Eczema: Tips on how to manage atopic dermatitis in spring and summer

 

• Eczema is a chronic skin condition. People with eczema can experience flare-ups where symptoms get worse and other times have no symptoms.
• People with eczema can experience flare-ups because of certain triggers, including those in the environment.
• Seasonal changes can trigger eczema flare-ups, so people may need to take extra care to manage eczema at certain times of the year.

Eczema is a common skin condition that causes dry, itchy, and cracked skin.

Managing the condition can be stressful and irritating.

People with eczema can work with their doctors and dermatologists to manage their symptoms and reduce their chances of having flare-ups.

People with eczema should also know how weather and temperature changes can impact their symptoms.

From here, they can take steps to manage their symptoms, including taking special care to manage symptoms in the spring and summer.

 

Common eczema symptoms

While there are different types of eczema, the most common type is atopic dermatitisTrusted Source.

People with atopic dermatitis may experience the following symptomsTrusted Source:

• Dry and itchy skin
• Red patches of inflamed areas
• Thickening of the skin in affected areas

Eczema can affect any area of the body, but certain age demographics are more likely to have certain areas affected.

For example, infants and toddlers will likely have their scalps and faces affected.

When people scratch the affected areas, the areas may ooze, bleed, or crust. These areas are then at a higher risk for infection, worsening the person’s skin condition.

People with eczema will have times when eczema symptoms get worse. These flares are when symptoms can be the most irritating.

There may be other times when symptoms go away altogether.

Seasonal changes with eczema

People with eczema can experience flare-ups because of many triggers.

Learning to avoid triggersTrusted Source or modify certain behaviors can be helpful in the management of eczema.

Eczema triggers related to seasons can include the following:

• Fast temperature changes
• Pollen, which may be more common in the spring
• Dry air
• Sweating and humidity
• Hot or cold weather
• Sunburn or overheating

Depending on someone’s specific triggers, they may experience exacerbations of symptoms during the spring and summer months.

Dr.Jacqueline Eghrari-Sabet, an allergy and immunology specialist who is the telehealth medical director for the Allergy & Asthma Network, explained to Medical News Today how eczema can worsen based on seasonal influence.

A main reason for the seasonal change is exposure to certain allergens that are more present at certain times of the year.

Eczema management in the spring and summer

Treatment for eczema involves action steps to minimize symptoms and avoid triggers.

Avoiding triggers can help reduce flare-ups and the severity of symptoms.

People can work with their doctors to develop treatment plans based on their unique needs.

Sometimes, the use of medication is necessary to help with symptom management, including the use of topical and systemic medications.

Some treatment for eczema will remain constant, as noted by pediatrician Dr.
Nivedita More with Bayside Medical Group at Stanford Medicine Children’s Health in California.

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Streptococcal Infections: How And Why To Perform The Rapid Test.

Streptococcal infection: the rapid test is used to check whether a person with a sore throat (pharyngitis) has streptococcal pharyngitis, i.e. an infection of the throat and tonsils caused by the bacterium Streptococcus pyogenes, also called group A β-haemolytic Streptococcus

Many sore throats are of viral origin and may resolve spontaneously within a few days; some people, however, suffer from streptococcal pharyngitis.

It is important to diagnose and treat this type of infection promptly because of the high probability of infection and the development of secondary complications, especially in children.
The rapid test, also known as rapid antigen detection test (RADT), can detect the presence of specific antigens for group A streptococcus, providing a result in 10-12 minutes

The U.S. Food and Drug Administration (FDA) has recently approved the use of a molecular test that can detect the presence of genetic material belonging to group A streptococcus in pharyngeal swabs in just eight minutes.

A positive rapid test indicates the presence of an infection with group A streptococcus, the bacterium that causes streptococcal pharyngitis.

A negative rapid test, on the other hand, indicates that the person with a sore throat most likely does not have streptococcal pharyngitis although, in children and adolescents, a pharyngeal swab culture test is recommended as confirmation.
It is recommended to consult the paediatrician and perform the rapid test in the case of:
Acute onset sore throat lasting more than a week, or recurrent sore throat;
Reddened (inflamed) throat and/or tonsils with white or yellow plaques or streaks
Fever of 38°C or higher
Skin rashes
Hoarseness lasting more than two weeks
Small red spots on the palate
Difficulty swallowing
Headaches, muscle aches
Nausea or vomiting
Pain and swollen cervical lymph nodes
Blood in saliva and mucus

According to the 2012 guidelines provided by the Infectious Diseases Society of America (IDSA), the test is not recommended if other symptoms attributable to a viral-type infection are also present, such as: Cough, rhinorrhoea (runny nose), mouth ulcers.
Streptococcus, the test is performed by taking an oro-pharyngeal sample and a rapid test is possible

In this case, specific antigens of group A beta-haemolytic Streptococcus are sought, and therefore the test has an absolute specificity and sensitivity of 96 %.

