Hashimoto’s thyroiditis aggravated by goitrogenic diet presenting as rhabdomyolysis worsened by alcohol intake

Abstract

Hashimoto’s thyroiditis (HT) is the most common form of primary hypothyroidism. Several muscular manifestations like pain, weakness, stiffness and elevated muscle enzymes have been noticed in hypothyroidism. Alcohol is also known to cause myositis and rhabdomyolysis. Patients with thyroid should avoid certain foods like broccoli, cauliflower and cabbage as they contain goitrogens. This is a case of a young man who presented with severe muscle aches and pain and was found to have rhabdomyolysis. Further evaluation revealed an underlying HT. Moreover, he had been consuming raw broccoli, which is goitrogenic, and alcohol which worsened the rhabdomyolysis. He was managed with levothyroxine and intravenous fluids, following which he improved.

Background

Rhabdomyolysis is the disintegration of skeletal muscle and is characterised by muscle necrosis and the release of intracellular muscular components like myoglobin, creatine kinase (CK), aldolase, lactate dehydrogenase (LDH), aspartate aminotransferase and potassium into the circulation.¹ It can cause limb weakness, swelling, myalgia and passing of dark-coloured urine in the absence of haematuria. Myoglobinuria may be present. Hashimoto’s thyroiditis (HT) is a common form of primary hypothyroidism, where there is an autoimmune destruction of the thyroid gland. Proximal muscle weakness, pain or cramps are the musculoskeletal symptoms associated with hypothyroidism.² The condition can be worsened by the consumption of a large quantity of foods containing goitrogens. Several pharmaceutical agents and alcohol are known to cause rhabdomyolysis.³ Since both hypothyroidism and alcohol can cause rhabdomyolysis, this case projects the importance of assessing the thyroid status regularly and changing the diet if necessary.

Case presentation

A 36-year-old man presented with muscle aches and pains since 1 month, which had become severe over the last 1 week. He also noticed dark discolouration of urine since 2 days. He did not have any symptoms like weight gain, cold intolerance, dry skin, pedal oedema or constipation. On enquiring about his diet, he has been consuming large multiple servings of raw broccoli along with alcohol (90 mL brandy/day) for the past 2 weeks. He was not on any regular medications.

On presentation, he was conscious, oriented and afebrile. He was overweight with a body mass index of 26.72 kg/m² (weight 90 kg and height 177 cm). He had a hoarse voice, mild facial puffiness, mild pedal oedema and macroglossia. There was no obvious neck swelling. His pulse rate was 60/min and blood pressure was 130/80 mm Hg. Neurologically, he had sluggish deep tendon reflexes, but there was no muscle weakness, hypertrophy or rigidity. Other systemic examinations were normal.

Investigations

His blood investigations like complete blood counts, electrolytes, calcium, phosphorus, magnesium and haemoglobin A1c were normal. His renal functions were deranged with urea 76 mg/dL (10–40) and creatinine 1.87 mg/dL (0.9–1.3). His liver enzymes were elevated, that is, serum glutamic oxaloacetic transaminase 104 U/L (0–35) and serum glutamic pyruvic transaminase 72 U/L (0–45). His fasting lipid profile showed triglycerides 589 mg/dL (<150), low-density lipoprotein 199 mg/dL (<130), high-density lipoprotein 32 mg/dL (40–60) and very low-density lipoprotein 40 mg/dL (6–38). His ECG showed sinus bradycardia, but echocardiography was normal. Ultrasound abdomen revealed fatty liver (grade 2) and chest X-ray was normal. His LDH and CK levels were elevated, 375 U/L (114–240) and 739 U/L (24–190), respectively. Antinuclear antibody profile was negative. His urinary examination showed myoglobinuria, without pyuria or haematuria. His thyroid profile showed thyroid-stimulating hormone 68 μIU/mL (0.40–4.20), T3 20.6 ng/dL (40–181) and T4 0.88 µg/dL (4.60–10.50) and positive antithyroid peroxidase antibody of 2372 U/mL (<35), suggestive of HT. Ultrasound of neck revealed thyroiditis.

