Answer: Take extensive history. We want to find out if increase in easinophils in due to some parasitic infection, autoimmune disease or just a response to an allergy.
History:
The family history showed intermittent asthma in a sibling and an aunt with arthritis, but no other pulmonary or autoimmune diseases. The review of systems showed no vomiting/diarrhea, fever/chills, or other symptoms.
SO, we know a large increase in easinophils are not due to any autoimmune disease. So, what next? Could it be an allegic rxn?
Answer: Do a physical Exam:
The pertinent physical exam revealed a child with normal growth parameters and extensive dermatitis involving the face, neck, trunk and extremities. He had no adenopathy or hepatosplenomegaly. He had no other rashes. The laboratory evaluation showed his complete blood count at 12 months of age to have a white blood count of 8.4 x 1000/mm2 with 4500 polymorphonuclear cells, 1600 lymphocytes and 2300 eosinophils.
So, what is your diagnosis?
The diagnosis of eosinophila secondary to atopic dermatitis was made. He was to follow-up with his primary care physician to monitor the eosinophila which should improve with improved control of his atopic dermatitis.
known as atopic eczema, is an atopic, hereditary, and non-contagious skin disease characterized by chronic inflammation of the skin.
The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food, and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are the mo
Atopic dermatitis often occurs together with other atopic diseases like hay fever, asthma and conjunctivitis. It is a familial and chronic disease and its symptoms can increase or disappear over time
So, why an increase in easinophils?
Easoniphils along with mast cells play a role in the allergic responses. When the allergen binds to antibody on a mast cell, mast cell will degranulate and release histamines. Morever, it will also secrete certain cytokines which will recruite easinophils to the site of allergen. Easophils contribute to the tissue injury by releasing toxic enzymes and oxygen radicals.
Exercise-induced anaphylaxis (EIA) is a syndrome in which patients experience the symptoms of anaphylaxis, which occur only after increased physical activity. The symptoms include pruritus and urticaria (typically with giant hives), and, without emergency intervention, the patient may develop hypotension and collapse. Now increasingly recognized as more children and teenagers participate in physical activities and sports, EIA quite possibly will become more common in the future. Those affected by the syndrome are typically accomplished athletes and have a history of atopy, but anyone can be affected.
The types of physical activities that have triggered episodes of EIA have included walking, dancing, racquet sports, swimming, jogging, bicycling, skiing, basketball, and sprinting. Hot humid weather and cold weather can precipitate episodes in some patients. If a patient has recurrent EIA, the episodes tend to be worse in the summer months. The first reported case of EIA was in 1979 by Maulitz and coworkers and was food-related, occurring in a 31-year-old patient who had ingested shellfish prior to long-distance running. Since then, many different allergens have been reported in the literature to have caused EIA, including shrimp, oyster, celery, cheese sandwiches, pizza, wheat gliadin, eggs, peaches, grapes, chick peas, pears, poppy seeds, and snails (which have been reported to have cross-reactivity with dust mites).
In 1980, Sheffer and Austen provided the first report of patients with EIA. Sixteen patients, aged 12-54 years, experienced EIA without a specific allergen exposure. Ten of these patients had onset of EIA in their teenage years, indicating that those who care for pediatric patients should be aware of this syndrome.
EIA has been categorized in a few different ways in the literature. Classic EIA is the most common type. Sheffer and Austen (1980) originally described 4 phases in the sequence of symptomatology of classic EIA. A prodromal phase is characterized by fatigue, warmth, pruritus, and cutaneous erythema. The early phase follows, with the urticarial eruption that progresses from giant hives (about 10-15 mm in diameter) to become confluent and may include angioedema of the face, palms, and soles. Then, the fully established phase occurs, which can include hypotension, syncope, loss of consciousness, choking, stridor, nausea, and vomiting and can last 30 minutes to 4 hours. The final phase is the late or postexertional phase, which is characterized by prolonged urticaria and headache persisting for 24-74 hours.
Another type of EIA is variant-type EIA, which is similar to classic EIA, except the typical giant hives are not observed. In their place are small punctate skin lesions, more typical of cholinergic urticaria, but the syndrome does lead to hypotension and collapse if allowed to progress. The variant type of EIA accounts for approximately 10% of cases.
Familial EIA has been described involving patients with a family history of EIA and atopy. No inheritance pattern has been established.
Two forms of food-dependent EIA have been described. Inherent in the definition of food-dependent EIA is that the food or exercise alone does not produce symptoms. First, specific-food EIA exists in which a specific food is known to be the offending allergen. Second, non–specific-food EIA exists in which no specific food is known, but eating any food prior to exercise causes symptoms of EIA.
The last type of EIA described is medication- or drug-dependent EIA. This category includes patients who develop the syndrome only after ingesting a specific medication and then exercising. The offending medications that have been reported include nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, antibiotics, and cold remedies.
In EIA, an exercise-induced lowering of the mast cell degranulation threshold exists, which causes the release of histamine and other mediators and leads to the progression from pruritus and urticarial rash to the symptoms of anaphylaxis. In the food-dependent subset, this process is influenced by immunoglobulin E (IgE) mast cell sensitization by a known or unknown food. If the offending food is known, the amount of the specific food ingested has an effect on whether the patient has symptoms. The mechanism by which exercise lowers the mast cell degranulation threshold is unknown. Previous observations suggest that increased physical activity has a direct effect on mast cell releasability and does not result in an increased sensitivity to histamine.
Once the histamine and other mast cell mediators, including leukotrienes, are released, they cause the smooth muscle contraction responsible for the wheezing and GI symptoms. The histamine and other mast cell mediators also cause the vascular dilatation that leads to the escape of plasma into the tissues, causing urticaria and angioedema, and results in hypotension and shock.
Prevalence is not well established. In one study, 9% of total episodes of childhood anaphylaxis and 20% of episodes in children older than 8 years were triggered by exercise.
Case reports from Germany, Italy, Japan, United States, and Thailand are provided in the literature.
Deaths of children have been reported, but they are rare. Infrequently, patients must alter their lifestyle and physical activity significantly; in some patients, the syndrome causes them to be unable to perform daily activities without the risk of anaphylactic syndrome.
No racial predilection is known.
One study showed a slight male predominance, but most other studies show no overwhelming difference between sexes.
EIA has been reported from as young as 4 years into adulthood. In a study of 16 patients, 10 patients (63%) had onset in their teenage years.
Risk factors for EIA include personal or family history of EIA or atopy, male sex (in one study), exposure to food allergen, and extremes of weather. Beta-blocker medications can aggravate anaphylactic episodes.
So, what do you think is the best treatment for this hypersensitivity?
Treatments:
1.Discontinue exercise at the first sign of erythema or any skin inflammation)
2. Subcutaneous epinephrine is the drug of choice if the symptoms progress to anaphylaxis. SO, what does epinephrine do?
3. Airway maintenance, oxygen therapy, fluid resuscitation, vasoactive drugs, and cardiopulmonary support should be used if necessary.
4. Patients can be treated with oral antihistamines
5. Prevention remains the best treatment for patients who have EIA. For food- or drug-dependent EIA, avoiding the offending food or drug 12 hours prior to exercise is essential, and, if no offending food is known, avoiding the ingestion of any food 6-8 hours prior to exercise is sometimes necessary.