Occult Pulmonary Neuroendocrine Tumor Causing Severe Hyperparathyroidism: Diagnostic Challenges and Clinical Outcomes.

Background/Objective: Ectopic tumoral production of parathyroid hormone (PTH) is rare. The incidence of hyperparathyroidism and osteitis fibrosa cystica (OFC) secondary to ectopic PTH secretion has only been reported in case reports, although infrequent. Case Report: We report a case of a well-differentiated pulmonary neuroendocrine tumor (NET) producing PTH that presented with severe hypercalcemia and OFC. Surgical removal of the pulmonary tumor resulted in resolution of hypercalcemia. Immunocytochemical analysis of the tumor tissue revealed PTH-positive staining. Recovery was complicated by severe hypocalcemia due to hungry bone syndrome. Discussion: To the best of our knowledge, this is the first documented case of a pulmonary NET causing OFC via PTH. We further describe the successful identification and resection of a rare NET and restoration of calcium homeostasis with aggressive calcium and vitamin D repletion. Conclusion: Although a rare cause of severe hypercalcemia and OFC, ectopic tumoral production of PTH must be considered in the differential diagnosis. Furthermore, resection of these tumors secreting PTH can lead to a protracted and severe high risk of hungry bone syndrome, which requires aggressive treatment to maintain calcium homeostasis.

Association of Need for Tracheotomy With Decreasing Mechanical In-Exsufflation Flows in Amyotrophic Lateral Sclerosis.

Although patients with lower motor neuron and myopathic disorders can prolong their lives by depending on continuous noninvasive ventilatory support, most patients with amyotrophic lateral sclerosis (ALS) cannot and must use tracheostomy mechanical ventilation to prolong survival. This case demonstrates that this occurs because amyotrophic lateral sclerosis patients' upper motor neuron reflex laryngeal closure and stridor cause upper airway collapse that renders mechanical insufflation-exsufflation (MIE) ineffective in expulsing airway secretions as well as for permitting continuous noninvasive ventilatory support. A decrease in MIE-exsufflation flows is a marker for a decrease in upper airway patency that renders MIE ineffective. As airway secretions accumulate and baseline oxyhemoglobin saturation decreases, tracheotomy becomes necessary for further survival. This case demonstrates an association between diminishing MIE-exsufflation flow and need to resort to tracheotomy.