensive disease and in older patients.
PV involves mucosa in 50-70% of patients. This may limit oral intake secondary to dysphagia. Blistering and erosions secondary to the rupture of blisters may be painful and limit the patient's daily activities.
Patients with PV typically heal without scarring unless the disease is complicated by severe secondary infection.
Race
PV affects all races. The prevalence of PV is high in regions where the Jewish population is predominant.3 For example, in Jerusalem, the prevalence of PV was estimated at 1.6 cases per 100,000 population; in Connecticut, the prevalence was 0.42 cases per 100,000 population.4 Incidence of PV in Tunisia is estimated at 2.5 cases per million population per year (3.9 in women, 1.2 in men), while in France, the incidence is 1.3 cases per million population per year (no significant difference between men and women).5 In Finland, where few people of Jewish or Mediterranean origin live, the prevalence is low, at 0.76 cases per million population.6
Sex
Male-to-female ratio is approximately equal. In adolescence, girls are more likely to be affected than boys.
Age
Mean age of onset is approximately 50-60 years; however, the range is broad, and disease onset in older individuals and in children has been described. Patients are younger at presentation in India than in Western countries.7
Clinical
History
Mucous membranes: PV presents with oral lesions in 50-70% of patients, and almost all patients have mucosal lesions. Mucosal lesions may be the sole sign for an average of 5 months before skin lesions develop, or they may be the sole manifestation of the disease.
Skin: Most patients develop cutaneous lesions. The primary lesion of PV is a flaccid blister, which usually arises on normal-appearing skin but may be found on erythematous skin. New blisters usually are flaccid or become flaccid quickly. Affected skin often is painful but rarely pruritic.
Drug-induced PV: Drugs reported most significantly in association with PV include penicillamine, captopril, and other thiol-containing compounds. Rifampin and emotional stress have recently been reported as triggers for PV.8
Physical
Mucous membranes typically are affected first in PV. Mucosal lesions may precede cutaneous lesions by months. Patients with mucosal lesions may present to dentists, oral surgeons, or gynecologists.
Mucous membranes
Intact bullae are rare in the mouth. More commonly, patients have ill-defined, irregularly shaped, gingival, buccal or palatine erosions, which are painful and slow to heal. The erosions extend peripherally with shedding of the epithelium.
The mucous membranes most often affected are those of the oral cavity, which is involved in almost all patients with PV and sometimes is the only area involved. Erosions may be seen on any part of the oral cavity. Erosions can be scattered and often extensive. Erosions may spread to involve the larynx with subsequent hoarseness. The patient often is unable to eat or drink adequately because the erosions are so uncomfortable.
Other mucosal surfaces may be involved, including the conjunctiva,9 esophagus,10 labia, vagina, cervix, penis, urethra, and anus.
Skin: The primary lesion of PV is a flaccid blister filled with clear fluid that arises on normal skin or on an erythematous base. The blisters are fragile; therefore, intact blisters may be sparse. The contents soon become turbid, or the blisters rupture producing painful erosions, which is the most common skin presentation. Erosions often are large because of their tendency to extend peripherally with the shedding of the epithelium.

Early, small blister filled with clear fluid arises on healthy skin.
[ CLOSE WINDOW ]
Early, small blister filled with clear fluid arises on healthy skin.

Flaccid blister filled with clear fluid arises on healthy skin.
[ CLOSE WINDOW ]
Flaccid blister filled with clear fluid arises on healthy skin.
Vegetating PV: Ordinary PV erosions may develop vegetation. Lesions in skin folds readily form vegetating granulations. In some patients, erosions tend to develop excessive granulation tissue and crusting, and these patients display more vegetating lesions. This type of lesion tends to occur more frequently in intertriginous areas and on the scalp or face. The vegetating type of response can be more resistant to therapy and can remain in one place for long periods of time.

An erosion.
[ CLOSE WINDOW ]
An erosion.
Nails: Acute paronychia, subungual hematomas, and nail dystrophies have been reported with PV.11,12
Pemphigus in pregnancy: Occurrence in pregnancy is rare. When present, maternal autoantibodies may cross the placenta, resulting in neonatal pemphigus. Neonatal pemphigus is transient and improves with clearance of maternal autoantibodies.13
Nikolsky sign: In patients with active blistering, firm sliding pressure with a finger separates normal-appearing epidermis, producing an erosion. This sign is not specific for PV and is found in other active blistering diseases.
Asboe-Hansen sign: Lateral pressure on the edge of a blister may spread the blister into clinically unaffected skin.

Causes
The cause of PV remains unknown; however, several potentially relevant factors have been identified.
Genetic factors: Predisposition to pemphigus is linked to genetic factors.14 Certain major histocompatibility complex (MHC) class II molecules, in particular alleles of human leukocyte antigen DR4 (DRB1*0402) and human leukocyte antigen DRw6 (DQB1*0503), are common in patients with PV.15,16,17,18
Age: Peak age of onset is from 50-60 years. Infants with neonatal pemphigus remit with clearance of maternal autoantibodies. The disease may present in childhood or in older persons.
Disease association: Pemphigus occurs in patients with other autoimmune diseases, particularly myasthenia gravis and thymoma.19

SERVICES OFFERED AT WWW.MANUSCRIPTEDIT.COM

Substantive Editing
Full translation & Scientific editing
English Proofreading
Camera-ready formatting
Target journal formatting
Editing research proposals
Journal selection
Journal submission
Response to reviewers
Poster creation/design
Editorial support to journal publishers
Medical Writing and Editing Services

Under eye wrinkle

Causes of wrinkles under the eyes

The problem begins when our skin elasticity starts to weaken and it can no longer bounce back. Unfortunately as we grow older our collagen level comes down, which are needed to give the skin elastic quality. The result is more pronounced when lines and wrinkles develops around and under the eyes. Under eye pigmentation and wrinkle is rarely hereditary and associated with dieases like atopic dermatitis & melasma .

Prevention

Apart from sleep, eyes are constantly active. Working on as a computer, watching the television, reading, playing sport which are all extremely demanding on the eye and skin and muscles that support it.

With this in mind, one should try to rest his/her eyes as often as possible. In a day long work at a computer , take a two-minute break every hour by closing eyes. This will give the muscles chance to relax, which in turn would help prevent wrinkles through intense muscle stimulation. www.manuscriptedit.com

Acne(Pimple)

Acne vulgaris (commonly called acne/pimple) is a common skin condition, caused by changes in pilosebaceous units, sebaceous unit consist of a hair follicle, and sebaceous gland. Androgen stimulates the sebaceous unit and increases its activity as a result it helps formation of acne. It is characterized by noninflammatory follicular papules or comedones , inflammatory papules, pustules, and nodules. Acne vulgaris affects the face, upper part of chest, and back.

Acne is most common during adolescence, affecting more than 85% of teenagers, and frequently continues into adulthood. The cause in adolescence is generally an increase in male sex hormones, which people of both genders accrue during puberty. For most people, acne diminishes over time and tends to disappear .However, there was no way to predict how long it would take to disappear entirely. www.manuscriptedit.com

What is the use of Botulinum toxin (BOTOX)?

Other than its original intended use to treat blepharospasm (eye spasm) and strabismus (misalignment of the eye), this product has a cosmetic applications . Recently FDA has approved Botulinum toxin (type-A)for cosmetic use to improve look by treating fine lines and superficial wrinkles. However, facial expressions seen during smiling, frowning or squinting can also cause dynamic wrinkles and BOTOX is used effectively in these condition. It is also found useful in the treatment of early signs of aging, facial wrinkles produced during expression by using Botox.
www.manuscriptedit.com