CLINICAL DERMATOLOGY

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Bacterial infections:

PYODERMAS: Primary & Secondary

PRIMARY:

Impetigo:

It is a superficial, highly contagious bacterial infection, seen commonly in preschool and to an extent school going young children. It is also rarely seen in adults who practice close contact sports.

Causes:

1.  Staphylococcus aureus

2.  Group A beta-hemolytic streptococci (GABHS) Streptococcus pyogenes

3.  Nongroup A streptococci (groups B,C,G)

4.  Streptococcus pneumoniae

5.  Coagulase negative  staphylococci – Staphylococcus epidermidis

6.  Enterococci

Features:

Incubation period:

Streptococcus: 1-3 days after exposure

Staphylococcus: 4 - 10days after exposure

There are 2 types:

1.  Non-Bullous impetigo

2.  Bullous impetigo

Non-Bullous Impetigo:

The non-bullous type is more common and is more commonly caused by Staphylococcus aureus these days. It evolves from a small vesicle to pustule, which progresses into a honey colored crusted plaque. This eventually dries leaving fine crusts and heals without scarring.

Crowding, poor hygiene, minor skin trauma, intimate sports facilitate spreading in others.

Bullous Impetigo:

It is caused primarily by group 2 Staphylococcus aureus – phage group 2 and type 71. It is characterized by painless flaccid bullae and moist erosions with surrounding erythema. Sometimes, bullae spread with central clearing and may form annular lesions.

Complications:

1.  Osteomyleitis

2.  Septic arthritis

3.  Pneumonia

4.  Septicemia

5.  Cellulitis

6.  Post streptococcal Glomerulonephritis (Streptococcal strains are more associated, characteristically with a latent period of 18-21 days following impetigo)

7.  Staphylococcal scalded skin syndrome (SSSS)

Other Primary (pyoderma) bacterial infections are:

Superficial: Folliculitis, Follicular impetigo

Deep: Furuncle, Carbuncle, Ecthyma, cellulitis, erysipelas, paronychia, necrotizing fascitis

Diet in Atopic Dermatitis:

1. Prenatal followed by postnatal probiotic supplementation decreases the risk of atopic dermatitis in new borns.

2. Postnatal prebiotic supplementation decreases the risk of atopic dermatitis.

3. Elimination diets are only appropriate for patients who have a food allergy that has been proven by oral food challenge.

4. Maternal allergen avoidance diets do not prevent atopic dermatitis.

5. Exclusive breastfeeding and supplementation with hydrolyzed formula is protective against atopic dermatitis for high-risk infants.

6. For infants at normal risk, breastfeeding is not protective for atopic dermatitis.

Dietary Exclusion and food allergy:

Diagnosis of an IgE-mediated food allergy relies on a combination of medical history, skin prick test, serum IgE testing, and oral food challenges. History, skin prick test, and allergen-specific serum IgE are not diagnostic because of their limited positive predictive value for clinical allergy. The diagnostic criterion standard is a double-blind, placebo-controlled food challenge, which is often impractical in clinical practice, and is appropriately replaced by a single-blind or open food challenge. A challenge is preceded by the elimination of suspected foods for 2 to 8 weeks and is administered in a supervised medical setting to enable treatment of hypersensitivity reactions. If the challenge does not elicit symptoms, an allergy to that food allergy is not present. A food allergy is confirmed if the challenge elicits symptoms that correlate with medical history, blood testing, and skin prick results.

For patients with atopic dermatitis and a proven food allergy, elimination diets are appropriate and may decrease the severity of atopic dermatitis. Nutritionist consultation is indicated to avoid nutritional deficiencies and growth restriction. In addition, because food allergies often spontaneously resolve, patients should be reassessed regularly to avoid unnecessary elimination. For patients without a proven food allergy, elimination diets should not be pursued to manage atopic dermatitis,  because there is no evidence to suggest that this approach is helpful. In addition, these diets may cause nutritional deficiencies, growth deficits, and anaphylaxis on re-exposure to previously tolerated foods.

Maternal diet and breastfeeding:

A detailed review found no significant protective effect of an antigen avoidance diet during pregnancy, lactation, or both for prevention the of atopic dermatitis in infants up to 18 months of age. In addition, maternal antigen avoidance during pregnancy was associated with a decreased mean gestational weight gain and birth weight and increased risk of preterm birth.

In 2008, the American Academy of Pediatrics summarized the evidence for maternal and infant nutrition in the context of AD, that restriction of maternal diet during pregnancy and lactation does not affect subsequent AD development. Exclusive breastfeeding for 4 months in high-risk infants was reported to be protective against AD. A meta-analysis of 18 prospective studies and the German Infant Nutritional Intervention studies found decreased AD incidence in high-risk infants who were breastfed compared to those fed cow’s milk formula. This protective effect also applied to hydrolyzed formula. Conversely, no significant effect of exclusive breastfeeding on AD was observed for infants in the general population.

