Page 1 of 1: Very high eosinophilia ...........

nadu · Credits: 17470 My Scrapbook

Q.Very high eosinophilia is caused by all parasitic infections EXCEPT :

1. Trichinosis

2. Visceral larva migrans

3. Tropical pulmonary eosinophilia

4. Hydatid disease

SATVIK · Credits: 958 My Scrapbook

The role of eosinophilia in diagnosing parasitic infection is worth mentioning.
Indeed a very good explanation given in Harrison,
14th ed ,pg no-1164.
it says markedly high eosinophilia is caused by tropical pulm eosinophlia,early stages of fluke infection,during the stage of muscle invasion in trichinosis and with heavy infections in visceral larva migrans.
Leakage of fluid from echinococcal cysts causes intermittent increase in eosinophilia.

so the answer is option D.

nadu · Credits: 17470 My Scrapbook

thanx

gongu · Credits: 4772 My Scrapbook

hydatid disease

shanoo · Credits: 230 My Scrapbook

answer is hydatid disease.

siddhesh · Credits: 206 My Scrapbook

hey frds..apart from options which other parasitic conditions are there which dont cause high eosinophilia??..one is invasive amoebiasis.

jabby · Credits: 3703 My Scrapbook

Hydatid disease

robin · Credits: 1719 My Scrapbook

In fact among the protozoan parasites, Isospora is the only one that causes eosinophilia. This is strictly among protozoans only.

josephdhar · Credits: 1143 My Scrapbook

hello look at this HES

Hypereosinophilic syndrome (HES) encompasses a wide range of clinical manifestations sharing 3 features defined by Chusid et al: (1) a peripheral eosinophil count of greater than 1.5 X 109/L for longer than 6 months; (2) evidence of organ involvement, thus excluding benign eosinophilia; and (3) an absence of other causes of eosinophilia, such as parasite infestation (most common cause of eosinophilia worldwide), allergy (most common cause of eosinophilia in the United States), malignancy, and collagen-vascular disease.

HES is a clonal proliferation of eosinophils. By definition, HES is an idiopathic condition.

* Some have speculated that HES is not primarily a disease of eosinophils but rather a disease of T cells that secrete cytokines that result in such clonal proliferations. Such clonal eosinophils are activated and have more eosinophilic mediators than normal eosinophils.
* Some cases of HES turn into leukemia, and, as such, chromosomal abnormalities are at the root of some cases of HES. A study from the NIH6 found chromosomal abnormalities in 8 of 33 patients examined. Such abnormalities can include the Philadelphia chromosome.
The signs and symptoms are dependent on the organ system involved.

* Mucocutaneous signs
*
o Urticarial wheals and angioedema are common.
o Dermatographism occurs in as many as 75% of patients.
o Erythematous, pruritic papules and plaques are the other major dermatologic manifestation.
o Blistering lesions and necrotic ulcers secondary to dermal microthrombi have been reported.
o Petechiae, generalized erythroderma, erythema annulare centrifugum, and Raynaud phenomenon are other cutaneous manifestations.
o Splinter hemorrhages can result from cardiac thromboemboli.
o Ulcers can occur on virtually any mucosal surface.
* Cardiac signs
*
o Signs of heart disease vary depending on the stage of involvement, and they become more prominent in the latter stages of the disease.
o Splinter hemorrhages, arrhythmias, murmurs (particularly mitral and tricuspid regurgitation), restrictive cardiomyopathy, cardiomegaly, as well as other CHF manifestations all occur and have a worse prognosis. The symptoms of HES can resemble restrictive cardiac disease.
* Neurologic signs
*
o Acute neurologic deficits are usually the result of thromboembolic disease.
o Primary CNS involvement manifests as changes in mental status, ataxia, increased deep muscle tone, increased deep tendon reflexes, and a positive Babinski sign. Seizures can occur but are less common.
o When peripheral nerves are involved, patients exhibit sensory and/or motor deficits. Radiculopathies, muscle atrophy from denervation, and mononeuritis multiplex have been reported. Generalized weakness has been noted but is not a diagnostic sign of HES.
* Pulmonary signs
*
o Pleural effusions are common as a result of CHF.
o Diffuse or focal crackles may be appreciated as a result of pulmonary infiltration by eosinophils or by ensuing pulmonary fibrosis.
o Pleuritic chest pain and hypoxia can be caused by pulmonary emboli originating from the right side of the heart.
* GI signs
*
o Because HES can affect every abdominal organ, complaints of abdominal pain need to be immediately evaluated.
o Bowel necrosis, with the classic "pain out of proportion to examination," due to thromboembolic disease is life threatening.
o Splenomegaly is common.
* Rheumatologic signs
*
o Joint effusions can occur.
o The characteristic color changes of Raynaud phenomenon may be observed.
* Ocular signs: Occasional visual blurring may occur.

Therapy is geared toward reducing organ damage. Corticosteroids are the initial drugs of choice, and prednisone produces a response in approximately 66% of patients. A response to prednisone manifests as a reduction in the eosinophil count within 48 hours. Usually, the response is more rapid.

Imatinib, which blocks the effects of platelet-derived growth factor, has transformed the care of a large subset of patients with HES and can be helpful. It can lead to a sustained drop in the eosinophil count. However, because the causes of HES are variable, predicting the responsiveness of a patient to imatinib mesylate therapy remains difficult.

For conditions unresponsive to prednisone, chemotherapeutic and biologic agents can be used. The toxicity of these agents should always be considered, and the risk-benefit ratio of these treatments must be assessed.

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