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In 2021, the scientific community was marked by the introduction of vaccine against COVID-19. This is major step in overcoming the pandemic, but it does not mean that several side effects or precautions are not related to the immunization; however, the current level of statistical evidence concerning potential negative effects is low, as logically expected at this point. We aim to introduce a female case who was confirmed with subacute thyroiditis after COVID-19 vaccination. Prompt recognition of subacute thyroiditis avoids unnecessary investigations, hospitalizations or even exposure to antibiotics as seen in this case. Early intervention with anti-inflammatory medication releases the symptoms. The association with vaccine against COVID-19 might be incidental or not; more evidence is needed but as far as we might think nowadays, the connection is possible, thus the importance of specific awareness. [ABSTRACT FROM AUTHOR]

Introduction. Up to 50-70% of the population (women seem more affected than men) have a thyroid nodule (TN) of various dimensions, especially less than 1 cm. The incidence is age-related, but the prevalence is also consistent in women of reproductive age. The investigations in order to conceive usually involve the thyroid panel and the accidental ultrasound detection of a TN is a relatively frequent scenario. The relationship with low fertility rate is less strong, with the exception of autoimmune thyroid background. Aim. To introduce a series of cases with TN detected during investigations for fertility. Method. These are two case reports. The hormonal and imagery profile is provided. Case 1. We present the case of a 26-year-old non-smoking female coming from a nonendemic area. She is nulipara. The personal and family medical history is irrelevant. She has regular menses and seeks for fertility. The gynecological exam is normal, so she was referred for endocrine assays. The thyroid blood tests showed normal TSH (1.3 μUI/mL), calcitonin (4.3 pg/ mL; N: 1-4.8 pg/mL) and TPO antibodies (10 UI/mL; N<35 UI/mL). Thyroid ultrasound shows right lobe of 4.9/2.1/2.1 cm, and left lobe of 4.6/1.7/1.4 cm. The right lobe is displayed by a hypoechoic TN (peripheral halo, vascularised) of 2.1/1.5/3.2 cm, with another of 0.7/0.4/0.4 cm, without lymph nodes involvement. Due to high dimensions and ultrasound features, the patient was referred for surgery. Case 2. A 34-year-old smoking female, coming from a nonendemic area, was admitted for fertility issues. She has four healthy children (the oldest 8 years ago), with the same partner. She presents irregular menses for the last five months. TPOAb are positive (270 UI/mL), with a normal thyroid function (TSH = 2.3 μUI/mL; N: 0.5-4.5 μUI/mL). The thyroid ultrasound pattern is hypoechoic, with a few TN of maximum 0.3 cm. The clinical examination accidentally revealed lipomas at the skull of 2 cm (confirmed at computed tomography). The lipid profile was normal, unrelated to thyroid and skull anomalies. Conclusions. Both cases had thyroid anomalies most probably unrelated to fertility issues. [ABSTRACT FROM AUTHOR]

Ectopic Cushing syndrome or ectopic ACTH (Adrenocorticotropic Hormone) syndrome, a rare but severe condition, is due to a non-pituitary ACTH excess or exceptionally a non-hypothalamic CRH (Corticotropin - Releasing Hormone) hyper-production, usually due to a neoplasia which may be of endocrine or nonendocrine origin. Our objective is to introduce a brief literature regarding ectopic Cushing syndrome based on five micro-chapters: clinical evaluation, lab tests, imaging assays, therapy options and as discussions – the current limits of the topic. This actually comes with a twist in every aspect since a lot of data are yet to be clarify about this complex medical entity. Clinical presentation may be suggestive for Cushing syndrome but a few characteristics are more frequently seen as hyperpigmentation, rapid onset up even becoming an endocrine emergency, male preponderance, potential weight loss instead of weight gain, as oppose to Cushing disease or adrenal Cushing syndrome. Hypokalaemia is a hallmark of this particular situation. Additional tests are necessary to identify the source of ACTH excess and this twist is necessary in addition to traditional suppression tests for glucocorticoid axes. Some authors describe another twist in recognition of syndrome presentation: that actually there are two subtypes – one caused by a very aggressive tumour with rapid evolution and another with a lent slope of clinical features appearance caused by a occult neoplasm. Another twist is the fact that, in cases without a clear tumour origin, bilateral adrenal removal is actually necessary until adequate identification of source is done (if ever). Overall, a complex multidisciplinary team is necessary, the prompt recognition and therapy is life saving and numerous limits of both diagnosis and management are still a matter of debate [ABSTRACT FROM AUTHOR]

