Pediatric Aphthous Ulcers

Immunology, Infectious Diseases No Responses »
May 132012

Commonly termed canker sores, aphthous ulcers, or aphthous stomatitis, have been the focus of study and research for many years, although the exact etiology of the lesions has yet to be identified. Categorized as an idiopathic disease, aphthous ulcers are frequently misdiagnosed, treated incorrectly, or simply ignored.

Causes

Precipitating factors include trauma, salivary gland dysfunction, stress, genetic predisposition, local infections, nutritional deficiencies, GI disorders, systemic disorders, food allergy or hypersensitivity, hormonal fluctuations, and chemical exposure.

Clinical Presentation

The diagnosis of aphthous ulcers (canker sores) is primarily clinical. Patients typically describe a prodromal stage of a burning or pricking sensation of the oral mucosa 1-2 days before the ulcer appears.

Aphthous ulcers occur on areas of the mouth in which the mucosa is nonkeratinized and loosely attached, particularly the buccal mucosa, the labial mucosa, the floor of the mouth, the ventral surface of the tongue, and the soft palate. Ulcers may appear as single or multiple lesions, and they are easily distinguished from primary or secondary viral infections, bacterial infections (eg, necrotizing ulcerative gingivitis), dermatologic conditions (lichen planus, cicatricial pemphigoid, pemphigus), and traumatic injuries (contusions, lacerations, burns) by the healthy appearance of adjacent tissues and the lack of distinguishing systemic features.

Diagnosis

The diagnosis of aphthous ulcers (canker sores) is usually based on the history and clinical Continue reading »

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Atopic Dermatitis (Eczema)

Immunology, Skin No Responses »
Dec 262010
  • Atopic dermatitis is a chronic relapsing and remitting inflammatory skin disease characterized by dermatitis with typical morphology and distribution.
  • Eczema is a generic term for a constellation of clinical signs, whereas atopic dermatitis is a term that specifically connotes an allergic contribution to the etiology of the eczema.
  • The overall prevalence of atopic dermatitis in the United States is 17% among school-aged children, leading to considerable disease-related morbidity, including irritability, secondary skin infections, sleep disturbance, school absenteeism, and poor self-image.
History
  • Age of onset is a consideration, with 45% of affected individuals manifesting atopic dermatitis in the first 6 months of life, 60% by the first year, and 85% by school age.
  • Pruritus is a cardinal feature of eczema, often described as the “itch that rashes.” Scratching leads to further compromise in the skin barrier and augments inflammation.
  • Xerosis (dry skin) also involves nonlesional skin. (In other conditions, commonly mistaken for atopic dermatitis (seborrheic dermatitis, nummular eczema, and psoriasis), the uninvolved skin is generally healthy.)
  • Patients may have a personal and family history of atopy (asthma, hay fever, food allergy).
  • Exacerbating factors include food allergens (most frequently egg, milk, wheat, soy, peanut, tree nuts, shellfish) and inhalant allergens (e.g., pet dander, house dust mite).
  • Systemic involvement, with failure to thrive, chronic diarrhea, and/or recurrent infections should prompt consideration of underlying systemic disease, such as immunodeficiency (e.g., Wiskott-Aldrich syndrome, Netherton syndrome, immune dysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome, and hyper-IgE syndrome), or malabsorption (e.g., zinc deficiency or cystic fibrosis).
Physical Examination
  • Xerosis
  • Morphology of lesions
    • Acute lesions: pruritic papules with excoriation and serous exudation
    • Chronic lesions: lichenified papules and plaques
    • Superficial linear abrasions from scratching
    • Indistinct lesional borders, unlike that of psoriasis

  • Areas of involvement. Although atopic dermatitis may appear anywhere on the body, characteristic patterns include:
    • Infants: cheeks, forehead, and extensor surface of extremities
    • Children/adolescents: flexor surface of extremities popliteal and antecubital fossae, and ventral surface of wrists and ankles Continue reading »
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Introduction to DiGeorge Syndrome

Genetics, Immunology No Responses »
Dec 142010

DiGeorge syndrome (DGS) now understood to be the chromosome 22q11.2 deletion syndrome was originally described as 3 syndromes found on 2 continents.Dr. DiGeorge was the first to provide clinical examples in humans that demonstrated the thymus was involved in immune function.

Pathophysiology

As the name chromosome 22q11.2 deletion syndrome implies, the syndrome is the result of a 2-3 million base pair (Mb) deletion on the long arm of chromosome 22. This area is prone to microdeletion because of the presence of nonallelic, flanking, low-copy repeat DNA sequences in the region, which lead to unequal crossing over between the two chromosome 22s during meiosis.

Frequency

Estimates of the incidence of chromosome 22q11.2 deletion syndrome range from 1 per 2000-4000 in the general population. It is a frequent cause of cleft palate and congenital heart defects.

Sex

Males and females appear to be equally affected.

Age

This is a congenital condition, but age at diagnosis largely depends on the severity and the types of birth defects. Thus, those with more serious cardiac defects, hypocalcemia, or both observed in classic DGS are diagnosed in the neonatal period. Recurrent infections usually present in patients older than 3-6 months. Some individuals without hypocalcemia who have normal immune Continue reading »

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