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Case Presentation A 64-year-old man presented for consideration for lung transplant. He had a history of previous tobacco use, OSA on CPAP therapy, and gastroesophageal reflux disease. He worked as a design engineer. The patient had a 4-year history of dyspnea on exertion, followed with periodic CT scan of the chest. Nine months prior to his evaluation for lung transplant, the patient developed worsening of dyspnea, dry cough, poor appetite, and weight loss. At times, the cough was violent and associated with chest pressure. He was prescribed systemic corticosteroids and antibiotics without improvement. Four months later, the patient noted sudden onset of severe chest pain and worsening dyspnea. A CT scan of the chest demonstrated extensive pneumomediastinum in addition to changes consistent with pulmonary fibrosis. An esophagogram showed thickening of the distal esophagus, but no signs of perforation. He was prescribed supplemental oxygen and advised to stop the use of CPAP. The patient sought a second opinion. A CT scan of the chest showed improvement of the pneumomediastinum and extensive fibrotic lung disease. Pulmonary function tests (PFTs) were consistent with a restrictive pattern, decreased diffusing capacity (Dlco), and a preserved residual volume over total lung capacity ratio. The patient was prescribed systemic corticosteroids with no improvement of his symptoms. Repeat PFTs showed further decline of Dlco, and he was referred for lung transplant evaluation.

A 51-year-old man was admitted for evaluation of new-onset generalized seizures in the context of progressive and significant behavioral change. His medical history was only notable for previous outbreaks of genital herpes. He took no medications. He had occasional social alcohol use and no illicit drug use but was a 35-pack-year current smoker. The patient had no relevant occupational exposure history but had recently traveled to Panama. Initially, the patient's significant other noticed a progressive flattening of his affect. The patient then started to experience episodes of "passing out" that led to injuries prompting ED visits. He was prescribed antiseizure medications and scheduled for an outpatient workup. However, with progressive gait instability, lethargy, and an increase in frequency of generalized seizures, the patient was admitted for treatment of suspected viral encephalitis. Despite initiation of antimicrobial and antiviral therapy, the patient's level of alertness continued to decline, ultimately leading to intubation for airway protection.

A 40-year-old woman (a nonsmoker) with history of idiopathic thrombocytopenic purpura and a platelet count > 90,000 cells/μL without specific medication was referred to pulmonary clinic for evaluation of multiple pulmonary nodules. The patient presented to an outside hospital with fatigue, lack of energy, and dyspnea on exertion for 2 years. She denied fever, cough, chest pain, or weight loss. An initial chest radiograph showed bilateral multiple pulmonary nodules. A chest CT scan revealed multiple nodular lesions, varying in size, in all lobes of both lungs. There was no mediastinal lymphadenopathy or pleural effusion. There was no significant hypermetabolic activity on a subsequent fluorodeoxyglucose PET scan/CT scan, and there had been no significant change. She underwent CT scan-guided percutaneous transthoracic biopsy and bronchoscopy with transbronchial biopsies, all of which were inconclusive. An open lung biopsy was considered.

A 60-year-old woman was referred to the pulmonary clinic for evaluation of lung nodules. Her medical history was notable for hypothyroidism, anxiety, and a ruptured breast implant for which incomplete surgical resection and evacuation had been performed 10 years previously. She was a lifelong nonsmoker and worked as a gym instructor. The patient denied occupational exposures and had not traveled recently. Medications included levothyroxine and alprazolam. Except for a 1-month history of occasional dry cough, the review of systems was negative. The patient's physician queried whether the previously ruptured silicone breast implant may have played a role in the genesis of the nodules and referred the patient to our institution for further management. The lack of systemic symptoms relative to the degree of lung involvement provided an early diagnostic clue.

Rationale: Although there have been reports of pulmonary toxicity with low-dose amiodarone, it is generally believed that low-dose therapy is safe. Methods: The clinical data for eight patients identified from a retrospective chart review are presented. Results: All of the patients were receiving amiodarone, 200 mg/d, for an average of 2 years. The average age was 77 years (range, 65 to 89 years). Seven of the eight patients were male. Seven of the eight patients presented with dyspnea on exertion, and three of the eight patients presented with cough. All of the patients had a clinical diagnosis of amiodarone-induced pulmonary toxicity. Open-lung biopsies were obtained on two patients that were consistent with amiodarone-induced pulmonary toxicity. None of the patients were in congestive heart failure. Treatment involved cessation of amiodarone. In addition, three patients received corticosteroids. Five of the patients improved symptomatically with this conservative approach, and four patients improved radiographically. One patient died with progressive respiratory insufficiency (presumably from amiodarone pulmonary toxicity). One patient was unavailable for follow-up. Conclusion: Amiodarone-induced pulmonary toxicity can occur at a daily dose of 200 mg. Clinicians must remain alert to this possibility even with this low-dose therapy.

A 40-year-old woman (a nonsmoker) with history of idiopathic thrombocytopenic purpura and a platelet countgt; 90,000 cells/μL without specific medication was referred to pulmonary clinic for evaluation of multiple pulmonary nodules. The patient presented to an outside hospital with fatigue, lack of energy, and dyspnea on exertion for 2 years. She denied fever, cough, chest pain, or weight loss. An initial chest radiograph showed bilateral multiple pulmonary nodules. A chest CT scan revealed multiple nodular lesions, varying in size, in all lobes of both lungs. There was no mediastinal lymphadenopathy or pleural effusion. There was no significant hypermetabolic activity on a subsequent fluorodeoxyglucose PET scan/CT scan, and there had been no significant change. She underwent CT scan-guided percutaneous transthoracic biopsy and bronchoscopy with transbronchial biopsies, all of which were inconclusive. An open lung biopsy was considered.

Nontuberculous mycobacteria (NTM) are increasingly recognized as important pulmonary pathogens. Mycobacterium avium intracellulare complex (MAC) causes most lung infections due to NTM. Patients with preexisting lung disease or immunodeficiency are at greatest risk for developing MAC infection. The majority of MAC pulmonary cases, however, occur in immunocompetent elderly women in association with nodular infiltrates and bronchiectasis. More recently, pulmonary disease has also been described in immunocompetent patients after exposure to MAC-contaminated hot tubs. We describe a case of aggressive MAC lung disease in a young immunocompetent female patient without preexisting lung disease whose clinical and pathologic characteristics do not fit into any of these categories and may represent a unique manifestation of MAC lung disease.