Case Report: Beyond metabolism: subclinical hypothyroidism associated with chronic alveolar hypoventilation

Subclinical hypothyroidism, characterized by elevated thyroid-stimulating hormone levels with normal thyroid hormone levels, is frequently overlooked as a cause of respiratory dysfunction. While thyroid disorders are known to affect multiple organ systems, their role in precipitating chronic alveolar hypoventilation remains under-recognized in clinical practice.

We report the case of a 48-year-old man with a body mass index (BMI) of 24.2 kg/m² who presented with a three-month history of excessive daytime sleepiness, morning headache, and mild exertional breathlessness. Physical examination revealed no obvious signs suggestive of thyroid or primary respiratory pathologies. Arterial blood gas analysis demonstrated compensated type II respiratory failure with hypercapnia (pCO₂, 62 mmHg) and compensatory metabolic alkalosis (HCO₃^-, 33 mEq/L). Pulmonary function tests revealed mildly decreased respiratory muscle strength, with a maximum inspiratory pressure (MIP) of 50 cmH₂O (45% predicted) and a maximum expiratory pressure (MEP) of 70 cmH₂O (47% predicted). Polysomnography confirmed sleep-related hypoventilation with an apnea-hypopnea index (AHI) of 3.2 events/h, oxygen desaturation index (ODI) of 2.8 events/h, and oxygen saturation nadir of 86%, effectively excluding obstructive sleep apnea (OSA). Thyroid function tests revealed subclinical hypothyroidism with elevated TSH (8.7 μIU/mL) but normal free thyroxine (T4) (1.2 ng/dL) and triiodothyronine (T3) (110 ng/dL) levels. Elevated anti-thyroid peroxidase antibody levels (120 IU/mL) suggested autoimmune thyroiditis.

Levothyroxine (50 μg/day) was initiated with a target TSH of 0.4-2.5 μIU/mL as per the European Thyroid Association guidelines, along with lifestyle modifications, including breathing exercises and moderate aerobic activity. After 2 months, the TSH level decreased to 2.1 μIU/mL. Complete normalization of gas exchange was achieved within 3 months (pCO₂: 44 mmHg, HCO₃^-: 26 mEq/L, pH: 7.41, TSH: 2.6 μIU/mL), with resolution of all symptoms. The patient's body weight remained stable throughout the follow-up period. Sustained improvement with no recurrence was documented at 6 months and 1 year.

This case highlights the important temporal association between subclinical hypothyroidism and chronic alveolar hypoventilation. Although causality cannot be definitively established, the complete resolution following levothyroxine therapy suggests a clinically relevant relationship. This emphasizes the importance of thyroid function screening in patients with unexplained respiratory compromise after the exclusion of common causes.