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icd 10 ataxia
Ataxia-telangiectasia is an autosomal backward anarchy acquired by a birthmark in the ATM gene mapped to chromosome 11q22.3. The ATM gene artefact is complex in the apprehension of damaged DNA and plays a analytical role in the progression of the corpuscle aeon from G1 to S appearance and G2 to M phase.[1] In the accident of DNA damage, ATM kinase phosphorylates p53 (a bump suppressor protein), which serves as a transcriptional activator of genes that arrest the corpuscle aeon or advance to apoptosis.[2] This adjournment allows the corpuscle to adjustment the damaged DNA. In the absence of ATM kinase, p53 is clumsy to anticipate the corpuscle from advanced to the abutting appearance of the corpuscle cycle, which may advance to the manual of inappropriate abiogenetic advice to the babe cells.
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The abundance of ataxia-telangiectasia is about 1 in 20,000-100,000 in the United States[3] and is best arresting in ethnicities with a aerial abundance of consanguinity.
The analytic manifestations of ataxia-telangiectasia arise amid 1-4 years of age and accommodate accelerating cerebellar ataxia, dysarthric speech, oculomotor apraxia, telangiectasia of the conjunctivae, choreoathetosis, allowed deficiency, and common infections.[4] These patients additionally accept an added accident of diabetes mellitus; radiation sensitivity; and cancer, decidedly leukemia and lymphoma.[4]
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Laboratory abnormalities accommodate animated AFP levels, immunoglobulin deficiency, alternate translocations amid chromosomes 7 and 14, acutely depleted levels of ATM protein, and radiosensitivity approved by in vitro assay. Cerebellar decline may additionally be apparent on MRI.[5] A serum AFP akin 2 accepted deviations aloft accustomed for age, forth with analytic manifestations, is analytic for ataxia-telangiectasia.[6] The action can additionally be diagnosed with accelerated immunoblotting appraisal for ATM, which is acutely depleted in best patients with ataxia-telangiectasia.[7]
Management of ataxia-telangiectasia is targeted against ache manifestations. Intravenous immunoglobulin backup analysis can be acclimated for individuals with common and astringent infections.[8] Antibiotic prophylaxis may be advised in patients with alternate sinopulmonary infections.[8]
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Physical and anatomic analysis should be accomplished aboriginal to aerate functionality and abbreviate contractures and scoliosis.
Patients should be monitored for signs of aboriginal cancer, such as weight loss, bruising, localized swelling, or pain. Analytic tests involving ionizing radiation should be abhorred to abbreviate the accident for DNA mutations and consecutive cancer.
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The cast for ataxia-telangiectasia is poor attributable to its multisystem involvement. Currently, there are no disease-modifying agents for the ataxic symptoms, and abounding patients advance blight and pulmonary ache from alternate infections. The average age of afterlife is about 25 years, and no therapies accept apparent to decidedly adapt the advance of the disease.
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