The Negative Pricing of the May 2020 WTI Contract

This paper sheds light on the negative pricing of the May 2020 WTI futures contract (CLK20) on April 20, 2020. The super contango of early 2020, triggered by COVID-19 lockdowns and geopolitical tensions, incentivized cash and carry (C&C) traders to be long CLK20 and short distant contracts, while simultaneously booking storage at Cushing. Our investigation reveals that C&C arbitrage largely contributed to the lack of storage capacity at Cushing in April 2020 and the price crash relates to the reversing trades of many long CLK20 traders without pre-booked storage. Additional aggravating factors included a liquidity crush, staggering margin calls and potential price distortions due to the trade-at-settlement mechanism. The analysis suggests that claims from experts that hold index trackers responsible for the crash are unwarranted: Index trackers did not trigger the negative pricing, nor widen the futures-spot spread by rolling their positions to more distant contracts ahead of maturity.

Testicular Adrenal Rest Tumors in a Patient With Congenital Adrenal Hyperplasia.

Ultrasound is the imaging examination of choice for evaluation of suspected testicular pathology. The differential diagnosis of bilateral testicular lesions includes malignancy such as lymphoma and metastases, infection, and, uncommonly, adrenal rest tumors. We present a patient who developed bilateral testicular adrenal rest tumors after years of poorly controlled congenital adrenal hyperplasia, possibly due to chronically elevated adrenocorticotropic hormone stimulating the growth of testicular stem cells. Our patient also has a testicular ultrasound appearance that is hyperechogenic, rather than hypoechogenic as commonly described in the literature. Treatment adherence is important in the management of congenital adrenal hyperplasia, as testicular adrenal rest tumors may eventually lead to infertility.

Isolated ACTH deficiency following immunization with the BNT162b2 SARS-CoV-2 vaccine: a case report.

BACKGROUND: The global COVID-19 pandemic requires urgent development of new vaccines. Endocrinological adverse effects following the new mRNA vaccine against COVID-19 have been reported in several cases. Specific to the involvement of pituitary function; however, only a single case with hypophysis has been reported. This is the first case of isolated adrenocorticotropic hormone (ACTH) deficiency (IAD) following mRNA vaccination against COVID-19. CASE PRESENTATION: A healthy 31-year-old man received the BNT162b2 SARS-CoV-2 mRNA vaccine. The first injection was uneventful. One day after the second injection, he noticed general fatigue and fever. In the following several days, he additionally developed headaches, nausea, and diarrhea. Four days after the vaccine injection, he visited a hospital with worsening of these symptoms. Physical examination revealed slight disorientation but no other deficits. Laboratory tests revealed hyponatremia, hypoglycemia, and extremely low plasma ACTH and serum cortisol levels (ACTH < 1.5 pg/ml, cortisol 1.6 µg/dl). He was diagnosed with adrenal crisis and was emergently treated with hydrocortisone. The symptoms responded well and he recovered within a few days. Magnetic resonance images after the replacement with hydrocortisone revealed an atrophic pituitary gland. The patient was referred to our tertiary hospital for further endocrinological examination. Pituitary endocrine load tests revealed isolated adrenocortical response deficiency. After other clinical assessments, he was diagnosed as having isolated ACTH deficiency. After initiation of hydrocortisone replacement, there has been no recurrence of symptoms related to adrenocortical insufficiency nor involvement of other pituitary functions. CONCLUSION: This is the first reported case of IAD potentially associated with COVID-19 immunization. Recent reports have emphasized the importance of adjuvants in the mRNA vaccine that induce the endocrinological adverse effects through disturbance of the autoimmune system, but details are still unclear. Given the broad and rapid spread of vaccinations against COVID-19, it is clinically important to consider that there could be cases with a rare but emergent adrenal crisis even among those who present common symptoms of adverse effects following inactive SARS-CoV-2 mRNA vaccination.

Secondary Adrenal Insufficiency After COVID-19 Diagnosed by Insulin Tolerance Test and Corticotropin-Releasing Hormone Test.

Coronavirus disease 2019 (COVID-19) can affect multiple organs and systems, including the endocrine system. Its symptoms can last for months, resulting in post-COVID-19 conditions, among others. A small number of patients have central adrenal insufficiency (CAI) months after recovery from COVID-19; nevertheless, its pathogenesis has not been fully elucidated. The insulin tolerance test (ITT) is a gold standard test assessing the hypothalamic-pituitary-adrenal axis, and the corticotropin-releasing hormone (CRH) test is useful for differentiating CAI into secondary (pituitary) and tertiary (hypothalamic) adrenal insufficiency. We present a case of new-onset CAI in a young female patient who had no medical history other than COVID-19. Adrenocorticotropin hormone and cortisol responded poorly to both insulin-induced hypoglycemia and CRH administration. These findings suggest that the pituitary gland may be the primary site of hypothalamic-pituitary-adrenal dysfunction, although magnetic resonance imaging of the pituitary gland was unremarkable. To our knowledge, this is possibly the first and only case report of new-onset secondary adrenal insufficiency after recovery from COVID-19 in which the ITT and the CRH test were performed and highly suggestive for the pathogenesis of not only post-COVID-19 CAI but also post-COVID-19 conditions.

Delayed Onset of Central Hypocortisolism in a Patient Recovering From COVID-19.

OBJECTIVE: The objective of this report is to highlight the possible but little-known association between coronavirus disease 2019 (COVID-19) and delayed onset of central hypocortisolism, which may be of significant clinical importance. METHODS: We describe a patient who developed new-onset central hypocortisolism in the convalescent phase of mild COVID-19, which has not been previously reported. RESULTS: A 47-year-old man with recent COVID-19 upper respiratory tract infection developed new-onset persistent dyspepsia and eosinophilia for which multiple investigations were normal. He was eventually diagnosed with central hypocortisolism, as evidenced by 8 AM cortisol level of 19 nmol/L (normal, 133-537 nmol/L) and adrenocorticotropic hormone of 7.1 ng/mL (normal, 10.0-60.0 ng/mL). He was started on hydrocortisone, which led to resolution of both dyspepsia and eosinophilia. At the same time, an interesting thyroid function trend was observed-an initial increase in both free thyroxine and thyroid stimulating hormone was followed by temporary central hypothyroidism before subsequent spontaneous recovery. On follow-up 3 weeks later, the patient remained hypocortisolemic. CONCLUSION: COVID-19 may be associated with the delayed onset of central hypocortisolism in its convalescent phase. Although various mechanisms are possible, hypothalamic-pituitary activation during systemic illness, followed by a rebound decrease in activity after recovery, is consistent with the clinical course and thyroid function trend in this patient. It is essential that physicians consider endocrinopathies in the differential diagnosis of such cases, given the risk of life-threatening adrenal crises and their possible contribution to persistent symptoms following recovery from COVID-19.