A 68-year-old Caucasian female was admitted to a referral pulmonary institute for additional testing for suspected sarcoidosis. She had been treated with drugs for hyperthyroidism for about 35 years. However, around 12 months prior to the admission, she developed weakness, malaise, and a feeling of heart palpitations. An endocrinologist evaluated the patient multiple times. Since the hormone values (T3, T4, and TSH) were still irregular even after the prescribed therapy, she was treated surgically three months before the hospitalization. A total thyroidectomy was performed and definitive pathohistological findings revealed a polynodous goiter with numerous diffuse noncaseating granulomas whose morphology, number, and localization were typical of thyroid sarcoidosis (Figures 4C,D). Once the diagnosis of thyroid sarcoidosis was suspected, the patient was referred to a pulmonologist for further evaluation. At admission, she denied having any other comorbidity except thyroidectomy-associated hypothyroidism, which was managed with oral levothyroxine 50 mcg daily. She reported a positive family history of pulmonary tuberculosis. The psycho-social history as well as the physical examination were unremarkable.
Blood laboratory findings at the admission revealed elevated values of serum ACE, while other biochemical parameters, including the levels of serum calcium and calcium in 24-h urine, were within reference range (Table 1). Chest X-ray and HRCT scans were without lesions in the lung parenchyma and lymphadenopathy. Pulmonary function tests and gas exchange at rest and during exertion were preserved. Histopathological examination of transbronchial and bronchial biopsies revealed non-necrotizing granulomas consistent with sarcoidosis (Figures 4A,B). The ultrasound examination of the upper abdomen as well as the ophthalmological examination did not reveal any sarcoidosis extension. Considering family history, a thorough assessment of pulmonary tuberculosis was done, and it was excluded since acid-fast staining of the patient's sputum and lung biopsies showed the absence of acid-fast bacilli, while cultures of Mycobacterium tuberculosis and other mycobacteria later on grew negative. The patient also had a negative result on the QuantiFERON TB-Gold In-Tube test. Other causes of granulomatous inflammation, such as fungal infection, were excluded as well, since fungal cultures of sputum and lung biopsies grew negative, while staining of lung biopsies was negative for fungal infection. During the cardiac evaluation, a heart rhythm disorder was recorded (left bundle branch block and first-degree atrioventricular block). Positron emission tomography/computed tomography was performed due to the suspicion of cardiac sarcoidosis; however, only bilateral hilar accumulation of radiopharmaceutical was observed. Once this diagnostic algorithm was finished, we decided not to administer steroids treatment, and the patient was discharged with thyroid substitution therapy (oral levothyroxine 50 mcg per day), while the cardiologist recommended conservative therapeutic approach of heart rhythm disorder. At the follow-up pulmonology visit 3 months later, the patient denied having any respiratory symptoms; the chest X-ray revealed no pathological alternations; and the serum ACE levels were now within the reference range. Without changing the treatment, she was followed every 3 months for the next 12 months until she stopped coming to scheduled controls.
Patients agreed to our treatment plan and were thankful for the assistance provided. Since the patients stopped visiting our pulmonary institute after a certain period of follow-up, we contacted them by phone at the time of writing the study and received information that both patients are being monitored by endocrinologists, and periodically have check-ups with local pulmonologists, without symptoms characteristic of sarcoidosis.