A 66-Year-Old Man with Abnormal Thyroid Function Tests
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SYMPTOMS TO DIAGNOSIS GREGORY W. RUTECKI, MD, Section Editor YAZAN N. ALHALASEH, MD ZAID A. ABDULELAH, MD AHMAD O. ARMOUTI, MD AYMAN A. ZAYED, MD, MSc, FACE, FACP Department of Internal Medicine, King Istishari Hospital, Amman, Jordan King Hussein Medical Center, Professor of Medicine and Chief, Division of Endocrinology, Hussein Cancer Center, Amman, Jordan Amman, Jordan Diabetes, and Metabolism, Department of Internal Medicine, Jordan University Hospital, Amman, Jordan A 66-year-old man with abnormal thyroid function tests 66-year-old man presented to the emer- daily and atorvastatin 20 mg daily. He was A gency department with increasing short- compliant with his medications. ness of breath and productive cough, which Though he usually received an infl uenza had begun 5 days earlier. Three years previ- vaccine every year, he did not get it the previ- ously, he had been diagnosed with chronic ob- ous year. Also, 3 years previously, he received structive pulmonary disease (COPD). the 23-valent pneumococcal polysaccharide One week before the current presentation, vaccine (PPSV23), and the year before that he developed a sore throat, rhinorrhea, and na- he received the pneumococcal conjugate vac- sal congestion, and the shortness of breath had cine (PCV13). In addition, he was immunized started 2 days after that. Although he could against herpes zoster and tetanus. speak in sentences, he was breathless even at The patient had smoked 1 pack per day for rest. His dyspnea was associated with noisy the past 38 years. His primary care physician breathing and cough productive of yellowish had advised him many times to quit smoking. sputum; there was no hemoptysis. He reported He had enrolled in a smoking cessation pro- He presented fever, but he had no chills, night sweats, chest gram 2 years previously, in which he received pain, or paroxysmal nocturnal dyspnea. The re- varenicline in addition to behavioral counsel- with an acute view of other systems was unremarkable. ing in the form of motivational interviewing exacerbation His COPD was known to be mild, in and a telephone quit-line. Nevertheless, he of COPD Global Initiative for Chronic Obstructive continued to smoke. Lung Disease (GOLD) grade 1, group A. His He was a retired engineer. He did not drink requiring postbronchodilator ratio of forced expiratory alcohol or use illicit drugs. hospitalization volume in 1 second (FEV1) to forced vital capacity (FVC) was less than 0.70, and his ■ PHYSICAL EXAMINATION FEV1 was 84% of predicted. Apart from mild On physical examination, the patient was sit- intermittent cough with white sputum, his ting up in bed, leaning forward. He was alert COPD had been under good control with in- and oriented but was breathing rapidly and haled ipratropium 4 times daily and inhaled looked sick. He had no cyanosis, clubbing, pal- albuterol as needed. He said he did not have lor, or jaundice. His blood pressure was 145/90 shortness of breath except when hurrying on mm Hg, heart rate 110 beats per minute and level ground or walking up a slight hill (Modi- regular, respiratory rate 29 breaths per minute, fi ed Medical Research Council dyspnea scale and oral temperature 38.1°C (100.6°F). His grade 1; COPD Assessment Test score < 10). oxygen saturation was 88% while breathing In the last 3 years, he had 2 exacerbations of room air. His body mass index was 27.1 kg/m2. COPD, 1 year apart, both requiring oral pred- His throat was mildly congested. His neck nisone and antibiotic therapy. veins were fl at, and there were no carotid Other relevant history included hyperten- bruits. His thyroid examination was normal, sion and dyslipidemia of 15-year duration, for without goiter, nodules, or tenderness. which he was taking candesartan 16 mg twice Intercostal retractions were noted around doi:10.3949/ccjm.86a.19024 the anterolateral costal margins. He had no 666 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 86 • NUMBER 10 OCTOBER 2019 Downloaded from www.ccjm.org on September 23, 2021. For personal use only. All other uses require permission. ALHALASEH AND COLLEAGUES chest wall deformities. Chest expansion was TABLE 1 reduced bilaterally. There was hyperresonance bilaterally. Expiratory wheezes were heard Initial laboratory results over both lungs, without crackles. a His heart had no murmurs or added sounds. Test Value Reference range There was no lower-limb edema or swelling. Hemoglobin 15.9 g/dL 13.5–17.5 g/dL The rest of his physical examination was un- White blood cell count 16.7 x 109/L 4.5–11.0 × 109/L remarkable. Neutrophils 85% 40%–75% Chest radiography showed hyperinfl a- tion without infi ltrates. Electrocardiography Lymphocytes 10% 20%–45% showed normal sinus rhythm, with a peaked P Monocytes 3% 2%–10% wave (P pulmonale) and evidence of right ven- Eosinophils 1% 1%–6% tricular hypertrophy, but no ischemic changes. Basophils 1% 0%–1% Results of initial laboratory testing are 9 9 shown in Table 1. Platelet count 260 x 10 /L 150–400 × 10 /L Assessment: A 66-year-old man with Sodium 136 mmol/L 135–145 mmol/L GOLD grade 1, group A COPD, presenting Potassium 5.1 mmol/L 3.5–5.2 mmol/L with a severe exacerbation, most likely due to Blood urea nitrogen 15 mg/dL 7–20 mg/dL viral bronchitis. Creatinine 1.0 mg/dL 0.5–1.1 mg/dL ■ INITIAL MANAGEMENT Glucose 110 mg/dL 70–140 mg/dL The patient was given oxygen 28% by Ven- Calcium 9.5 mmol/L 8.9–10.1 mmol/L turi mask, and his oxygen saturation went up Albumin 3.7 g/dL 3.5–5.5 g/dL to 90%. He was started on nebulized albuterol Alanine aminotransferase 32 U/L 7–35 U/L 2.5 mg with ipratropium bromide 500 μg every Aspartate aminotransferase 30 U/L 7–35 U/L 4 hours, prednisone 40 mg orally daily for 5 days, and ceftriaxone 1 g intravenously every Troponin I 0.21 ng/mL 0.00–0.40 ng/mL 24 hours. The fi rst dose of each medication Brain natriuretic peptide 73 pg/mL < 125 pg/mL was given in the emergency department. Sputum gram stain Negative Negative The patient was then admitted to a pro- Sputum culture and sensitivity Pending No growth gressive care unit, where he was placed on noninvasive positive pressure ventilation, Blood culture Pending No growth continuous cardiac monitoring, and pulse Partial pressure of oxygen 54 mm Hg 75–100 mm Hg oximetry. He was started on enoxaparin 40 Oxygen saturation 88% 94%–100% mg subcutaneously daily to prevent venous Arterial blood pH 7.37 7.35–7.45 thromboembolism, and the oral medications he had been taking at home were continued. Partial pressure of carbon 50 mm Hg 35–45 mm Hg dioxide Because he was receiving a glucocorticoid, his blood glucose was monitored in the fasting Serum bicarbonate 28 mmol/L 22–28 mmol/L state, 2 hours after each meal, and as needed. a Two hours after he started noninvasive Abnormal values are in bold. positive pressure ventilation, his arterial blood gases were remeasured and showed the follow- ■ HOSPITAL COURSE ing results: • pH 7.35 On hospital day 3, his dyspnea had slightly improved. His respiratory rate was 26 to 28 • Partial pressure of carbon dioxide (Paco2) 52 mm Hg breaths per minute. His oxygen saturation re- • Bicarbonate 28 mmol/L mained between 90% and 92%. • Partial pressure of oxygen (Pao2) 60 mm Hg At 10:21 pm, his cardiac monitor showed • Oxygen saturation 90%. an episode of focal atrial tachycardia at a rate CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 86 • NUMBER 10 OCTOBER 2019 667 Downloaded from www.ccjm.org on September 23, 2021. For personal use only. All other uses require permission. THYROID FUNCTION TESTS TABLE 2 Thyroid function test results in patients with nonthyroidal illness Thyroid test Result Mechanisms Thyroid- Normal, Low TSH because of: stimulating high, or low • Suppression of hypothalamic-pituitary axis by infl ammatory cytokines hormone (TSH) • Abnormal TSH glycosylation • Decreased leptin resulting in low thyrotropin-releasing hormone, resulting in low TSH • Increased hypothalamic and pituitary type 2 iodothyronine deiodinase (D2) activity resulting in increased local T3 and thus decreased TSH Transient TSH increase during recovery from acute illness can be seen 6 Serum free Normal, Increased “direct” free T4 possibly because of inhibitors of T4 to its binding proteins 7 thyroxine (T4) high, or low Decreased free T4 index possibly because of very low binding protein concentrations Total T4 Normal or Decreased total T4 because of: low • Low production of its binding proteins • Decreased binding to thyroxine-binding globulin (inhibitors of T4 binding, glycosylated thyroxine-binding globulin) • Low TSH Total triiodo- Low Decreased type 1 iodothyronine deiodinase (D1) activities thyronine (T3) (by cytokines, increased cortisol, free fatty acids, and drugs) Low production of thyroxine-binding globulin Decreased binding to thyroxine-binding globulin (inhibitors of T3 binding, glycosylated thyroxine-binding globulin) Low TSH a Reverse T3 High Increased type 3 iodothyronine deiodinase (D3) activity Decreased D1 activity a Except in patients with end-stage renal disease and in some patients with acquired immune defi ciency syndrome. of 129 beats per minute that lasted for 3 min- □ Serum TSH and total triiodothyronine utes and 21 seconds, terminating spontane- (T3) □ ously. He denied any change in his clinical Serum TSH and free T4 □ condition during the episode, with no chest Serum TSH and free T3 pain, palpitation, or change in dyspnea. There There are several tests to assess thyroid func- was no change in his vital signs. He had an- tion: the serum TSH, total T4, free T4, total other similar asymptomatic episode lasting 4 1 T3, and free T3 concentrations.