Introduction: Thyroid dysfunction may cause a wide range of neurological disorders in children. Hypothyroidism is associated with peripheral nerve demyelination. However, minimal data are available in pediatric population.
Purpose: To describe a case of newly diagnosed Hashimoto thyroiditis (HT) suffering acute-onset rapidly progressive peripheral polyneuropathy.
Case Report: A 12-year-old girl presented for the first time to our Department because of a 2-week history of left upper limb weakness and paresthaesia. She was newly diagnosed with mild hypothyroidism due to HT and started on levothyroxine (LT4). On physical examination, she had diminished touch sensation on left upper limb and bilateral absence of knee reflexes. Electrophysiological study was indicative of acute sensory polyneuropathy and cerebrospinal fluid (CSF) examination revealed slightly elevated albumin with normal cell count. Based on these findings, the patient received intravenous immunoglobulin treatment with the suspicion of Guillain-Barré syndrome. The following days clinical deterioration was recorded; she had wide based standing, her gait was slightly ataxic and she developed acute onset moderately severe, continuous, burning pain affecting her left foot. Meanwhile, thyroid function evaluation questioned the need for LT4 substitution therapy since thyroid stimulating hormone levels were suppressed and free thyroxine concentration was elevated; HT was confirmed by high titers of antithyroid antibodies. Further detailed history and physical examination revealed signs and symptoms of hyperthyroidism (weight loss, tremor, anxiety, sleeplessness, palpitations, diarrhea). Based on negative thyroid stimulating immunoglobulin a diagnosis of iatrogenic hyperthyroidism was made. LT4 was discontinued and beta-blocker was prescribed because of severe tachycardia and hypertension leading to gradual clinical and biochemical improvement. Despite the normalisation of thyroid hormones, deterioration of weight loss and neuropathic pain alongside with secondary amenorrhea necessitated further evaluation of sensory polyneuropathy including anorexia nervosa. Potential causes of neuropathy (vitamin deficiency, metabolic, toxic, infectious, inflammatory, autoimmune, paraneoplastic, inherited) were excluded. On 6-month follow-up, the patient is euthyroid, while signs and symptoms of hyperthyroidism have resolved; she gained the lost weight and her menstruation normalised; however, glove and stocking distribution neuropathy has improved but persists. Based on this clinical course, HT can be considered the cause of neuropathy explaining also the slightly elevated CSF albumin levels.
Conclusion: This case experiencing the wide spectrum of thyroid dysfunction, from hypothyroidism to hyperthyroidism and finally to euthyroidism underlies the necessity of thyroid function evaluation in children with acute polyneuropathy. Symptoms of neuropathy may precede the diagnosis of hypothyroidism and persist despite normalisation of thyroid hormone levels.
19 - 21 Sep 2019
European Society for Paediatric Endocrinology