Covid-19 and Cushing’s Disease in a Patient with ACTH-secreting Pituitary Carcinoma

Abstract

Summary

The pandemic caused by severe acute respiratory syndrome coronavirus 2 is of an unprecedented magnitude and has made it challenging to properly treat patients with urgent or rare endocrine disorders. Little is known about the risk of coronavirus disease 2019 (COVID-19) in patients with rare endocrine malignancies, such as pituitary carcinoma. We describe the case of a 43-year-old patient with adrenocorticotrophic hormone-secreting pituitary carcinoma who developed a severe COVID-19 infection. He had stabilized Cushing’s disease after multiple lines of treatment and was currently receiving maintenance immunotherapy with nivolumab (240 mg every 2 weeks) and steroidogenesis inhibition with ketoconazole (800 mg daily). On admission, he was urgently intubated for respiratory exhaustion. Supplementation of corticosteroid requirements consisted of high-dose dexamethasone, in analogy with the RECOVERY trial, followed by the reintroduction of ketoconazole under the coverage of a hydrocortisone stress regimen, which was continued at a dose depending on the current level of stress. He had a prolonged and complicated stay at the intensive care unit but was eventually discharged and able to continue his rehabilitation. The case points out that multiple risk factors for severe COVID-19 are present in patients with Cushing’s syndrome. ‘Block-replacement’ therapy with suppression of endogenous steroidogenesis and supplementation of corticosteroid requirements might be preferred in this patient population.

Learning points

  • Comorbidities for severe coronavirus disease 2019 (COVID-19) are frequently present in patients with Cushing’s syndrome.
  • ‘Block-replacement’ with suppression of endogenous steroidogenesis and supplementation of corticosteroid requirements might be preferred to reduce the need for biochemical monitoring and avoid adrenal insufficiency.
  • The optimal corticosteroid dose/choice for COVID-19 is unclear, especially in patients with endogenous glucocorticoid excess.
  • First-line surgery vs initial disease control with steroidogenesis inhibitors for Cushing’s disease should be discussed depending on the current healthcare situation.

Background

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had a significant impact on the health care systems to date. The clinical presentation of coronavirus disease 2019 (COVID-19) is diverse, ranging from asymptomatic illness to respiratory failure requiring admission to the intensive care unit (ICU). Risk factors for severe course include old age, male gender, comorbidities such as arterial hypertension, diabetes mellitus, chronic lung-, heart-, liver- and kidney disease, malignancy, immunodeficiency and pregnancy (1). Little is known about the risk of COVID-19 in patients with rare endocrine malignancies, such as pituitary carcinoma.

Case presentation

This case concerns a 43-year-old man with adrenocorticotrophic hormone (ACTH)-secreting pituitary carcinoma (with cerebellar and cervical drop metastases) with a severe COVID-19 infection. He had previously received multiple treatment modalities including surgery, radiotherapy, ketoconazole, pasireotide, cabergoline, bilateral (subtotal) adrenalectomy and temozolomide chemotherapy as described elsewhere (2). His most recent therapy was a combination of immune checkpoint inhibitors consisting of ipilimumab (3 mg/kg) and nivolumab (1 mg/kg) (anti-CTLA-4 and anti-PD-1, respectively) every 3 weeks for four cycles, after which maintenance therapy with nivolumab (240 mg) every 2 weeks was continued. Residual endogenous cortisol production was inhibited with ketoconazole 800 mg daily. He had stabilized disease with a decrease in plasma ACTH, urinary free cortisol and stable radiological findings (2). Surgical resection of the left adrenal remnant was planned but was not carried out due to the development of a COVID-19 infection.

