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Case Study Spinal Gout

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Case Study Spinal Gout
Objectives: Retrospective case discussion of a patient who was empirically treated for spinal gout and review of relevant literature. that presented with lower extremity weakness
Results: A 77 year old male presented with new onset paraparesis that developed over 3 days. CT and MRI imaging was suggestive of spinal gout but patient refused a spinal biopsy. He was empirically treated with high dose steroids and his lower extremity weakness started improving in 3 days.
Conclusion: Although gout is common, spinal gout is extremely rare. …..
Keywords: Spinal gout, paraparesis, tophi

Introduction:

Case Report:
A 77 year old, African American male, with past medical history of hypertension, untreated hepatitis C and gout came to the ED with complaints
…show more content…
Thus, he was started empirically on high dose steroids for three days and then tapered down with Prednisone orally. His lower extremity strength improved to 4/5 during his hospitalization by day 3. He was discharged on oral prednisone and sent to acute rehab. He was later re-admitted 2 months later for a gluteal abscess and at that time lower extremity muscle strength was 5/5 in his lower extremities and he was ambulatory. Consent was obtained from the patient to publish his case and any case related …show more content…
Hyperuricemia can occur due to decreased renal uric acid excretion or increased uric acid production. Non-modifiable risk factors include male gender, postmenopausal, advanced age, or Pacific Islander descent. Modifiable risk factors for gout include obesity, diet with high meat or seafood content, alcohol, drinks with high fructose or sucrose, hypertension, chronic kidney disease, organ transplant recipients and certain medications such as thiazide or loop diuretics. Although these risk factors inc hyperuricemia, not all individuals will develop signs or symptoms of gout. There are 28 genome loci that have been identified to be associated with gout (TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and

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