Severe proximal myopathy secondary to Hashimoto’s thyroiditis

Abstract

Muscular symptoms in hypothyroidism are common, including myalgia, fatigue and cramps; however, a significantly raised creatine kinase and muscle weakness are rare. Differential diagnosis of patients presenting with muscle weakness and a raised creatine kinase is wide, and hypothyroidism is rarely considered. We report this case of a 30-year-old female presenting with proximal muscle weakness as her primary symptom, hypothyroid symptoms of 3-month duration and a significantly raised creatine kinase. After ruling out other causes of a raised creatine kinase, thyroxine replacement was commenced, which led to complete resolution of her proximal weakness, myalgia and normalisation of creatine kinase level. This case illustrates severe proximal myopathy can be secondary to hypothyroidism, symptoms can resolve with thyroxine replacement and emphasises the importance of measuring thyroid function in patients with proximal weakness/myalgia and a significantly raised creatine kinase.

Background

Myopathy can present with muscle weakness/myalgia and typically has a raised creatine kinase. There are numerous causes of myopathy including infectious, autoimmune and iatrogenic. Hypothyroidism commonly presents with muscular symptoms including myalgia, fatigue and cramps, however is rarely considered as a cause of proximal myopathy and a significantly raised creatine kinase.^{1 2}

Case presentation

A 30-year-old female part-time teacher was referred by her general practitioner with a 3-month history of global muscle weakness, myalgia and frequent muscle spasms. She also reported a history of cold intolerance, weight gain and tiredness for 2–3 months. She delivered her son 3–4 months prior to these symptoms and, 2 months after delivery, noticed palpitations, insomnia and tiredness that resolved spontaneously.

She was a non-smoker, did not consume alcohol and had no other past medical history. She was not on any prescription or over the counter medications or food supplements. There was no family history of thyroid problems. Clinical examination revealed a normal built young woman. Vital signs were within normal limits. Examination of the respiratory system, cardiovascular system, abdomen and extremities were unremarkable. There was evidence of proximal, symmetrical muscle weakness with muscle tenderness, dry skin and a small non-tender symmetrical goitre. There was no sensory disturbance or signs of encephalopathy. The deep tendon reflexes were normal. Her creatine kinase was elevated at 5124 U/L.

Investigations

Hypothyroidism was suspected initially due to her clinical presentation; however, given the extent of creatine kinase level rise and muscle weakness with tenderness, investigations were performed to exclude other causes of myopathy. These included viral screen (cytomegalovirus, Epstein-Barr virus and hepatitis B and C), 9 am serum cortisol, serum prolactin, serum vitamin B12 and 25OH vitamin D, all of which were normal. Rheumatological screening tests (including ESR, rheumatoid factor and auto-antibody screen) were normal. The liver autoimmune profile was checked in view of a raised bilirubin of 24 μmol/L (normal range <21) and ALT at the level 77 IU/L (normal range –5 to 45), which was also normal.

Severe primary hypothyroidism due to Hashimoto’s thyroiditis was confirmed with a significantly raised thyroid-stimulating hormone (TSH) 190mU/L (normal range 0.35–4.7), free T4 <5 pmol/L (normal range 7.8–21) and free T3 2.7 pmol/L (normal range 3.8–6). Thyroid peroxidase antibodies were >1000 U/mL (normal 0–75).

Treatment

The patient was treated with intravenous fluids, and despite having an unclear diagnosis for the cause of her myopathy, she was commenced on levothyroxine replacement for her hypothyroidism.

Outcome and follow-up

Treatment with levothyroxine led to normalisation of creatine kinase and complete resolution of her proximal myopathy over a period of 4 months.

Discussion

The pathophysiology of increased creatine kinase in hypothyroidism is poorly understood. Myofiber degeneration and decreased rate of clearance of creatine kinase enzyme from circulation have been suggested.³ Slowed muscle contraction and relaxation in hypothyroid myopathy may be due to a shift in the distribution of muscle fibre types to slow-twitch from fast-twitch fibres.

Previous cases have reported statin-induced hypothyroid myopathy⁴; myopathy due to relative hypothyroidism resulting from rapid thyroid hormone reduction in a hyperthyroid patient⁵; and myopathy that resolved with thyroxine administration; however, this patient was clinically euthyroid on presentation and did not have proximal weakness on examination⁶; a hypothyroid patient with associated myopathy but with a TSH level far lower (50) than the patient in this case report.⁷ In our case, there was neither statin use nor any other precipitants. In contrast to a case reported by Scott KR et al,² where the serum creatine kinase was over 29 000 U/L, the serum creatine kinase elevation in our patient was modest (5124 U/L).

Although there have been previous reports of hypothyroidism presenting with overt myopathy, classical symptoms and signs of hypothyroidism were absent.⁸ Our case is noteworthy, in that there was a simultaneous onset of clinical symptoms of both hypothyroidism and proximal myopathy over a period of 3 months, with evidence of severe proximal myopathy on examination and complete resolution of symptoms and normalisation of creatine kinase with thyroxine replacement. The higher TSH level in this patient compared with previous cases suggests that the level of TSH does not necessarily correlate with the level of creatine kinase or degree of myopathy.⁶

There are no existing guidelines regarding the investigation of proximal weakness and raised creatine kinase. National Institute for Health and Care Excellence clinical knowledge summary does not advise routine measurement of creatine kinase in patients with persistent hypothyroid symptoms.⁹

Learning points.

• Hashimoto’s hypothyroidism can present with severe myopathy consisting of muscle weakness and myalgia.

• Symptoms of myopathy can be simultaneously present with hypothyroid symptoms and resolve with thyroxine administration.

• Expect the recovery of myopathy to lag behind by 3–6 months after normalisation of thyroid-stimulating hormone.

• Thyroid status and function should be routinely examined/tested in cases presenting with either myopathy or a raised creatine kinase.