In March 2021, he consulted our emergency department for severe respiratory complaints. He had been suffering from upper respiratory tract symptoms for one week, with progressive dyspnoea in the last three days. He tested positive for SARS-CoV-2 the day before admission. On examination, his O2 saturation was 72%, with tachypnoea (40/min) and bilateral pulmonary crepitations. His temperature was 37.2°C, blood pressure 124/86 mmHg and pulse rate 112 bpm. High-flow oxygen therapy was initiated but yielded insufficient improvement (O2 saturation of 89% and tachypnoea 35/min). He was urgently intubated for respiratory exhaustion.

Investigation

Initial investigations showed type 1 respiratory insufficiency with PaO2 of 52.5 mmHg (normal 75–90), PaCO2 of 33.0 mmHg (normal 36–44), pH of 7.47 (normal 7.35–7.45) and a P/F ratio of 65.7 (normal >300). His inflammatory parameters were elevated with C-reactive protein level of 275.7 mg/L (normal <5·0) and white blood cell count of 7.1 × 10⁹ per L with 72.3% neutrophils. His most recent morning plasma ACTH-cortisol level (measured using the Elecsys electrochemiluminescence immunoassays on a Cobas 8000 immunoanalyzer [Roche Diagnostics]) before his admission was 213 ng/L (normal 7.2–63) and 195 µg/L (normal 62–180) respectively, while a repeat measurement 3 weeks after his admission demonstrated increased cortisol levels of 547 µg/L (possibly iatrogenic due to treatment with high-dose hydrocortisone) and a decreased ACTH of 130 ng/L.

Treatment

On admission, he was started on high-dose dexamethasone therapy for 10 days together with broad-spectrum antibiotics for positive sputum cultures containing Serratia, methicillin-susceptible Staphylococcus aureus and Haemophilus influenzae. Thromboprophylaxis with an intermediate dose of low molecular weight heparin (tinzaparin 14 000 units daily for a body weight of 119 kg) was initiated. A ‘block-replacement’ regimen was adopted with the continuation of ketoconazole (restarted on day 11) in view of his endocrine treatment and the supplementation of hydrocortisone at a dose depending on the current level of stress. The consecutive daily dose of hydrocortisone and ketoconazole is shown in Fig. 1.

Figure 1View Full Size
Figure 1
‘Block-replacement’ therapy with ketoconazole and hydrocortisone/dexamethasone. Dexamethasone 10 mg daily was initially started as COVID-19 treatment, followed by hydrocortisone at a dose consistent with current levels of stress. Ketoconazole was restarted on day 11 and titrated to a dose of 800 mg daily to suppress endogenous glucocorticoid production.

Citation: Endocrinology, Diabetes & Metabolism Case Reports 2022, 1; 10.1530/EDM-21-0182

Outcome and follow-up

He developed multiple organ involvement, including metabolic acidosis, acute renal failure requiring continuous venovenous hemofiltration, acute coronary syndrome type 2, septic thrombophlebitis of the right jugular vein, and critical illness polyneuropathy. He was readmitted twice to the ICU, for ventilator-associated pneumonia and central line-associated bloodstream infection respectively. He eventually recovered and was discharged from the hospital to continue his rehabilitation.

Discussion

We describe the case of a patient with severe COVID-19 infection with active Cushing’s disease due to pituitary carcinoma, who was treated with high-dose dexamethasone followed by ‘block-replacement’ therapy with hydrocortisone in combination with off-label use of ketoconazole as a steroidogenesis inhibitor. His hospitalization was prolonged by multiple readmissions to the ICU for infectious causes. Our case illustrates the presence of multiple comorbidities for a severe and complicated course of COVID-19 in a patient with active Cushing’s disease.

Dexamethasone was initially chosen as the preferred corticosteroid therapy, in analogy with the RECOVERY trial, in which dexamethasone at a dose of 6mg once daily (oral or i.v.) resulted in lower 28-day mortality in hospitalized patients with COVID-19 requiring oxygen therapy or invasive mechanical ventilation (3). However, the optimal dose/choice of corticosteroid therapy is unclear, especially in a patient population with pre-existing hypercortisolaemia. A similar survival benefit for hydrocortisone compared to dexamethasone has yet to be convincingly demonstrated. This may be explained by differences in anti-inflammatory activity but could also be due to the fact that recent studies with hydrocortisone were stopped early and were underpowered (45).