The test is called rapid because the result is available in 10 to 15 minutes.

With the rapid swab it is also possible to detect the presence of both viable and non-viable elements (still present 24/48 hours after the start of antibiotic therapy, although no longer able to develop into colonies when a culture test is performed).

With the rapid or direct test, however, it is not possible to detect microbial agents other than group A

beta-haemolytic Streptococcus.
 

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5 things your nails indicate about your health

Nails are an essential component of your body but are often ignored.You can cover up your nails with colorful nail paints but you can't cover up the physical health conditions they may indicate.The appearance of your nails can sometimes provide clues about your underlying health conditions.Here are five nail signs and what they tell about your overall fitness and health.

The shape and texture of your nails

Concave, spoon-shaped nails can be a sign of iron deficiency anemia.Brittle, thin, or cracked nails can be a sign of a thyroid problem.Nails curving around the fingertips can be a sign of lung disease, heart disease, and inflammatory bowel disease.Pitting or rippling nails can be a sign of psoriasis, an autoimmune skin condition that causes inflammation.

If your nails are discolored

Discoloration of the nails can sometimes indicate an underlying health condition.For instance, nails that are yellow or brown in color can be a sign of a fungal infection.Yellowish-pink or brownish-red spots on nails that extend from the cuticle to the tip of the nail indicate you have psoriasis.Yellow nails can also be a sign of jaundice.

If your nail growth is slow, rapid, or inconsistent

Slow nail growth may be a sign of anemia.On the contrary, rapid nail growth can be a sign of a hyperactive thyroid, a condition in which the thyroid gland produces too much hormone.If your nails grow unevenly or in spurts, it can be a sign of an underlying medical condition such as diabetes or a blood circulatory problem.

If your nails are scooping outward

Lifting nails, often known as onycholysis, is a disorder when the fingernails are seen to be parting from their nail beds.It can happen as a result of excessive exposure to water or overly vigorous manicure sessions, and the nail colors typically change to an opaque white, green, or occasionally even yellow.This typically denotes a thyroid condition or psoriasis in cases of trauma.

If your nails have beau's lines

Beau's lines are horizontal ridges that run across the nails and it can be a sign of serious underlying conditions.It can indicate uncontrollable diabetes, where your blood sugar levels become high and can damage your blood vessels and nerves.It also indicates zinc deficiency in your diet. If someone is going through chemotherapy, beau's lines can appear on their nails as well.

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Pemphigus: Updated Review and Emerging Therapies.

 Overview of Pemphigus,

Pemphigus is defined as a group of autoimmune, blistering disorders caused by circulating autoantibodies that bind to desmogleins (Dsg), which are proteins that are vital to epidermal intercellular adhesion.1 Binding of these autoantibodies to their targets causes acantholysis (or loss of keratinocyte to keratinocyte adhesion), which ultimately results in the formation of intraepithelial blisters in skin and mucous membranes.1 Unfortunately, pemphigus disorders can potentially be life-threatening and have a devastating impact on quality of life.

Pemphigus vulgaris and pemphigus foliaceus, which comprise 90–95% of pemphigus diagnoses, will be described here.2,3 Other types of pemphigus include Immunoglobulin A (IgA) pemphigus, Paraneoplastic pemphigus, Drug-induced pemphigus, Pemphigus vegetans, Pemphigus erythematosus (Senear-Usher syndrome), Pemphigus herpetiformis, Atypical pemphigus, and Neonatal pemphigus.

Pemphigus diseases are different from pemphigoid diseases. Pemphigoid diseases are the other main group of autoimmune blistering disorders and are characterized by autoantibodies against structural proteins of the dermal–epidermal junction.6 Pemphigus diseases demonstrate a positive Nikolsky’s sign (extension of a blister when pressure is applied to the side of the blister), whereas Pemphigoid diseases do not.1

Diagnosis of pemphigus disorders is often aided by clinical presentation, direct immunofluorescence microscopy of a perilesional biopsy, serology, and histopathology of a lesional biopsy.7

Systemic corticosteroids represent the first-line treatment in all forms of pemphigus.7 Adjuvant medications include azathioprine and mycophenolate compounds.7 Rituximab, an anti-CD20 monoclonal antibody that induces B-cell depletion, has been shown to improve patient survival.8 Currently, rituximab in conjunction with corticosteroids is first-line for treatment of moderate to severe pemphigus, thus allowing for a major corticosteroid-sparing effect and decreasing the risk of steroid-associated adverse events.7

Pemphigus vulgaris (PV)

PV, the most common type of pemphigus, causes blisters on cutaneous and mucosal surfaces.

