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The symptoms associated with empty sella syndrome (ESS) include headache, giddiness, vomiting, visual field deficits, and endocrine problems, as well as the radiological appearance of an enlarged sella turcica. This case report highlights a 45-year-old female who had a COVID-19 infection 2 months back and presented with chronic headache, giddiness, and lethargy having persistent hyponatremia later diagnosed as empty sella syndrome on brain magnetic resonance imaging. In this case, we tried to correlate all of these clinical and radiological features as COVID-19 sequelae due to post-Covid hypothalamic-pituitary axis dysfunction.Copyright © 2023 Authors. All rights reserved.
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Objectives: Endoscopic endonasal transsphenoidal adenomectomy (TSA) is the most frequently performed skull base surgery, and researchers have recently focused on preserving nasal function. The endoscopic transseptal approach is a promising procedure due to its reduced injury to the nasal mucosa; however, there are no studies comparing rhinological and neurosurgical outcomes concurrently with the standard endoscopic transnasal approach. Therefore, we conducted this study to investigate whether the transseptal approach could reduce nasal morbidities with comparable neurosurgical outcomes. Methods: We retrospectively reviewed 25 patients who underwent endoscopic endonasal transseptal TSA for pituitary adenoma without encasement of internal carotid artery from January 2019 to December 2020. Another 25 patients who received transnasal approach from January 2017 to December 2018 were selected as controls. Patients with diseases affecting the nasal cavity/olfaction or usage of a nasoseptal flap were excluded for a better comparison of the two procedures. We collected data from radiological studies, endocrine studies, endoscopic evaluations, 22-item sinonasal outcome tests (SNOT-22) and Top International Biotech Smell Identification Test (TIBSIT) for comparison. Results: Lower postoperative SNOT-22 and Lund-Kennedy endoscopic scores were observed in the transseptal group. The effect size of differences were classified as large effect (The absolute value of Cohen's d > 0.8). Nevertheless, the TIBSIT scores were not significantly different. The rates of gross total resection, recovery of hormonal abnormalities, and complications were not significantly different. After controlling possible confounding factors using multivariate analysis, the endoscopic transseptal approach remained an independent factor for lower SNOT-22 scores and Lund-Kennedy endoscopic scores. Conclusions: The endoscopic transseptal approach provides improved recovery of nasal mucosa and intact olfaction without compromising neurosurgical outcomes. Level of Evidence: 2b.
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This review is aimed at illustrating and discussing the neuroimmune endocrinological aspects of the SARS-CoV-2 infection in light of the studies on this topic that have so far appeared in the literature. The most characteristic findings and pending controversies were derived by PubMed and Scopus databases. We included original and observational studies, reviews, meta-analysis, and case reports. The entry of the coronavirus into susceptible cells is allowed by the interaction with an ecto-enzyme located on human cells, the angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 also targets the central nervous system (CNS), including hypothalamic-pituitary structures, as their tissues express ACE2, and ACE2 mRNA expression in hypothalamus and pituitary gland cells has been confirmed in an autoptic study on patients who died of COVID 19. SARS-CoV-2 infection may cause central endocrine disorders in acute phase and in post-COVID period, particularly due to the effects of this virus at CNS level involving the hypothalamic-pituitary axis. The aggression to the hypothalamus-pituitary region may also elicit an autoimmune process involving this axis, responsible consequently for functional disorders of the satellite glands. Adrenal, thyroid and gonadal dysfunctions, as well as pituitary alterations involving GH and prolactin secretions, have so far been reported. However, the extent to which COVID-19 contributes to short- and long-term effects of infection to the endocrine system is currently being discussed and deserves further detailed research.
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SARS-CoV-2 is a type of coronavirus that causes COVID-19 disease. The virus can infect various organs by triggering hormones, regulatory and messenger molecules, and immune-inflammatory responses. Given the vital role of thyroid in metabolism, it is important to understand the potential effects of SARS-CoV-2 on the thyroid gland. In this article, reports and studies examining the effects of SARS-CoV-2 infection on thyroid are reviewed, and possible effects of this virus on thyroid function are discussed. According to the available evidence, SARS-CoV-2 can adversely impact thyroid function directly by affecting the pituitary-thyroid axis or indirectly by triggering immune-inflammatory responses. COVID-19-dependent thyroid disorders have been biochemically observed in three forms: hypothyroidism, thyrotoxicosis, and nonthyroidal illness syndrome. Subacute thyroiditis has been one of the most common clinical conditions of SARS-CoV-2-dependent thyrotoxicosis. In addition, SARS-CoV-2 may cause recurrence of improved thyroid diseases or exacerbate current diseases. There is no evidence that thyroid disease, including thyroid cancer, increases the risk of COVID-19 or exacerbates its complications. According to current studies, COVID-19 medications, including glucocorticoids and anticoagulants, have no adverse effects on thyroid function in non-acute COVID-19 patients. Further studies are needed to investigate the interactions between SARS-CoV-2 infection and thyroid function.