Multiple risk factors for a complicated course of COVID-19 are present in patients with Cushing’s syndrome and might increase morbidity and mortality (67). These include a history of obesity, arterial hypertension and impaired glucose metabolism. Prevention and treatment of these pre-existing comorbidities are essential.

Patients with Cushing’s syndrome also have an increased thromboembolic risk, which is further accentuated by the development of severe COVID-19 infection (67). Thromboprophylaxis with low molecular weight heparin is associated with lower mortality in COVID-19 patients with high sepsis‐induced coagulopathy score or high D-dimer levels (8) and is presently widely used in the treatment of severe COVID-19 disease (9). Subsequently, this treatment is indicated in hospitalized COVID-19 patients with Cushing’s syndrome. It is unclear whether therapeutic anticoagulation dosing could provide additional benefits (67). An algorithm based on the International Society on Thrombosis and Hemostasis-Disseminated Intravascular Coagulation score was proposed to evaluate the ideal anticoagulation therapy in severe/critical COVID-19 patients, with an indication for therapeutic low molecular weight heparin dose at a score ≥5 (9).

Furthermore, the chronic cortisol excess induces suppression of the innate and adaptive immune response. Patients with Cushing’s syndrome, especially when severe and active, should be considered immunocompromised and have increased susceptibility for viral and other (hospital-acquired) infections. Prophylaxis for Pneumocystis jirovecii with trimethoprim/sulfamethoxazole should therefore be considered (67).

Additionally, there is a particular link between the pathophysiology of COVID-19 and Cushing’s syndrome. The SARS-CoV-2 virus (as well as other coronaviruses) enter human cells by binding the ACE2 receptor. The transmembrane serine protease 2 (TMPRSS2), expressed by endothelial cells, is additionally required for the priming of the spike-protein of SARS-CoV-2, leading to viral entry. TMPRSS2 was studied in prostate cancer and found to be regulated by androgen signalling. Consequently, the androgen excess frequently associated with Cushing’s syndrome might be an additional risk factor for contracting COVID-19 via higher TMPRSS2 expression (10), especially in women, in whom the effect of excess androgen would be more noticeable compared to male patients with Cushing’s syndrome.

Treating Cushing’s syndrome with a ‘block-replacement’ approach, with suppression of endogenous steroidogenesis and supplementation of corticosteroid requirements, is an approach that should be considered, especially in severe or cyclic disease. The use of this method might decrease the need for monitoring and reduce the occurrence of adrenal insufficiency (7). Our patient was on treatment with ketoconazole, which was interrupted at initial presentation and then restarted under the coverage of a hydrocortisone stress regimen. Ketoconazole was chosen because of its availability. Advantages of ketoconazole over metyrapone include its antifungal activity with the potential for prevention of invasive pulmonary fungal infections, as well as its antiandrogen action (especially in female patients) and subsequent inhibition of TMPRSS2 expression (10). Regular monitoring of the liver function (every month for the first 3 months, at therapy initiation or dose increase) is necessary. Caution is needed due to its inhibition of multiple cytochrome P450 enzymes (including CYP3A4) and subsequently greater risk of drug-drug interactions vs metyrapone (710). Another disadvantage of ketoconazole is the need for oral administration. In our patient, ketoconazole was delivered through a nasogastric tube. i.v. etomidate is an alternative in case of an unavailable enteral route.

