The systemic illness associated with SARS-CoV-2 infection results in hospitalization rate of 380.3 hospitalizations per 100,000 population, overwhelming health care systems. Vitamin D regulates expression of approximately 11,000 genes spanning many physiologic functions that include regulation of both innate and adaptive immune function. We investigate potential benefit of calcitriol therapy given to patients hospitalized with COVID-19. This was an open label, randomized clinical trial of calcitriol or no treatment given to hospitalized adult patients with COVID-19. Subjects were randomly assigned treatment with calcitriol 0.5 mcg daily for 14 days or hospital discharge; or no treatment [ 1 : 1 ] at time of enrollment. We enrolled 50 consecutive patients, 25 per trial arm. The change in peripheral arterial oxygen saturation to the inspired fraction of oxygen (SaO2/FIO2 ratio) on admission and discharge between the groups the control group had an average increase of +13.2 (+/- 127.7) on discharge and the calcitriol group had an increase of +91.04 (+/- 119.08) (p= .0305), suggesting an improvement in oxygenation among subjects who received calcitriol. Additionally, 12 patients in the control group required oxygen supplementation on admission and 21 of them were discharged on room air. 14 subjects needed oxygen supplementation in the calcitriol group on admission while all 25 were discharged on room air. Other clinical markers showed the average length of stay was 9.24 (± 9.4) in the control group compared to 5.5 (± 3.9) days in the calcitriol group (p= .14). The need for ICU transfer was 8 in the control group and 5 in the calcitriol group. There were 3 deaths and 4 readmissions in the control group and 0 deaths and 2 readmissions in the calcitriol group. This pilot study illustrates improvement in oxygenation among hospitalized patients with COVID-19 treated with calcitriol and suggests the need for a larger randomized trial.

days. At the time of presentation, her blood pressures were 90/50 mmHg, and despite the low B.P she had a heart rate of 40 beats /minute, and had the BMI of 14.3 kgm -2 . According to the patient, she had her menarche at the age of thirteen years and her menstrual cycle had been completely normal until four months back when it suddenly stopped. The patient had an amenorrheic since then. The patient's attendant reported a history of weight loss in the patient with a gradual and progressive weight loss of 25 kg in the past 6 months with normal appetite but doing excessive exercise under the peer pressure of looking smart and healthy. Initial ECG was consistent with sinus bradycardia. Further workup revealed that her FSH, LH, and free T4 were reduced. Treatment course: She was initially kept inward to monitor her blood pressures with the fluid being given. Dopamine was started for the symptomatic bradycardia which was tapered off and stopped later on. After an interview with the patient and her family, a diagnosis of anorexia nervosa was reached with the patient being started on SSRI treatment. Thyroxine in the low dose was also given to bring FT4 to the normal range. Discussion: Patient Vitamin B12 was 179 pd/ml (N¼ greater than 201 pg/ml), Hemoglobin 11.2g/dl, Calcium 8.6 mg/dl (8.6-10.2), Thyroid stimulating hormone (TSH) 0.950 uIU/ml (N-0.4-4.2), free T4 (FT4) 0.85 ng/dl (N-0.89-1.76), free T3 (FT3) 1.20 pg/m ( N-l2.1-4.4), luteinizing hormone (LH) < 0.07 mIU/ml , follicle stimulating hormone (FSH) 1.07 mIU/ml, Estradiol < 11.80 pg/ml, and folate of 4.78 ng/ml (2.6-12.2). Conclusion: Anorexia nervosa can have a profound impact on endocrine organs. Long-term anorexia can lead to disruption of the hypothalamus-pituitary axis (HPA) and can lead to amenorrhea. These patients can have thyroid dysfunction which can lead to diagnostic confusion. Most of the endocrinal disorders improve with nutritional support.Peer pressure can lead to adopting an unhealthy lifestyle with dire consequences. A thorough history is very important in assessing such patients.

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Immune checkpoint inhibitors are widely used in the treatment of cancers. They are known to cause multisystem immune related adverse effects, including endocrinopathies. Primary thyroid dysfunction has been documented as an adverse effect of immunotherapy. We report a case of primary hypothyroidism detected in a patient after treatment with anti -PD-L1 agent, Atezolizumab. The patient presented with altered mental status 6 months after the initiation of immunotherapy. TSH was measured as part of the workup for encephalopathy, revealing TSH >20 with undetectable free T3, free T4. Anti TPO antibodies were elevated to >7500 IU/ml with anti thyroglobulin antibodies elevated to about 50U/ml. Thyroid ultrasound showed a diffusely heterogeneous gland with no other abnormalities. Patient was detected to have metastatic disease to the brain and spinal cord likely causing her change in mental status and was treated with steroids and radiation after which she improved. She was started on Levothyroxine 50mcg daily and discharged on the same dose. This case illustrates the need for measurement of TSH in all patients prior to the initiation of immunotherapy given the possibility of development of primary thyroid dysfunction mediated by inflammatory thyroiditis in these settings.