Case presentation

A 62-year-old woman presented to an outpatient clinic with approximately four weeks of progressive fatigue, generalized muscle pain, weakness, and increasing difficulty rising from bed and walking. Her medical history included hypothyroidism, cerebrovascular accident with residual visual sequelae, prior deep venous thrombosis of the left lower extremity, type 2 diabetes mellitus, dyslipidemia, and prior right lower-extremity varicose vein surgery. Her medications included levothyroxine 125 mcg daily, metformin 750 mg, and rosuvastatin 20 mg daily, which she had been taking for approximately four months before presentation.

At the first outpatient visit, vital signs were stable, including blood pressure of 129/77 mmHg and a pulse of 87 beats per minute. Cardiopulmonary examination was normal, and neurologic examination did not reveal focal deficits. Given the patient’s progressive weakness, generalized myalgia, and history of hypothyroidism and statin exposure, laboratory evaluation was requested, including complete blood count, renal function, hepatic profile, inflammatory markers, thyroid function, urinalysis, and CK.

At a second outpatient visit, the patient returned with the requested laboratory results and ultrasound findings.

Initial laboratory testing demonstrated severe hyperCKemia with CK of 8,586 U/L. C-reactive protein (CRP) was elevated at 150.6 mg/L, erythrocyte sedimentation rate (ESR) was 66 mm/hour, lactate dehydrogenase (LDH) was 437 U/L, aspartate aminotransferase (AST) was 219 U/L, and alanine aminotransferase (ALT) was 210 U/L. Serum creatinine was preserved at 0.48 mg/dL. Hemoglobin was 11.7 g/dL, hematocrit was 34.9%, and platelet count was 437,000/mm3. Thyroid testing showed a thyroid-stimulating hormone (TSH) of 3.5 µIU/mL and a free thyroxine (T4) of 1.4 ng/dL, arguing against overt hypothyroidism as the sole explanation for the degree of CK elevation.

On examination at the second outpatient visit, the patient had diffuse muscle tenderness and decreased strength involving both the upper and lower extremities. Cardiopulmonary examination remained normal, and no focal neurologic deficits were identified.

Abdominal ultrasound demonstrated hepatic steatosis (Figure 1), and thyroid ultrasound was consistent with chronic thyroiditis (Figure 2).

Figure 1: Abdominal ultrasound demonstrating hepatic steatosisAbdominal ultrasound obtained from the patient presented in this case. The arrow indicates the hepatic parenchyma demonstrating diffuse increased echogenicity consistent with hepatic steatosis

Figure 2: Thyroid ultrasound consistent with chronic thyroiditisThyroid ultrasound obtained from the patient presented in this case. The arrow indicates the heterogeneous thyroid parenchyma consistent with chronic thyroiditis

Given the marked CK elevation, progressive weakness, statin exposure, and elevated inflammatory markers, severe rosuvastatin-associated myopathy was suspected. The differential diagnosis included toxic statin myopathy, statin-associated immune-mediated inflammatory myopathy, polymyositis, and hypothyroid-related myopathy. At the second outpatient visit, rosuvastatin was discontinued, urgent rheumatology and endocrinology referrals were arranged, and autoimmune testing was requested, including antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), anti-Jo-1 antibody, anti-Mi-2 antibody, and anti-SRP antibody. Because of the marked CK elevation, progressive weakness, and the risk of complications, the patient was also urgently referred to the emergency department of a public hospital for further evaluation and stabilization. According to information subsequently provided by the patient’s family, she was hospitalized for four days. The author did not have access to the hospital records and therefore could not verify the investigations performed, treatment administered, or clinical response during admission.

After discharge, the patient continued specialist care within the public hospital system and did not return to the author’s outpatient clinic. Subsequent laboratory tests through day 54 were ordered by other treating physicians at other clinical facilities but were performed by the laboratory associated with the author’s clinic; therefore, the results remained accessible in the clinic record. The author could not verify the subsequent specialist management, the completion of the requested autoimmune testing, the recovery of muscle strength, final specialist diagnosis, or long-term clinical outcome.

Serial laboratory follow-up demonstrated persistent hyperCKemia with gradual improvement (Table 1). CK increased to 9,239 U/L on day 22 and then decreased to 7,018 U/L on day 38 and 3,550 U/L on day 54. AST and ALT peaked at 342 U/L and later decreased to 233 U/L and then 120 U/L. Renal function remained preserved throughout follow-up, with a creatinine of 0.54 mg/dL on day 54.

Clinical day | CK (U/L) | AST (U/L) | ALT (U/L) | CRP (mg/L) | ESR (mm/hour) | Creatinine (mg/dL)
Day 1 | 8,586 | 219 | 210 | 150.6 | 66 | 0.48
Day 22 | 9,239 | 342 | 342 | NA | 13 | NA
Day 38 | 7,018 | 233 | 233 | 16.1 | NA | NA
Day 54 | 3,550 | 120 | 120 | 304.2* | 120 | 0.54

On day 54, inflammatory markers again increased, with a CRP of 304.2 mg/L and an ESR of 120 mm/hour. Concurrent urinalysis and urine culture demonstrated urinary tract infection due to Escherichia coli with >100,000 colony-forming units (CFU)/mL, limiting the interpretation of inflammatory markers as direct markers of myositis activity at that time.