The mean age of onset is 50 to 60 years of age, and it affects both sexes equally.9 The reported incidence is between 0.1 and 0.5 per 100,000 people per year, but can be higher in certain groups, such as Ashkenazi Jews.9

In terms of etiology, genetics are thought to confer susceptibility to the disease. Environmental factors, including stress, diet, and infection, may trigger immune dysregulation, leading to flares.9 Patients with PV have autoantibodies against Dsg3 or both Dsg3 and Dsg1.9

In 80% of PV cases, patients initially present with intraoral blisters that frequently rupture, resulting in painful erosions.9 In 75% of PV cases, cutaneous lesions arise after the first oral blisters.9 Physical exam may reveal vesicles, erosions, or bullae on erythematous or normal-appearing skin.9Diagnostic clues favoring PV include mucosal lesions, positive Nikolsky’s sign, positive direct immunofluorescence microscopy results (i.e., intercellular deposits of IgG, complement component 3, or both), and serum antibodies against Dsg3.7

As in all forms of pemphigus, corticosteroids are first-line in the treatment of PV.7 There is an accepted algorithm for the management of PV developed by international experts, which resulted from a Delphi consensus based on the European Dermatology Forum and the European Academy of Dermatology and Venereology guidelines.7

Despite advances in treatment, patients with PV should be monitored closely. Patients can experience relapses and complications, such as infection. In fact, septicemia is the leading cause of death in PV, indicating that there is still much progress to be made with PV management.9

Pemphigus foliaceus (PF)

Unlike PV, PF is characterized by skin involvement only, with the sparing of mucosal surfaces.

PF is less common than PV. The mean age of onset is 50 to 60 years of age, and it affects both sexes equally.10Endemic pemphigus foliaceus, which is also known as Fogo selvagem, is common in Brazil and other South American countries.10, 11

Regarding etiology, genetics are thought to confer susceptibility to the disease, while environmental factors, such as the use of certain drugs, act as triggers. In particular, penicillamine and captopril, which contain sulfhydryl groups that are speculated to interact with the sulfhydryl groups in Dsg1 and Dsg3, are associated with drug-induced PF.10

Most patients with PF are not severely ill.10 Patients may suffer from burning, pruritus, and pain.10 The onset is usually subtle with a few scattered lesions involving the seborrheic areas (i.e., the scalp, face, chest, and upper back).10 The lesions are characterized by erythema, “puff pastry-like” scaling, and crusting.3 Intact blisters are rarely seen because they are superficial and rupture easily.10 PF may stay localized for years or quickly progress to generalized involvement, leading to exfoliative erythroderma.10

The diagnosis of PF is supported by crusted erosions, lack of mucosal lesions, positive Nikolsky’s sign, positive direct immunofluorescence microscopy results (i.e., intercellular deposits of IgG, complement component 3, or both), and serum antibodies against Dsg1.7

As in all forms of pemphigus, systemic corticosteroids are first-line in the treatment of PF.7 The treatment algorithm for PF is similar to that of PV.7 However, in localized forms of PF with a limited number of lesions, topical or intralesional corticosteroids can be used.12

Prior to corticosteroid therapy, PF was fatal in approximately 60% of patients.10 Fortunately, steroids and other immunosuppressive therapies have greatly reduced mortality.10 In terms of prognosis, PF is a benign disease that responds well to treatment and may remit.10

Pemphigus: Emerging Therapies

There are many new treatments currently being tested for pemphigus.3,8,13,14,15 Second and third generation anti-CD20 monoclonal antibodies, such as veltuzumab, ocrelizumab, and obinutuzumab, have higher binding affinities and induce a more robust B-cell depletion compared to rituximab.3,13 The development of these next generation anti-CD20 monoclonal antibodies could lead to major progress in the treatment of pemphigus. Bruton tyrosine kinase (BTK) inhibitors, which downregulate several B-cell functions, and efgartigimod, an engineered Fc fragment derived from human IgG1, are also being studied for use in pemphigus treatment.13,14,15 Recently, researchers have engineered chimeric autoantibody receptor (CAAR)-T cells that recognize Dsg domains to selectively target autoreactive B-cells, which could become a precise therapy for pemphigus in the future.3,8 Other novel, potential therapies include cytokine inhibitors, anti-CD25 monoclonal antibodies, autologous hematopoietic stem cell transplantation, and polyclonal regulatory T cell (PolyTreg) therapy.13 Hopefully, one or more of these emerging therapies will soon be shown to be safe and effective in the treatment of pemphigus, and ultimately improve survival and quality of life for these patients.

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#Streptococcus #dermatitis #shingless #sunburnn #skindiseases #vulgariss #rosaceaa #skinmoless

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