steroid induced myopathy can cause dyspnea in cancer patients

As a paraneoplastic endocrine syndrome resulting from the adrenocorticotropic hormone production by his lung cancer, cortisol-induced myopathy can occur and present several features consistent with the myopathy that occurs with exogenous intake of corticosteroids. Because the injury caused by steroids is to type 2 and type 4 collagen, the tempo of steroid-induced myopathy is usually weeks to months, which would be consistent with this patient’s time course. The myopathy is painless, and muscle enzyme levels are not elevated. Most notable in this patient is the normal alveolar-arterial (A-a) gradient (A-a gradient = PAO2 = FIO2 (PB [barometric pressure] − PH2O [water vapor pressure]) − PaCO2/R [respiratory quotient] = 21%(760 − 47) −72/0.8 = 60 − 58 = 2), which is consistent with a neuromuscular process as the cause of his respiratory dysfunction.

Because of the tumor size at initial presentation, with the resultant postobstructive pneumonia, there is the potential for recurrence of this infectious process on the basis of expansion of the tumor size. If hypoxemia were to occur owing to such a problem, the A-a gradient should be abnormal. The stability of the chest radiograph also argues against the recurrence of a postobstructive process.

The timeline for radiation pneumonitis, which is usually within the first 8 months, is consistent with this patient’s course. The effects of radiation on the lung characteristically include a decrease in FEV1 and impairment in DLCO. As the consequences of the injury become more progressive, oxygenation is affected. In such a situation, the A-a gradient would be abnormal, which is not the situation in this patient.

Immune checkpoint blockade can induce inflammatory adverse effects, termed immune‐related adverse events. Although any organ system can be affected, the lung can be a site of injury, with resultant checkpoint inhibitor pneumonitis (CIP). The median time to onset is about 2.8 months, with a range from 9 days to 19 months. Present thinking is that cytotoxic antigen-directed T-cell responses induced by the checkpoint inhibitors and directed against lung tissue drive the pathogenesis of CIP. Acute interstitial pneumonia, ARDS, cryptogenic organizing pneumonia, ground-glass opacities, nonspecific interstitial pneumonia, and hypersensitivity pneumonitis are some of the radiographic manifestations of CIP. Even though the time course of this patient’s illness is consistent with CIP, he had neither radiographic nor A-a gradient findings expected with CIP.123456

Footnotes

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