Finally, as a general point, the first-line treatment of a patient with a novel diagnosis of Cushing’s disease is transsphenoidal surgery. Recent endocrine recommendations pointed out the possibility of initial disease control with steroidogenesis inhibitors in patients without an indication for urgent intervention during a high prevalence of COVID-19 (7). This would allow the optimalization of metabolic parameters; emphasizing that the short-to mid-term prognosis is related to the cortisol excess and not its cause. Surgery could then be postponed until the health situation allows for safe elective surgery (7). This decision depends of course on the evolution of COVID-19 and the healthcare system in each country and should be closely monitored by policymakers and physicians.

Declaration of interest

The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding

This work did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.

Patient consent

Written informed consent for publication of their clinical details and/or clinical images was obtained from the patient.

Author contribution statement

J M K de Filette is an endocrinologist-in-training and was the main author. All authors were involved in the clinical care of the patient. All authors contributed to the reviewing and editing process and approved the final version of the manuscript.

References

Adrenal: How the SARS-CoV-2 virus undermines our body’s ‘fight’ response

Researchers in Europe say they have shown for the first time that the SARS-CoV-2 virus attacks the human stress system by limiting how our adrenal glands can respond to the threat of Covid-19.

According to a study, the coronavirus targets the adrenal glands, thereby weakening the body’s ability to produce the stress hormones cortisol and adrenaline needed to help battle a serious infection.

Part of the body’s defence mechanism, these glands are indispensable for our survival of stressful situations, particularly with a coronavirus infection.

The research was published by a group of scientists in London, United Kingdom; Zurich, Switzerland; and Dresden and Regensburg in Germany, in the journal The Lancet Diabetes and Endocrinology last month (November 2021).

“The results of our latest work now show for the first time that the virus directly affects the human stress system to a relevant extent,” says Dr Stefan Bornstein, director of the Medical Clinic and Polyclinic III and the Centre for Internal Medicine at the University Hospital in Dresden.

Whether these changes directly contribute to adrenal insufficiency, or even lead to long Covid is still unclear, he says.

This question must be investigated in further clinical studies.

Pointing to recent research showing the effect of inhaling steroids to prevent clinical deterioration in patients with Covid-19, the researchers say certain drugs may be able to help limit this effect of the SARS-CoV-2 virus.

“This evidence underlines the potentially important role for adrenal steroids in coping with Covid-19,” scientists at the University of Zurich say.

The researchers analysed the data of 40 deceased Covid-19 patients in Dresden and found that their tissue samples showed clear signs of adrenal gland inflammation.

From https://www.thestar.com.my/lifestyle/health/2021/12/22/how-the-sars-cov-2-virus-undermines-our-bodys-039fight039-response

COVID-19 Targets Human Adrenal Glands

COVID-19 develops due to infection with SARS-CoV-2, which particularly in elderly with certain comorbidities (eg, metabolic syndrome)

can cause severe pneumonia and acute respiratory distress syndrome. Some patients with severe COVID-19 will develop a life-threatening sepsis with its typical manifestations including disseminated intravascular coagulation and multiorgan dysfunction.

Latest evidence suggests that even early treatment with inhaled steroids such as budesonide might prevent clinical deterioration in patients with COVID-19.

This evidence underlines the potentially important role for adrenal steroids in coping with COVID-19.

The adrenal gland is an effector organ of the hypothalamic–pituitary–adrenal axis and the main source of glucocorticoids, which are critical to manage and to survive sepsis. Therefore, patients with pre-existing adrenal insufficiency are advised to double their doses of glucocorticoid supplementation after developing moderate to more severe forms of COVID-19.

Adrenal glands are vulnerable to sepsis-induced organ damage and their high vascularisation and blood supply makes them particularly susceptible to endothelial dysfunction and haemorrhage. Accordingly, adrenal endothelial damage, bilateral haemorrhages, and infarctions have been already reported in patients with COVID-19.

Adrenal glands contain the highest concentration of antioxidants to compensate enhanced generation of reactive oxygen species, side products of steroidogenesis, which together with elevated intra-adrenal inflammation can contribute to adrenocortical cell death.