Conclusions:

There is insufficient evidence to suggest a benefit from supplementation with vitamin D, Evening Primrose Oil, Borage Oil, fish oil, zinc sulphate, selenium, vitamin E, pyridoxine, sea buckthorn seed oil, hempseed oil, sunflower oil, and docosahexaenoic acid for atopic dermatitis. 

Evidence suggests that prebiotic supplementation in infants and prenatal followed by postnatal probiotic supplementation decrease the risk of atopic dermatitis. 

Elimination diets are only appropriate for patients who have a food allergy that is proven by oral food challenge. Maternal allergen avoidance diets during pregnancy or lactation do not prevent atopic dermatitis.. 

Exclusive breastfeeding for 4 months or breastfeeding supplemented with hydrolyzed formula is protective against atopic dermatitis in high-risk infants. For infants at normal risk, breastfeeding does not affect the incidence of atopic dermatitis.. 

1.  What is Alopecia Areata?

Alopecia areata (AA) is a common, inflammatory, non-scarring type of hair loss. There are many variations in the clinical presentation, ranging from small, patches of hair loss to a complete absence of body and scalp hair. Patients affected by AA are seen in all age groups, sexes, and ethnicities, and may experience frustration with the unpredictable nature of their disease and significantly affect the quality of life.

The cause of AA remains elusive though significant advancement has been made in the understanding of its causative pathophysiologic mechanisms, and it is believed to result at least in part from complex autoimmune-mediated hair follicle destruction. 

Patients with AA frequently experience marked impairment in psychological well-being, self-esteem, and may be more likely to suffer from psychiatric comorbidities.

2.  Are there many types of Alopecia Areata?

Several subtypes of alopecia areata have distinct presentations. Some of them have multiple patches of hair loss, some only on the  back of the scalp (oophiasic type), some sudden graying type, and some total loss of hair on the scalp,  eyebrows, eyelashes – aloepica totalis (AT) and some of them progress to hairloss of entire body areas – alopecia universalis (AU).

3.  What are the outcomes after treatment?

Factors that may contribute to improvement include AA subtype, extent of hair loss, duration of hair loss, age at onset, and family history. Approximately 5% of cases of patchy AA will progress to AT or AU. Extensive involvement indicates an unfavorable prognosis.

The ophiasis subtype can have a poorer outcome and may be less responsive to treatment, while the acute diffuse and total alopecia subtype generally has a favorable prognosis.

4.  Are there any other diseases or factors causing or associated with AA?

Increased risk of AA development is seen in patients with atopy, including atopic dermatitis, asthma, and allergic rhinitis has been reported. Multiple autoimmune diseases (including thyroid disease, psoriasis, and vitiligo) have been shown to have a high association with AA and also possibly with rheumatoid arthritis, celiac disease and type 1 diabetes. There are recent studies although not currently substantiated in AA, the circulating chemical mediators, the inflammatory cytokines certainly have the potential to adversely affect other organs, as seen in other autoimmune diseases like psoriasis, systemic lupus erythematosus, and rheumatoid arthritis.

Nutritional deficiencies including vitamin D and iron deficiency, are also more common in AA patients. Patients with AA have been found to have higher rates of sensorineural hearing loss.

There is a strong genetic component in AA with a 10-fold increased risk in first-degree relatives. Stress and psychological disorders are among the most commonly cited causes of AA by patients, but the exact association is still debatable. A recent study reported a high prevalence of anxiety, depression and sleep problems among patients with AA. Furthermore, reports of suicide in children and adults with AA are concerning. Food with high dietary soy oil content seems to increase resistance to AA in laboratory studies.

5.  What are the treatment options in Alopecia Areata?

Many therapies are available for the treatment of alopecia areata, including topical, systemic, and injectable modalities. However, these treatment methods produce variable clinical outcomes and there are nocurrently available treatments that induce and sustain remission. 

Intralesional corticosteroids are considered a first-line treatment method for limited disease. Topical corticosteroids may be used alone or in conjunction with other treatments, including intralesional corticosteroids. Minoxidil 5% foam or solution may be used as adjuvant therapy in alopecia areata. Alone, minoxidil may be insufficient to promote complete hair regrowth. Topical immunotherapy is another option with good improvement in many.

Short courses of oral corticosteroids are often sufficient to stimulate hair regrowth; however, the side effect profile precludes long-term use and the likelihood of relapse is significant.

Most recently, a novel therapeutic option using a group of medications called JAK inhibitors shows promising results raising the hopes of AA patients and the treating doctors more than ever before and is presently available in Kuwait. Also, many existing medications used for other indications are being evaluated for their utility in AA. 

Overall, the treatment options for alopecia areata are increasing and there are new promising treatments in the horizon.