Endocrine Abstracts (2017) 49 EP1340 | DOI: 10.1530/endoabs.49.EP1340

Peripheral neuropathy in hypothyroidism - about a clinical case

José Marçalo, Alexandra Araújo, Carolina Faria, Ana Wessling, Maria Raquel Carvalho, Ema Nobre & Maria João Bugalho


Hospital de Santa Maria, Lisbon, Portugal.


Introduction: Hypothyroidism can affect the nervous system, commonly causing mono and polyneuropathies which show a variable frequency and pattern. Its mechanisms are not fully understood. Symptoms usually correlate better with the duration of the dysfunction rather than with its severity and typically improve significantly after medical therapy.

Case report: A 58-year-old woman was admitted at our hospital with a one-year history of progressive weakness of both lower extremities, more evident on her left limb. The patient reported a 20-year history of hypothyroidism medicated with levothyroxine 25mcg id and type 2 diabetes medicated with metformin 1000mg bid, without proper follow-up. She denied other relevant long-term medication or addictions. Fifteen days prior to admission, she was paraparetic and had lost her ability to walk. No other relevant personal or familial medical history was found. Neurological examination showed painless sensorimotor polyneuropathy and lower muscular strength on both legs. Laboratory results revealed hypothyroidism: TSH 37.1mU/L and FT4 0.5ng/dl. Serologic studies were negative and B12-deficiency was excluded, as well as other common causes of peripheral neuropathy. Lumbar MRI did not show spinal cord compression and cerebrospinal fluid analysis was inconclusive. Bilateral carpal tunnel syndrome and sensorimotor polyneuropathy, without criteria of Guillain-Barré syndrome, were found on electromyography (EMG). Furthermore, myopathic aspects compatible with muscular necrosis were detected, despite normal creatine kinase levels. Few weeks after progressively increasing levothyroxine dose, laboratory studies showed: TSH 10.2mU/L, FT4 1.27ng/dl, Anti-TPO 66U/mL. Unsatisfactorily controlled hyperglycemia persisted (HbA1c 10.2%). Paraparesis significantly improved and sensorimotor dysfunction subsided.

Conclusion: In general, sensorimotor peripheral neuropathy is common in diabetes and occasional in hypothyroidism. In the described case, it is difficult to ascertain the relative contribution of each nosological entity. Nevertheless, the clinical presentation, the EMG and the prompt response to levothyroxine, favor hypothyroidism as the main cause.

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