Furthermore, sepsis-associated critical illness-related corticosteroid insufficiency, which describes coexistence of the hypothalamic–pituitary–adrenal dysfunction, reduced cortisol metabolism, and tissue resistance to glucocorticoids, was reported in critically ill patients with COVID-19.

Low cortisol and adrenocorticotropic hormone (ACTH) responses during acute phase of infections consistent with critical illness-related corticosteroid insufficiency diagnosis (random plasma cortisol level lower than 10 μg/dL) were reported in one study with patients suffering from mild to moderate COVID-19 manifestations.

It is however possible those other factors triggered by COVID-19 such as hypothalamic or pituitary damage, adrenal infarcts, or previously undiagnosed conditions, such as antiphospholipid syndrome, might be responsible for reduced function of adrenal glands. However, contrary to this observation, a study with patients with moderate to severe COVID-19 revealed a very high cortisol response with values exceeding 744 nmol/L, which were positively correlated with severity of disease.

In this clinical study,

highly elevated cortisol concentrations showed an adequate adrenal cortisol production possibly reflecting the elevated stress level of those severely affected patients.

However, since ACTH measurements were not done, it is impossible to verify whether high concentrations of cortisol in those patients resulted from an increment of cortisol, or were confounded by reduced glucocorticoid metabolism.

A critical and yet unsolved major question is whether SARS-CoV-2 infection can contribute either directly or indirectly to adrenal gland dysfunction observed in some patients with COVID-19 or contribute to the slow recovery of some patients with long COVID.
We performed a comprehensive histopathological examination of adrenal tissue sections from autopsies of patients that died due to COVID-19 (40 cases), collected from three different pathology centres in Regensburg, Dresden, and Zurich (appendix pp 1–3). We observed evidence of cellular damage and frequently small vessel vasculitis (endotheliitis) in the periadrenal fat tissue (six cases with low and 13 cases with high density; appendix p 10) and much milder occurrence in adrenal parenchyma (ten cases with low and one case with moderate score; appendix p 10), but no evidence of thrombi formation was found (appendix p 10). Endotheliitis has been scored according to a semi-quantitative immunohistochemistry analysis as described in the appendix (p 4). Additionally, in the majority of cases (38 cases), we noticed enhanced perivascular lymphoplasmacellular infiltration of different density and sporadically a mild extravasation of erythrocytes (appendix p 10). However, no evidence of widespread haemorrhages and degradation of adrenocortical cells were found, which is consistent with histological findings reported previously.

In another autopsy study analysing adrenal glands of patients with COVID-19, additional signs of acute fibrinoid necrosis of small vessels in adrenal parenchyma, subendothelial vacuolisation and apoptotic debris were found.

Adrenal gland is frequently targeted by bacteria and viruses, including SARS-CoV,

which was responsible for the 2002–04 outbreak of SARS in Asia. Considering that SARS-CoV-2 shares cellular receptors with SARS-CoV, including angiotensin-converting enzyme 2 and transmembrane protease serine subtype 2, its tropism to the adrenal gland is therefore conceivable.

To investigate whether adrenal vascular cells and possibly steroid-producing cells are direct targets of SARS-CoV-2, we examined SARS-CoV-2 presence in adrenal gland tissues obtained from the 40 patients with COVID-19 (appendix pp 1–3). Adrenal tissues from patients who died before the COVID-19 pandemic were used as negative controls to validate antibody specificity. Using a monoclonal antibody (clone 1A9; appendix p 11), we detected SARS-CoV-2 spike protein in adrenocortical cells in 18 (45%) of 40 adrenal gland tissues (figure Bappendix p 12). In the same number of adrenal tissues (18 [45%] of 40), we have detected SARS-CoV-2 mRNA using in situ hybridisation (ISH; figure Aappendix p 12). The concordance rate between immunohistochemistry and ISH methods was 90% (36/40). Scattered and rather focal expression pattern of SARS-CoV-2 spike protein was found in the adrenal cortex (figure A and Bappendix p 12). In addition, SARS-CoV-2 expression was confirmed in 15 out of 30 adrenal gland tissues of patients with COVID-19 by multiplex RT-qPCR (appendix pp 6–7). The concordance between ISH, immunohistochemistry, and RT-qPCR techniques for SARS-CoV-2 positivity was only 23%, which is a technical limitation of our study possibly reflecting the low number of virus-positive cells. However, when considering triple-negative samples, an overall 53% consensus was found (appendix pp 7–8).

