Browsing by Subject "Rhabdomyolysis"

Now showing 1 - 3 of 3
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    A multistate transition model for statin‐induced myopathy and statin discontinuation
    (Wiley, 2021) Zhu, Yuxi; Chiang, Chien-Wei; Wang, Lei; Brock, Guy; Milks, M. Wesley; Cao, Weidan; Zhang, Pengyue; Zeng, Donglin; Donneyong, Macarius; Li, Lang; Biostatistics and Health Data Science, Richard M. Fairbanks School of Public Health
    The overarching goal of this study was to simultaneously model the dynamic relationships among statin exposure, statin discontinuation, and potentially statin-related myopathic outcomes. We extracted data from the Indiana Network of Patient Care for 134,815 patients who received statin therapy between January 4, 2004, and December 31, 2008. All individuals began statin treatment, some discontinued statin use, and some experienced myopathy and/or rhabdomyolysis while taking the drug or after discontinuation. We developed a militate model to characterize 12 transition probabilities among six different states defined by use or discontinuation of statin and its associated myopathy or rhabdomyolysis. We found that discontinuation of statin therapy was common and frequently early, with 44.4% of patients discontinuing therapy after 1 month, and discontinuation is a strong indicator for statin-induced myopathy (risk ratio, 10.8; p < 0.05). Women more likely than men (p < 0.05) and patients aged 65 years and older had a higher risk than those aged younger than 65 years to discontinue statin use or experience myopathy. In conclusion, we introduce an innovative multistate model that allows clear depiction of the relationship between statin discontinuation and statin-induced myopathy. For the first time, we have successfully demonstrated and quantified the relative risk of myopathy between patients who continued and discontinued statin therapy. Age and sex were two strong risk factors for both statin discontinuation and incident myopathy.
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    LBSAT311 Rhabdomyolysis: A Rare Presentation Of Hashimoto Thyroiditis In An Adolescent Boy
    (Oxford University Press, 2022-11-01) Saroufim, Rita; Eugster, Erica A.; Pediatrics, School of Medicine
    Introduction: Hashimoto thyroiditis is the most common cause of hypothyroidism and is associated with a wide range of clinical presentations in children and adolescents. Hypothyroidism-induced rhabdomyolysis without precipitating factors is extremely rare, particularly in pediatric patients. We describe a previously healthy adolescent boy who came to our institution with vague symptoms and was found to have rhabdomyolysis secondary to hypothyroidism due to Hashimoto thyroiditis. Clinical Case: A 16 year old boy presented to the emergency department at Riley Hospital for Children due to a two week history of bilateral eye and lip swelling. Additional symptoms included fatigue, sleepiness, slowing of speech, decreased attention span and weight gain. He was not on any medications and had no history of allergies. There was no family history of endocrine or neuromuscular disorders. Physical exam revealed a height of 177 cm (75th tile), weight of 118.4 kg (99th %tile) and BMI at the 99th %tile. Exam was significant for slow generalized movements, facial edema, and delayed deep tendon reflexes in all extremities. The thyroid gland was normal. Laboratory evaluation revealed Creatinine-1.46 mg/dL (0.3-1.2), ALT-88 Units/L (7-52), AST-254 Units/L (13-39), TSH-32.2 mcU/mL (0.4-4.2), fT4 <0.2 ng/dL (0.6-1.5) and CK 20,500 Units/L (30-223). Thyroid peroxidase antibody was elevated at 686.1 IU/mL. A renal and bladder ultrasound showed trace intra-abdominal ascites and decreased echogenicity of the bilateral psoas muscles favoring edema and consistent with rhabdomyolysis. He received IV hydration and was started on levothyroxine 25 mcg daily that was increased over a 10 month period to achieve euthyroidism. Genetic testing for rhabdomyolysis revealed two variants of unknown significance. Acyl carnitine and carnitine profiles were normal ruling out a metabolic myopathy. His symptoms improved significantly after treatment with levothyroxine although his CK levels plateaued around 1,000 Units/L. Liver and kidney function normalized during follow up. Conclusion: Rhabdomyolysis is a rare but serious complication of hypothyroidism, the pathogenesis of which is unclear. Proposed hypotheses include impaired mitochondrial oxidative metabolism, decreased muscle carnitine and switching of muscle fibers from fast-twitching type II to slow-twitching type I due to thyroxine deficiency ultimately leading to myolysis and release of intracellular muscle contents into the circulation. It is important for clinicians to have a high index of suspicion for hypothyroidism in children who present with muscle weakness and high creatinine kinase levels. The etiology of the disproportionately mild elevation of TSH in the setting of an unmeasurable free T4 and severe clinical hypothyroidism in our patient remains a mystery.
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    Robust critical limb ischemia porcine model involving skeletal muscle necrosis
    (Springer Nature, 2023-07-18) El Masry, Mohamed S.; Gnyawali, Surya C.; Sen, Chandan K.; Surgery, School of Medicine
    This work sought to develop a robust and clinically relevant swine model of critical limb ischemia (CLI) involving the onset of ischemic muscle necrosis. CLI carries about 25-40% risk of major amputation with 20% annual mortality. Currently, there is no specific treatment that targets the ischemic myopathy characteristic of CLI. Current swine models of CLI, with tolerable side-effects, fail to achieve sustained ischemia followed by a necrotic myopathic endpoint. Such limitation in experimental model hinders development of effective interventions. CLI was induced unilaterally by ligation-excision of one inch of the common femoral artery (CFA) via infra-inguinal minimal incision in female Yorkshire pigs (n = 5). X-ray arteriography was done pre- and post-CFA transection to validate successful induction of severe ischemia. Weekly assessment of the sequalae of ischemia on limb perfusion, and degree of ischemic myopathy was conducted for 1 month using X-ray arteriography, laser speckle imaging, CTA angiography, femoral artery duplex, high resolution ultrasound and histopathological analysis. The non-invasive tissue analysis of the elastography images showed specific and characteristic pattern of increased muscle stiffness indicative of the fibrotic and necrotic outcome expected with associated total muscle ischemia. The prominent onset of skeletal muscle necrosis was evident upon direct inspection of the affected tissues. Ischemic myopathic changes associated with inflammatory infiltrates and deficient blood vessels were objectively validated. A translational model of severe hindlimb ischemia causing ischemic myopathy was successfully established adopting an approach that enables long-term survival studies in compliance with regulatory requirements pertaining to animal welfare.