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This special issue contains 7 articles on the principles of predictive, preventive and personalised (3P) medicine. Topics covered include: endothelin-1 and its potential as the diagnostic, prognostic and treatment target in the framework of 3P medicine;potential health risks associated specifically with the low body weight;management of COVID-19;wrist actigraphic approach;diagnosing hospital bacteraemia;and omics biomarkers in pituitary neuroendocrine tumors.
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CONTEXT: Involvement of the pituitary gland in SARS-CoV-2 infection has been clinically suggested by pituitary hormone deficiency in severe COVID-19 cases, by altered serum adrenocorticotropic hormone (ACTH) levels in hospitalized patients, and by cases of pituitary apoplexy. However, the direct viral infection of the gland has not been investigated. OBJECTIVE: To evaluate whether the SARS-CoV-2 genome and antigens could be present in pituitary glands of lethal cases of COVID-19, and to assess possible changes in the expression of immune-related and pituitary-specific genes. METHODS: SARS-CoV-2 genome and antigens were searched in the pituitary gland of 23 patients who died from COVID-19 and, as controls, in 12 subjects who died from trauma or sudden cardiac death. Real-time reverse transcription polymerase chain reaction (PCR), in situ hybridization, immunohistochemistry, and transmission electron microscopy were utilized. Levels of mRNA transcripts of immune-related and pituitary-specific genes were measured by the nCounter assay. RESULTS: The SARS-CoV-2 genome and antigens were detected in 14/23 (61%) pituitary glands of the COVID-19 group, not in controls. In SARS-CoV-2-positive pituitaries, the viral genome was consistently detected by PCR in the adeno- and the neurohypophysis. Immunohistochemistry, in situ hybridization, and transmission electron microscopy confirmed the presence of SARS-CoV-2 in the pituitary. Activation of type I interferon signaling and enhanced levels of neutrophil and cytotoxic cell scores were found in virus-positive glands. mRNA transcripts of pituitary hormones and pituitary developmental/regulatory genes were suppressed in all COVID-19 cases irrespective of virus positivity. CONCLUSION: Our study supports the tropism of SARS-CoV-2 for human pituitary and encourages exploration of pituitary dysfunction after COVID-19.
Subject(s)
COVID-19 , COVID-19/genetics , COVID-19 Testing , Humans , Pituitary Hormones , RNA, Messenger , SARS-CoV-2/geneticsABSTRACT
Background: Severe acute respiratory syndrome-coronavirus (SARS-CoV) and SARS-CoV-2 might affect the hypothalam-ic-pituitary-adrenal axis. This paper presents a rare case of pituitary insufficiency diagnosed after CoV disease (COVID)-19. Case Report: On December 7, 2020, a 67-year-old male patient presented to the Endocrinology Department of Lokman Hekim University with weakness, weight loss, and abdominal pain lasting for 3 weeks. In his medical history, he had a positive real-time polymerase chain reaction test result for SARS-CoV-2 based on the nasopharyngeal swab analyzed on September 30. Central hypothyroidism, secondary adrenal insufficiency, hypogonadotropic hypogonadism, and a low dehy-droepiandrosterone-sulfate level were detected in the laboratory examinations. Steroid therapy was initiated.