Treatment

He was started on oral levothyroxine, 100 µg as initial bolus dose followed by 50 µg/day, along with aggressive intravenous fluid administration (3000 mL of normal saline/day). Intravenous thiamine (100 mg three times per day) was also given.

Outcome and follow-up

By day 2 of admission, his renal parameters had started normalising. As the patient had shown symptomatic improvement, electromyography and muscle biopsy were not done. He was discharged on day 4 of admission with a normal creatinine and CK levels. He was prescribed oral levothyroxine 50 µg/day. He was also advised to avoid alcohol and goitrogenic foods like broccoli, cauliflower and cabbage. On follow-up after 2 months, the patient was asymptomatic. His blood reports showed a normal thyroid and lipid profile, liver and renal parameters, LDH and CK levels.

Discussion

Hypothyroidism is known to cause musculoskeletal problems including myopathy. About one-third patients with hypothyroidism present with proximal muscle weakness, cramps or pain and stiffness. Elderly age group, alcoholism and patients with diabetes, renal and hepatic diseases are at higher risk of developing hypothyroid myopathy. However, hypothyroid-induced rhabdomyolysis is a rare scenario and can be precipitated by trauma, exercise, alcohol and drugs like statins.^{4 5}

Rhabdomyolysis can present with a wide spectrum of manifestations, ranging from asymptomatic elevations in serum muscle enzymes to acute kidney injury. The classic triad includes myalgia, transient muscle weakness and passing of dark-coloured urine. However, this triad is present in less than 10% of the patients.⁶ Trauma is the most common aetiology. The nontraumatic causes include seizures, heat exposure, endocrine disorders, electrolyte imbalance, infections and heavy exercise.^{1 7}

Several hypotheses have been proposed with regards to the mechanism of rhabdomyolysis in hypothyroidism. These include impaired mitochondrial oxidative metabolism, induction of insulin-resistant state and decreased muscle carnitine levels.^{8 9} Thyroxine deficiency results in abnormal glycogenolysis, mitochondrial oxidative metabolism and triglyceride turnover. This in turn can lead to impaired muscular function by causing a transition of fast-twitching type 2 muscle fibres to slow-twitching type 1 fibres. There is also low myosin ATPase activity and low ATP turnover in the skeletal muscles.¹⁰

The pathophysiology of alcohol-induced rhabdomyolysis depends on the duration of intoxication. In short-term cases, immobilisation and coma are the main contributing factors while in long-term alcohol abuse, acid–base and electrolyte imbalances like hypokalaemia, hypophosphatemia, hypocalcaemia and hypomagnesaemia are the main underlying factors.^{11 12} However, there can also be the direct toxic on skeletal muscles by the disruption of the ATP pump, breakdown of the muscle membrane and alteration of sarcoplasmic reticulum. The induction of cytochrome P450 may cause disintegration of skeletal muscles.^{13 14}

Diet can also play an important role in hypothyroidism. Foods like collards, brussels sprouts, Russian kale, broccoli, cauliflower and cabbage contain goitrogens. These compounds when consumed in very large amounts can cause thyroid dysfunction. However, these goitrogenic compounds are mostly deactivated when the foods are cooked.

The common oral manifestations in hypothyroidism include macroglossia, dysgeusia, poor periodontal health, delayed eruption and wound healing and altered tooth morphology.¹⁵ Macroglossia occurs due to accumulation of matrix glycosaminoglycans in the interstitial space.

Our patient presented with symptoms of myalgia and was found to have rhabdomyolysis due to HT. His condition was worsened following consumption of alcohol and large quantities of raw broccoli.

Learning points.

• Rhabdomyolysis is a rare complication of hypothyroidism.

• Alcohol can also cause or precipitate rhabdomyolysis.

• Foods containing goitrogenic compounds when consumed raw and in large quantities can cause thyroid dysfunction.

• Hypothyroidism can have oral manifestations like macroglossia, dysgeusia, poor periodontal health, delayed eruption and wound healing and altered tooth morphology.

Ethics statements

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