Figure thumbnail gr1
FigureDetection of SARS-CoV-2 in human adrenal gland from a patient who died due to COVID-19
Finally, to confirm the identity of infected cells, we have performed an ultrastructural analysis of adrenal tissue from a triple-positive patient case (by immunohistochemistry, ISH, and RT-qPCR), and found numerous SARS-CoV-2 virus-like particles in cells enriched with liposomes, which are typical markers of adrenocortical cells (figure C). The cortical identity of SARS-CoV-2 spike positive cells was also shown using serial tissue sections, demarcating regions with double positivity for viral protein and StAR RNA (appendix p 12). Furthermore, susceptibility of adrenocortical cells to SARS-CoV-2 infection was confirmed by in-vitro experiments (appendix p 7) showing detection of viral spike protein in adrenocortical carcinoma cells (NCI-H295R) cultured in a medium containing SARS-CoV-2 (figure D), and its absence in mock-treated control cells (figure E). We showed an uptake of viral particles in the adrenocortical cells, by ISH, immunohistochemistry, RT-qPCR and electron microscopy (figure A–C). Mechanistically, an uptake of SARS-CoV-2 like particles might involve expression of ACE2 in vascular cells (appendix p 13) and perhaps of the shorter isoform of ACE2 together with TMPRSS2 and other known or currently unknown virus-entry facilitating factors in adrenocortical cells (appendix p 13). An example of such factor is scavenger receptor type 1, which is highly expressed in adrenocortical cells.

Several forms of regulated cell necrosis were implicated in sepsis-mediated adrenal gland damage.

One of the prime examples of regulated necrosis triggered by sepsis-associated tissue inflammation is necroptosis. The necrotic process is characterised by loss of membrane integrity and release of danger-associated molecular patterns, which further promote tissue inflammation (necroinflammation) involving enhanced activation of the complement system and related activation of neutrophils. Whether necroptosis might be involved in COVID-19-associated adrenal damage is currently unknown. In our study, we showed prominent expression of phospho Mixed Lineage Kinase Domain Like Pseudokinase (pMLKL) indicating necroptosis activation in adrenomedullary cells (appendix p 14) in adrenal glands of COVID-19 patients. However, since we have also observed pMLKL expression in adrenal glands obtained from autopsies done before the COVID-19 pandemic (controls), necroptosis activation in medullary cells might be a rather frequent and SARS-CoV-2 independent event. However, contrary to the adrenal medulla, pMLKL positivity in the adrenal cortex was only found in virus-positive regions (appendix p 14). This finding suggests that SARS-CoV-2 infection might have directly triggered activation of necroptosis in infected cells in the adrenal cortex, whereas pMLKL expression in the adrenal medulla seems rather an indirect consequence of systemic inflammation.

In summary, in our study of 40 patients who died from COVID-19, we did not observe widespread degradation of human adrenals that might lead to manifestation of the adrenal crisis. However, our study shows that the adrenal gland is a prominent target for the viral infection and ensuing cellular damage, which could trigger a predisposition for adrenal dysfunction. Whether those changes directly contribute to adrenal insufficiency seen in some patients with COVID-19 or lead to its complications (such as long COVID) remains unclear. Large multicentre clinical studies should address this question.
WK, HC, and SRB declare funds from Deutsche Forschungsgemeinschaft (project number 314061271, TRR 205/1 [“The Adrenal: Central Relay in Health and Disease”] to WK and SRB; HA 8297/1-1 to HC), during the conduct of this Correspondence. All other authors declare no competing interests. We thank Maria Schuster, Linda Friedrich, and Uta Lehnert for performing some of the immunohistochemical staining and in-situ hybridisation.