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Relevance: Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. The prevalence rates of PCOS depend on the diagnostic criteria used and the characteristics of the population sample, and in the general population of women of reproductive age, the prevalence of the syndrome ranges from 6-9% to 19.9% [1,2]. According to modern criteria adopted by the consensus in Rotterdam, then systematically updated by ESHRE / ASRM (2014), the presence of two of the three criteria in a patient simultaneously allows to diagnose PCOS if other pathological conditions are excluded (thyroid pathology, congenital adrenal hyperplasia, adrenogenitalsyndrome, androgen-secreting tumors, Itsenko-Cushing syndrome). Modern international diagnostic criteria include the following signs: (1) signs of polycystic ovaries according to information from pelvic ultrasound investigation (the presence of more than 10 follicles in each ovary);(2) oligo-anovulation;(3) clinical (presence of hirsutism) or biochemical (increased androgen levels) development of ovarian hyperandrogenism [3, 4]. Polycystic ovary syndrome is closely related to many diseases, including metabolic syndrome. Although insulin resistance is an important risk factor for metabolic syndrome and other diseases associated with PCOS, hyperandrogenismmay also be an independent risk factor for type 2 diabetes, obesity, cardiovascular disease (CVD), and metabolic syndrome in female patients. Obesity is the most common symptom in PCOS patients (33-88%), which has a large impact on fertility and can lead to adverse effects such as menstrual irregularities, anovulation, infertility and abortion. Therefore, weight management in early PCOS is essential to improve fertility and quality of life. Hyperandrogenism plays a decisive role in abdominal obesity in obese women during adolescence, adulthood and menopause [5]. Although some studies have shown a negative association between plasma androgen levels (A4, DHEA and DHEAS) and obesity [6,7]. But the mechanism of how androgens affect fat cells in women is poorly understood. A number of observations show that among obese women with PCOS, metabolic disorders associated with insulin resistance and obesity, in many cases, play a more important role in the mechanism of anovulation in PCOS than excess androgens. In recent years, it has been established that in PCOS there is a frequent combination of hyperandrogenism and insulin resistance. With insulin resistance, there is a decrease in the response of insulin-sensitive tissues to the hormone insulin with its sufficient level in the blood. Insulin resistance is found in 30-70% of patients with PCOS who are overweight or obese, and in patients with normal body weight it occurs in 20-25% of cases. The above facts, as well as our own observations, prompted us to analyze the studied women of fertile age with impaired reproductive system against the background of overweight and obesity. Considering the above, the aim of this study was to identify the relationship between insulin resistance and reproductive disorders in women with overweight and obesity. Material and research methods. The study included 123 women with clinical development of HA and impaired reproductive function, who consulted the consultative clinic of the RSSPMC of Obstetrics and Gynecology of the Ministry of Health of the Republic of Uzbekistan. The criteria for inclusion in the main group were: age of women from 18 to 35 years (average age was 25.8 .. 3.28 years), absence of pregnancy, body mass index over 25 kg / m2. Exclusion criteria from the main group: type 1 and 2 diabetes, pituitary tumors, hypogonadotropichypogonadism, congenital adrenal hyperplasia, hypothyroidism, severe somatic pathology. All patients who applied for the consultation underwent: (1) Collection of anamnestic information. (2) Measurement of anthropometric indicators (height, weight, waist and hip circumference) and assessment of body hair growth using the Ferriman-Hallway scale. (3) Body mass index was
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Coronavirus disease (COVID-19), the ongoing global pandemic, is caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Recent evidence shows that the virus utilizes angiotensin-converting enzyme 2 (ACE2) as a spike protein receptor for entry into target host cells. The bovine ACE2 contains key residues for binding to the spike protein receptor-binding domain. This study evaluated the hypothesis that bovine gonadotroph expresses ACE2, and spike protein suppresses luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion from cultured bovine anterior pituitary (AP) cells. ACE2 mRNA expression and ACE2 protein expression were detected in the bovine AP cells using reverse transcription PCR and western blot analysis. Immunofluorescence microscopy analysis with the anti-ACE2 antibody revealed the co-localization of ACE2 and gonadotropin-releasing hormone (GnRH) receptor on the gonadotroph plasma membrane. Approximately 90% of GnRH receptor-positive cells expressed ACE2, and approximately 46% of ACE2-positive cells expressed the GnRH receptor. We cultured bovine AP cells for 3.5 days and treated them with increasing concentrations (0, 0.07, 0.7, or 7 pM) of recombinant spike protein having both S1 and S2 regions. The spike protein (0.07-7 pM) suppressed both basal and GnRH-induced LH secretion (P < 0.05). Spike protein (0.7-7 pM) suppressed GnRH-induced (P < 0.05), but not basal FSH secretion. In contrast, pre-treatment with ERK 1/2/5 inhibitor (U0126) partially restored the GnRH-induced LH and FSH secretion from the spike protein suppression. Collectively, the results indicate that gonadotrophs express ACE2, a receptor for coronavirus 2 spike protein, which in turn suppresses LH and FSH secretion from AP cells.
