Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the lethal causes of chronic liver disease globally. NAFLD can ultimately progress to non-alcoholic steatohepatitis (NASH) given persistent cellular insult. The crux of the problem lies in fat accumulation in the liver, such as increased fatty acid substrates owing to consumption of a high-fat diet, altered gut physiology, and excess adipose tissue. Being the hepatic manifestation of metabolic syndrome, insulin resistance is also among one of the many stimuli. Therefore, drugs, such as glucagon-like peptide-1 receptor agonist (GLP-1 RA) can play a significant role in reducing inflammation, in addition to weight loss and dietary habits. In this review article, we have reviewed the role of exenatide, liraglutide, and semaglutide in the management of NASH. Two of the agents, exenatide and semaglutide, have a predominant role in reducing alanine aminotransferase (ALT) levels, therefore reducing inflammation and promoting weight loss. However, these agents have a lesser impact on the degree of fibrosis. Liraglutide, on the other hand, has been shown to significantly decrease the degree of fibrosis and has been found helpful in reversing mild degrees of steatosis. Therefore, these agents warrant attention to the new perspective that has been presented so that future guidelines may incorporate and streamline individualized therapy.

Various factors can lead to thyroiditis, including any acute inflammatory process, especially viral illness. While coronavirus disease 2019 (COVID-19) has been linked to disorders of various systems, there is a lack of literature showing an association of coronavirus with the cause of Hashimoto's thyroiditis. Several possible mechanisms for this outcome have been proposed; chief among them is molecular mimicry. Here, we are reporting a case of Hashimoto's thyroiditis incited by COVID-19 in a 34-year-old obese female who presented with anxiety, behavioral changes, and repeated head movements. The patient had an elevated thyroid stimulating hormone (TSH) level, a low thyroxine (T4) level, and a positive anti-microsomal antibody screen. The patient also tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA. Ultrasound of the patient's neck showed an enlarged heterogeneous thyroid gland. Thyroid replacement therapy with intravenous levothyroxine was started with the subsequent oral transition. Concurrently, she received antibiotics, steroids, and low-molecular-weight heparin for COVID-19. The patient exhibited significant improvement in her mental status, with an eventual return to baseline. The results of the thyroid panel obtained at the outpatient follow-up were normal. Although there is a paucity of data to show COVID-19 as a cause of this painless thyroiditis, this case demonstrates such causality between these two.

Thrombotic thrombocytopenic purpura (TTP) is a thrombotic microangiopathy (TMA) caused by severely reduced ADAMTS13 or the von Willebrand factor-cleaving protease (VWFCP) enzyme resulting in low platelet and red blood cell counts along with severe renal, cardiac, and neurological dysfunction. Plasmapheresis is the treatment of choice. Mitomycin, a widely used chemotherapeutic agent for gastrointestinal (GI) cancers anal and breast cancers, has been reported to occasionally cause severe TTP and hemolytic uremic syndrome (HUS) cases. Here, we present a case of a 57-year-old African American transgender patient who presented with worsening kidney function, thrombocytopenia, and anemia following mitomycin therapy for her anal squamous cell carcinoma. Peripheral smear showed numerous schistocytes, and the patient was diagnosed with TTP because of low ADAMTS13 levels. The patient was started on plasmapheresis and steroid with ultimate improvement in condition. TTP is a rare condition that can be idiopathic or acquired. Further research is required to assess the complexity of the underlying mechanism. Early diagnosis and aggressive management often lead to a favorable outcome.

Todd's paresis or phenomenon (TP) is a focal weakness in a part of the body after a seizure. Seizure is an abrupt change in behavior caused by the cerebral cortex's electrical hyper-synchronization of neuronal networks. After the seizure, there is usually a transition period from the ictal state to the pre-seizure baseline level of awareness and function, referred to as the postictal period. Postictal symptoms include many systems, including sensory, motor, and psychosis. This phenomenon is named after Robert Bentley Todd, who first described it. Todd's paresis can be confused with other conditions, most commonly a stroke. Postictal ocular manifestation may be accompanied by aphasia or hemiplegia, but isolated gaze palsy is rarely reported. We are reporting a rare and first known isolated ophthalmoparesis and ptosis as postictal findings with no structural abnormalities present in imaging studies and complete resolution over three weeks on its own as an atypical postictal phenomenon. Patients with an underlying structural abnormality of the brain are more susceptible to Todd's phenomenon. Unusual manifestations of Todd's phenomenon are rare but clinically relevant and are decisive in therapeutic decision-making. Our patient presents a rare manifestation of Todd's phenomenon as ptosis and ophthalmoparesis in an elderly male with no underlying structural brain abnormalities that resolved within three weeks. Further research into the causes is needed to distinguish it from a stroke

Novel outbreaks with COVID-19 can cause multiple systemic manifestations, including autoimmune disease. Among all the infections, respiratory complications are the most apparent symptoms. Guillain-Barre syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy often related to previous infectious exposure. GBS emerged as a potentially severe complication of coronavirus disease 2019 (COVID-19) since its declaration as a global pandemic. We report the first case of COVID-19-induced acute motor axonal neuropathy variant of Guillain-Barre syndrome (GBS) from New York, USA. Our patient was a 66-year-old woman who had recently tested positive for COVID-19 and presented with bilateral upper and lower extremity weakness. Electromyogram studies showed acute demyelinating polyradiculoneuropathy. She was diagnosed with an acute motor axonal neuropathy variant of GBS. She was successfully treated with intravenous immunoglobulins (IVIGs) with marked improvement. In six months, she regained her strength back to normal. Whether GBS incidence in COVID-positive patients is based on molecular mimicry or antiganglioside antibodies is unclear. Physicians should be aware of GBS as a potentially serious complication associated with COVID-19. Further investigations and trials should be conducted better to understand the mechanism of GBS in patients of COVID-19.