Supplementary Material

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Resolution of pituitary microadenoma after coronavirus disease 2019: a case report

This article was originally published here

J Med Case Rep. 2021 Nov 1;15(1):544. doi: 10.1186/s13256-021-03127-3.

ABSTRACT

BACKGROUND: This report describes the case of a patient whose pituitary microadenoma resolved after he contracted coronavirus disease 2019. To our knowledge, this is one of the first reported cases of pituitary tumor resolution due to viral illness. We present this case to further investigate the relationship between inflammatory response and tumor remission.

CASE PRESENTATION: A 32-year-old man in Yemen presented to the hospital with fever, low blood oxygen saturation, and shortness of breath. The patient was diagnosed with coronavirus disease 2019. Past medical history included pituitary microadenoma that was diagnosed using magnetic resonance imaging and secondary adrenal insufficiency, which was treated with steroids. Due to the severity of coronavirus disease 2019, he was treated with steroids and supportive care. Three months after his initial presentation to the hospital, brain magnetic resonance imaging was performed and compared with past scans. Magnetic resonance imaging revealed changes in the microadenoma, including the disappearance of the hypointense lesion and hyperintense enhancement observed on the previous scan.

CONCLUSIONS: Pituitary adenomas rarely undergo spontaneous resolution. Therefore, we hypothesized that tumor resolution was secondary to an immune response to coronavirus disease 2019.

PMID:34724974 | DOI:10.1186/s13256-021-03127-3

CDC Expands Eligibility for COVID-19 Booster Shots

 

For Immediate Release: Thursday, October 21, 2021
Contact: Media Relations
(404) 639-3286

Today, CDC Director Rochelle P. Walensky, M.D., M.P.H., endorsed the CDC Advisory Committee on Immunization Practices’ (ACIP) recommendation for a booster shot of COVID-19 vaccines in certain populations. The Food and Drug Administration’s (FDA) authorization and CDC’s recommendation for use are important steps forward as we work to stay ahead of the virus and keep Americans safe.

For individuals who received a Pfizer-BioNTech or Moderna COVID-19 vaccine, the following groups are eligible for a booster shot at 6 months or more after their initial series:

For the nearly 15 million people who got the Johnson & Johnson COVID-19 vaccine, booster shots are also recommended for those who are 18 and older and who were vaccinated two or more months ago.

There are now booster recommendations for all three available COVID-19 vaccines in the United States. Eligible individuals may choose which vaccine they receive as a booster dose. Some people may have a preference for the vaccine type that they originally received, and others may prefer to get a different booster. CDC’s recommendations now allow for this type of mix and match dosing for booster shots.

Millions of people are newly eligible to receive a booster shot and will benefit from additional protection. However, today’s action should not distract from the critical work of ensuring that unvaccinated people take the first step and get an initial COVID-19 vaccine. More than 65 million Americans remain unvaccinated, leaving themselves – and their children, families, loved ones, and communities– vulnerable.

Available data right now show that all three of the COVID-19 vaccines approved or authorized in the United States continue to be highly effective in reducing risk of severe disease, hospitalization, and death, even against the widely circulating Delta variant. Vaccination remains the best way to protect yourself and reduce the spread of the virus and help prevent new variants from emerging.

The following is attributable to Dr. Walensky:

“These recommendations are another example of our fundamental commitment to protect as many people as possible from COVID-19. The evidence shows that all three COVID-19 vaccines authorized in the United States are safe – as demonstrated by the over 400 million vaccine doses already given. And, they are all highly effective in reducing the risk of severe disease, hospitalization, and death, even in the midst of the widely circulating Delta variant.”

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