Hot flashes (HF), transitory episodes of erythema, heat sensation, anxiety followed by chills, are described in carcinoid syndrome, mastocytosis, medullary thyroid cancer, hyperthyroidism, pheochromocytoma, alcohol consumption, side effects of drugs, and infections. They are pivotal among menopause-related vasomotor symptoms beside genitourinary syndrome in addition to sleep disturbances (40-60% of females), and metabolic changes. HF affect 70% of women (20% of them have a severe impairment of life quality); they last for 4-7 years, starting 4-6 years before last menstruation. The main HF cause is ovarian-derivate estrogen deprivation which activates complex endocrine and neuroendocrine mechanisms involving noradrenaline, 5-hydroxytriptamine (5-HT), calcitonin gen-related peptide, orexin, kisspeptin, neurokinin B, and epigenetic elements like modulation of tachykinin receptor 3, accelerated epigenetic aging (as found in Women's Health Initiative Observational Study), expression of central serotonin transporters. Estrogen deficiency uncouples the negative feedback with preoptic area of hypothalamus, responsible for thermoregulation by inducing an exacerbated vasodilatory response to a small increase of body temperature. TRPV1 (transient receptor potential vanilloid 1) in preoptic hypothalamic area may play a role by NE-α2ADR (norepinephrine- activated α2-adrenergic receptors) activation. Higher expression of serotonin transporter SLC6A4 causes a lack of 5-HT at synapsis which is a trigger for presynaptic 5-HT receptor feedback, thus a release of serotonin amount prevents hot flashes. Kisspeptin and neurokinin B which are co-expressed in infundibular nucleus of hypothalamus are involved in central thermoregulation and gonadotropin releasing hormone anomalies. The NKR3 (neurokinin 3 receptor) antagonist receptor improves HF. Understanding the pivotal role of central neurotransmitters in hot flashes is the basis of new therapeutically researches because otherwise estrogen replacement has a long list of side effects, and it is contraindicated in breast cancer-related hypogonadism. [ABSTRACT FROM AUTHOR]

Introduction. As opposed to secreting tumours, non-functioning pituitary adenomas are usually diagnosed at a later stage, when they are large enough to cause symptoms due to mass effect rather than because their associated endocrine dysfunction. We aim to introduce a case report with limited therapy options. Case presentation. We present the case of a 69 year-old male patient with a history of stroke, atrial fibrillation and type 2 diabetes, who was initially admitted to the neurology department three years ago for frontal headaches and visual disturbances. The MRI (magnetic resonance imaging) exam revealed a 15.4/26.7/19.5 mm sellar mass, with suprasellar and parasellar extension, minimal optic chiasm compression and pituitary stalk deviation. Initial pituitary hormone profile showed central hypogonadism and mild hyperprolactinemia. The patient underwent neurosurgery evaluation but at that point transsphenoidal surgery was contraindicated due to severe cardiovascular comorbidities and the patient was referred to the endocrinology department for further follow-up, where he presented a year later, after worsening of symptoms. The MRI revealed tumour enlargement (18.5/28/24.6 mm) and stationary hormonal profile. The diagnosis of nonfunctioning pituitary macroadenoma was once again confirmed, cabergoline was initiated as adjuvant therapy since surgery was still contraindicated because high cardiovascular risk. Stereotactic radiation was not an option due to tumour proximity to the optic chiasm, therefore the patient underwent conventional radiotherapy. Evaluation after 3 months showed stationary clinical picture while MRI scan 3 months revealed a mild tumour growth (4 mm in all diameters). Further cabergoline therapy 2 mg/week was prescribed and the patient needs carefull monitorization for worsening of symptoms and hypopituitarism. Conclusion. Surgery is the mainstay of therapy in case of large nonfunctioning pituitary macroadenomas. If contraindicated, the available options include radiotherapy and medical therapy like cabergoline, with varying results, mostly suboptimal. [ABSTRACT FROM AUTHOR]

Hereditary syndromes underlying neuroendocrine tumours are extremely heterogeneous and, despite the genetic background, their recognition may actually be done later in life in many cases. Our purpose is to introduce a case of neurofibromatosis type 1 -related pheocromocytoma on a patient within his six decade of life after multiple cardiovascular complications. A 53-year old male is admitted for loss of appetite with weight loss, decreased exercise tolerance, transient occipital headache, night sweats. His medical history revealed arterial hypertension, right carotid artery ischemic stroke, and a recently non-STEMI myocardial infarction diagnosed two months ago. The pathological family history illustrated mother and a brother prematurely dying of myocardial infarction (no date of skin anomalies). Clinical examination reveals café-au-lait spots, axillary freckles, skin neurofibromas and a large plexiform neurofibroma in the right thigh. Evaluation of the adrenal gland revealed highly elevated values of urinary metanephrines and normetanephrines. Computed tomography showed a left adrenal gland tumour of 31/39 mm. Thus neurofibromatosis type 1 in addition to a left pheocromocytoma was confirmed. A cardiologic examination before surgery was re-done. Given previous pathological history (cardiovascular events like stroke and nonSTEMI infarction) adrenalectomy was delayed for the moment in addition to second antiplatelet agent and the alpha blocker medication in increasing doses. The adrenal tumour removal is planned to be done as soon as cardiovascular risk is acceptable. The importance of endocrine check is seen in young patients with severe cardiovascular and neurological acute conditions that are actually caused by a hormonal excess like found in pheocromocytoma. Nevertheless, the spectrum of tumours associated with neurofibromatosis type 1 is heterogeneous and screening protocols are still a matter of debate. Delayed diagnosis worsts the overall prognosis [ABSTRACT FROM AUTHOR]