Background: In the US, serum thyroid-stimulating hormone (TSH) and thyroxine measurements are the fourth-and tenth-commonest laboratory tests ordered, respectively. Diagnosis of thyroid disorder requires clinical suspicion supported by laboratory values. However, in the setting of acute illness, both the clinical and laboratory pictures can be confounded. Objective: To study clinical outcomes and derangement patterns of inpatient thyroidfunction tests. Design: This retrospective study was conducted at an academic center on admissions aged ≥18 years and TSH tests performed over a 1-year period. Admissions with active pregnancy and/or prior thyroid-related diagnosis were excluded. Main Outcomes: Clinical outcomes were divided based on new diagnosis of thyroid-related disorder, newly prescribed thyroxine replacement, or antithyroid drugs/ endocrinology referrals, or both. In order to analyze the derangement patterns of abnormal TSH, only the results of the first test ordered were considered (as some admissions had multiple TSH tests ordered). Results: A total of 7,204 admissions aged ≥18 years had TSH tests done. Of these, 1,912 were excluded. Of the 5,292 admissions with no prior thyroid disorder or active pregnancy, 183 (3.46%) were assigned a new diagnosis of thyroid-related disorder, 54 (1.02%) received treatment/referral, and 46 (0.87%) received both a new diagnosis and treatment/referral. Based on the TSH results (reference range 0.42-4.0 mIU/L) of the 5,292 admissions, 4,312 (81.5%) and 980 (18.5%) admissions were flagged normal and abnormal, respectively. Of the 980 admissions with one or more abnormal TSH results, 21 (2.14%) had first ordered TSH <0.05 mIU/L, 855 (87.25%) admissions had first TSH result between 0.05-10 mIU/L, and lastly 104 (10.61%) were >10 mIU/L. Conclusion: There is low value in testing inpatients for thyroid disorders, and testing comes at significant expense to the health-care system.

Background: Necrotizing hypophysitis (NH) is an exceedingly rare clinical entity; we found only 5 reported cases in a literature review. CASE: A 34-year-old female with a history of primary hypothyroidism developed a headache, double vision, nausea, vomiting, decrease in appetite, galactorrhea, and weight loss. An MRI of the brain showed a 0.9 cm T2 hyperintense pituitary lesion with features suggestive of cystic degeneration or apoplexy of an adenoma There was effacement of the optic nerve anterior to the optic chiasm. Eye examination revealed optic nerve edema and a cranial nerve VI palsy. Laboratory studies revealed a normal prolactin 20.0 (3.3-26.7 ng/ml), and IGF-1 189 (RR: 66 - 303 ng/ml). The pituitary-adrenal axis and pituitary-gonadal axis appeared intact. After short treatment with dexamethasone, her primary symptom of severe headache improved but she later developed polyuria. The evaluation confirmed diabetes insipidus. Her headache worsened after the completion of the brief course of steroids. After a repeat MRI showed mild interval enlargement of the hypo-enhancing posterior pituitary, she underwent transsphenoidal pituitary tumor surgery. A biopsy showed necrotizing inflammation with foci of acute necrosis accompanied by polymorphonuclear cells. There was no granuloma seen. Special stains were negative for fungal, acid-fast, and bacterial organisms. Laboratory studies revealed negative ANA, negative ANCA, PR-3 Ab, MPO Ab, and anti-TPO Abs. The ACE enzyme was elevated at 85 (RR: 8-53 U/l), but the repeat test was within the normal range. A chest CT was not suggestive of pulmonary sarcoidosis. A post-surgery MRI demonstrated a decrease in pituitary size. Her headache worsened with a reduction in prednisone below 20 mg daily. In order to attempt further reduction in prednisone, azathioprine was started as a steroid-sparing agent. Titration of azathioprine up to 175 mg allowed prednisone to be reduced to the replacement dose of prednisone 5 mg daily. An MRI showed the pituitary mass to be unchanged. DISCUSSION: Hypophysitis is associated with diffuse enlargement and dysfunction of the pituitary gland. This case of NH is of unclear cause. There was no evidence of other inflammatory causes such as sarcoidosis, IgG4-related disease, ANCA-associated vasculitis, or infectious cause. As with typical lymphocytic hypophysitis, NH can present with sudden-onset hypopituitarism, neural compression, diabetes insipidus, and radiologic features of ischemic pituitary apoplexy. Signs and symptoms at diagnosis, as well as pituitary hormone abnormalities, vary on the degree of pituitary involvement. Pituitary adenoma commonly does not cause diabetes Insipidus. Radiologic findings consistent with ischemic pituitary apoplexy coupled with the presence of diabetes insipidus is suggestive of NH. A definitive diagnosis of NH, however, requires histopathology.

Background: Thyrotoxic periodic paralysis (TPP) can be a medical emergency as delay in diagnosis can lead to life-threatening arrhythmia. Periodic paralysis is more prevalent in the Asian population. We report a case of thyrotoxic periodic paralysis in a young Caucasian male. Case: A 24-year-old male with a past history of Graves’ disease, hypertension, and asthma was brought to the hospital due to leg weakness and fall. He was initially diagnosed with Graves’ disease 2 years ago. The patient could not take methimazole or metoprolol due to the affordability issue for the last 18 months. On presentation, he fell on the floor while attempting to stand up from the couch. He could not stand up or pick his cell phone. He remained on the floor for 2-3 hrs. A review of the system was positive for palpitation and fatigue and negative for diarrhea, weight loss, anxiety, sleep problem, and dry eyes. On arrival, he had a pulse of 100/min, BP of 157/85 mmHg with rest of vitals signs normal. Motor strength on bilateral lower extremities were 2/5. Upper extremity strength was normal. No thyromegaly or thyroid bruit was noted in the exam. The rest of the physical exam was normal. Labs showed Potassium 1.9 with a normal reference range (RR) of 3.5 - 5.1 mmol/l. His TSH was &lt; 0.01 (RR 0.35 - 5.00 MCU/ML), Free T4 was 5.0 (RR 0.6- 1.6 NG/DL), Total T3 was 425 (RR 87 - 180 NG/DL) and CK was 70 (RR 35- 232 U/L). EKG showed sinus rhythm at 90 bpm with no PR, T/ST, or QT abnormalities. He was given IV potassium and was also started on methimazole 10mg TID and metoprolol. His weakness and tachycardia were improved the next day. We discussed with him the options of medical management vs. surgery. He underwent a total thyroidectomy. Biopsy showed nodular hyperplasia consistent with graves’ disease. Discussion: Thyrotoxic periodic paralysis (TPP) is characterized by hypokalemia and episode of acute muscle weakness in lower extremities in the setting of hyperthyroidism. The pathophysiology of TPP remains uncertain. Hyperthyroidism is a hyperadrenergic state in which beta-2-adrenergic stimulation in muscle cells directly induces cellular K+ uptake by increasing cAMP, leading to activation of Na/K ATPase. The increase in the influx of intracellular K+ leads to hypokalemia and skeletal muscle weakness. Some studies show pathophysiology can be different in Caucasians compared to the Asian population that there could be abnormalities in Na and K channels other than Na/K ATPase. Potassium replacement should be done with caution as hypokalemia is due to intracellular shift and rebound hyperkalemia is common during the management. Beta-blocker may reverse adrenergic overstimulation of Na/K ATPase. It can help rapidly improve paralytic symptoms.

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