Subject(s)
Follicle Stimulating Hormone , Luteinizing Hormone , Pituitary Gland, Anterior , Spike Glycoprotein, Coronavirus , Angiotensin-Converting Enzyme 2 , Animals , COVID-19 , Cattle , Follicle Stimulating Hormone/metabolism , Luteinizing Hormone/metabolism , Pituitary Gland, Anterior/metabolism , Receptors, LHRH/metabolism , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/metabolismABSTRACT
A new dangerous respiratory disease COVID-19 was first reported in China in December 2019, the pathogen SARS-Coronavirus 2 (SARS-CoV-2), belonging to the beta coronavirus genus, which, in addition to SARS-CoV-2, includes SARS-CoV-1 and MERS-CoV. The genome of SARS-CoV-2 is almost 80% similar to SARS-CoV-1 and 50% to MERS-CoV. The mechanisms of infection of SARS-CoV-1 and SARS-CoV-2 are also similar and occur through the binding of the virus to the type 2 angiotensin-converting enzyme protein (ACE2), which is widely represented in the human body with predominant expression in endocrine tissues. In this connection, SARS-CoV-1 and SARS-CoV-2 affect the organs of the endocrine system, causing damage and hormonal changes that affect the prognosis of the course of COVID-19. This literature review is devoted to the analysis of changes in the organs of the endocrine system that occur during infection with SARS-CoV-1 and SARS-CoV-2, as well as the potential effect of hormones on susceptibility to SARS-CoV-2.
Subject(s)
Angiotensin-Converting Enzyme 2 , COVID-19 , Angiotensin-Converting Enzyme 2/genetics , Endocrine System , Humans , SARS-CoV-2ABSTRACT
Introduction: The COVID-19 epidemic has severely affected the life of people around the world. Periods of stress and psychological distress caused by this pandemic can affect a woman's menstrual cycle. The COVID-19 pandemic has had a significant impact on women's reproductive health. This narrative review was performed with aim to evaluate the effect of coronavirus on different aspects of each part of this axis and its relationship with women's health considering hypothalamic-pituitary-ovarian axis.
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INTRODUCTION: Angiotensin-converting enzyme 2 (ACE2) is the receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The effects of SARS-CoV-2 on normal pituitary glands function or pituitary neuroendocrine tumors (PitNETs) have not yet been elucidated. Thus, the present study aimed to investigate the potential risks of SARS-CoV-2 infection on the impairment of pituitary glands and the development of PitNETs. METHODS: PitNETs tissues were obtained from 114 patients, and normal pituitary gland tissues were obtained from the autopsy. The mRNA levels of ACE2 and angiotensin II receptor type 1 (AGTR1) were examined by quantitative real-time PCR. Immunohistochemical staining was performed for ACE2 in 69 PitNETs and 3 normal pituitary glands. The primary tumor cells and pituitary cell lines (MMQ, GH3 and AtT-20/D16v-F2) were treated with diminazene aceturate (DIZE), an ACE2 agonist, with various dose regimens. The pituitary hormones between 43 patients with SARS-CoV-2 infection were compared with 45 healthy controls. RESULTS: Pituitary glands and the majority of PitNET tissues showed low/negative ACE2 expression at both the mRNA and protein levels, while AGTR1 showed high expression in normal pituitary and corticotroph adenomas. ACE2 agonist increased the secretion of ACTH in AtT-20/D16v-F2 cells through downregulating AGTR1. The level of serum adrenocorticotropic hormone (ACTH) was significantly increased in COVID-19 patients compared to normal controls (p < 0.001), but was dramatically decreased in critical cases compared to non-critical patients (p = 0.003). CONCLUSIONS: This study revealed a potential impact of SARS-CoV-2 infection on corticotroph cells and adenomas.
Subject(s)
COVID-19 , Neuroendocrine Tumors , Humans , Peptidyl-Dipeptidase A/genetics , Pituitary Gland/metabolism , SARS-CoV-2ABSTRACT
The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is centralizing the interest of the scientific world. In the next months, long-term consequences on the endocrine system may arise following COVID-19. In this article, we hypothesized the effects of SARS-CoV-2 taking into account what learned from the severe acute respiratory syndrome coronavirus (SARS-CoV) that caused SARS in 2003.