Since the emergence of the COVID-19 pandemic at the end of 2019, a massive vaccination campaign has been undertaken rapidly and worldwide. Like other vaccines, the COVID-19 vaccine is not devoid of side effects. Typically, the adverse side effects of vaccination include transient headache, fever, and myalgia. Endocrine organs are also affected by adverse effects. The major SARS-CoV-2 vaccine-associated endocrinopathies reported since the beginning of the vaccination campaign are thyroid and pancreas disorders. SARS-CoV-2 vaccine-induced pituitary diseases have become more frequently described in the literature. We searched PubMed/MEDLINE for commentaries, case reports, and case series articles reporting pituitary disorders following SARS-CoV-2 vaccination. The search was reiterated until September 2022, in which eight case reports were found. In all the cases, there were no personal or familial history of pituitary disease described. All the patients described had no previous SARS-CoV-2 infection prior to the vaccination episode. Regarding the type of vaccines administered, 50% of the patients received (BNT162b2; Pfizer–BioNTech) and 50% received (ChAdOx1 nCov-19; AstraZeneca). In five cases, the pituitary disorder developed after the first dose of the corresponding vaccine. Regarding the types of pituitary disorder, five were hypophysitis (variable clinical aspects ranging from pituitary lesion to pituitary stalk thickness) and three were pituitary apoplexy. The time period between vaccination and pituitary disorder ranged from one to seven days. Depending on each case’s follow-up time, a complete remission was obtained in all the apoplexy cases but in only three patients with hypophysitis (persistence of the central diabetes insipidus). Both quantity and quality of the published data about pituitary inconveniences after COVID-19 vaccination are limited. Pituitary disorders, unlike thyroid disorders, occur very quickly after COVID-19 vaccination (less than seven days for pituitary disorders versus two months for thyroid disease). This is partially explained by the ease of reaching the pituitary, which is a small gland. Therefore, this gland is rapidly overspread, which explains the speed of onset of pituitary symptoms (especially ADH deficiency which is a rapid onset deficit with evocative symptoms). Accordingly, these pilot findings offer clinicians a future direction to be vigilant for possible pituitary adverse effects of vaccination. This will allow them to accurately orient patients for medical assistance when they present with remarkable symptoms, such as asthenia, polyuro-polydipsia, or severe headache, following a COVID-19 vaccination.

BACKGROUND:Type 1 autoimmune pancreatitis (AIP), also known as lymphoplasmacytic sclerosing pancreatitis (LPSP), is a rare cause of chronic pancreatitis, characterized by a fibro-inflammatory process. However, patients with AIP may have a good respon...

Renal tubular involvement in Sjögren's syndrome (SS) often described with renal tubular acidosis, nephrogenic diabetes insipidus, or rarely with Fanconi syndrome. SS presenting with clinical features of Bartter's syndrome or Gitelman's syndrome is rare. We report a case of a female patient who presented an acquired Bartter syndrome with a primary SS.

Background: Takayasu arteritis is a rare and chronic granulomatous vasculitis that affects the large vessels. Takayasu arteritis targets the aorta and its branches and is still of unknown etiology. It often affects female patients under 50 years of age. A relationship between Takayasu arteritis and tuberculosis has been suggested for a long time. Case presentation: We report a severe case of Takayasu arteritis in a 10-year-old Tunisian child revealed by renovascular hypertension with concomitant pulmonary tuberculosis. Conclusions: Our patient is among only a few cases of Takayasu arteritis published worldwide affecting young infants and adolescents, which underlines the strong relationship between Takayasu arteritis and tuberculosis.

Obstructive sleep apnea (OSA) may be linked to various factors that narrow the upper airways, such as obesity, adenotonsillar hypertrophy and craniofacial abnormalities. Hypothyroidism has also been described as a risk factor for OSA. However, the implication of goiter independently of thyroid function in the occurrence of OSA remains unclear. We present the case of a 66-year-old patient, with a large compressive multinodular goiter for whom total thyroidectomy was indicated. During the preoperative assessment, the patient showed a body mass index (BMI) of 37.8 kg/m2 with symptoms of OSA. Respiratory polygraphy confirmed the diagnosis of severe OSA (apnea hypopnea index: AHI=32) and treatment with continuous positive airway pressure (CPAP) was initiated prior to thyroid surgery. Surprisingly, after total thyroidectomy, OSA symptoms disappeared and the patient abandoned CPAP therapy. Subsequent respiratory polygraphy after thyroidectomy showed a decrease in AHI to a normal value (AHI < 5). Interestingly, there was no change in BMI or other factors explaining the resolution of OSA, except for thyroidectomy. This case report suggests that goiter can be considered a risk factor for OSA. However, prospective studies are needed to accurately assess the effects of goiter on occurrence of OSA according to its dimensions and local extension.