Mirizzi syndrome occurs in up to 6% of patients with cholecystolithiasis. It is generally caused by external compression of the common hepatic duct by a gallstone impacted in the neck of the gallbladder or the cystic duct, which can lead to fistulisation. The aim of this review was to highlight the proposed classifications for Mirizzi syndrome (MS) and to provide an update on modern approaches to the diagnosis of this disease. We conducted research on various internet databases and the total number of records was 993, but after a gradual process of elimination our final review consisted of 21 articles. According to the literature, the Cesendes classification is the most commonly used, but many new suggestions have appeared. Our review shows that the ultrasonography (US) is the most frequently used method of initial diagnosis, despite still having only average sensitivity. Magnetic resonance cholangiopancreatography (MRCP) and endoscopic retrograde cholangiopancreatography (ERCP) are good methods and are similarly effective, but only the latter can be simultaneously therapeutic. Some modern methods show very high sensitivity, but are not so commonly administered. Mirizzi syndrome is still a diagnostic challenge, despite the advancement of the available tools. Preoperative diagnosis is crucial to avoid complications during treatment. New research may bring a unification of classifications and diagnostic algorithms.

It is important to acknowledge the impact that COVID-19 has on the thyroid gland and how the thyroid gland status before and during infection affects SARS-CoV-2 severity. To this day those dependencies are not fully understood. It is known that the virus uses angiotensin-converting enzyme-2 as the receptor for cellular entry and it can lead to multiple organ failures due to a cytokine storm. Levels of proinflammatory molecules (such as cytokines and chemokines) which are commonly elevated during infection were significantly higher in observed SARS-CoV-2-positive patients. In terms of hypothyroidism, hyperthyroidism, and autoimmune thyroid diseases, there is no proof that those dysfunctions have a direct impact on the more severe courses of COVID-19. Regarding hyper- and hypothyroidism there was no consequential dependency between the frequency of SARS-CoV-2 infection morbidity and more severe post-infectious complications. When it comes to autoimmune thyroid diseases, more evaluation has to be performed due to the unclear relation with the level of antibodies commonly checked in those illnesses and its binding with the mentioned before virus. Nonetheless, based on analyzed works we found that COVID-19 can trigger the immune system and cause its hyperactivity, sometimes leading to the new onset of autoimmune disorders. We also noticed more acute SARS-CoV-2 courses in patients with mainly reduced free triiodothyronine serum levels, which in the future, might be used as a mortality indicating factor regarding SARS-CoV-2-positive patients. Considering subacute thyroiditis (SAT), no statistically important data proving its direct correlation with COVID-19 infection has been found. Nevertheless, taking into account the fact that SAT is triggered by respiratory tract viral infections, it might be that SARS-CoV-2 can cause it too. There are many heterogenous figures in the symptoms, annual morbidity distribution, and frequency of new cases, so this topic requires further evaluation.