Patient: Male, 24-year-old Final Diagnosis: Acute kidney injury • coagulopathy • liver failure • SARS-CoV-2 Symptoms: Cough • fever Medication: — Clinical Procedure: — Specialty: Gastroenterology and Hepatology • Infectious Diseases Objective: Unusual clinical course Background: Coronavirus disease 2019 (COVID-19) is a newly emerging disease that is still not fully characterized. It is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel virus that can be transmitted easily from human to human mainly by the respiratory route. Currently, there is no specific treatment for COVID-19 or a vaccine for prevention. The disease has various degrees of severity. It often presents with non-specific symptoms such as fever, headache, and fatigue, accompanied by respiratory symptoms (e.g., cough and dyspnea) and other systemic involvement. Severe disease is associated with hemophagocytic syndrome and cytokine storm due to altered immune response. Patients with severe disease are more likely to have increased liver enzymes. The disease can affect the liver through various mechanisms. Case Report: We report an unusual case of SARS-CoV-2 infection in a 24-year-old man with no previous medical illness, who presented with mild respiratory involvement. He had no serious lung injury during the disease course. However, he experienced acute fulminant hepatitis B infection and cytokine release syndrome that led to multiorgan failure and death. Conclusions: It is uncommon for SARS-CoV-2 infection with mild respiratory symptoms to result in severe systemic disease and organ failure. We report an unusual case of acute hepatitis B infection with concomitant SARS-CoV-2 leading to fulminant hepatitis, multiorgan failure, and death.

Background /Aims: Corona virus disease 2019 (COVID 19) is a pandemic infectious disease of 2020, which often presents with respiratory and gastrointestinal symptoms. The behavior of the virus and its full clinical picture has not been fully studied yet. Many case reports and case series have been running in order to elaborate different presentations and associations. Pulmonary and gastrointestinal features of COVID-19 infection are well outlined; however, neurological manifestations are less defined. Case presentation We report two adult cases of COVID-19 infection presented with acute Guillain-Barre Syndrome (GBS), and a literature review on the causal association between COVID-19 and GBS. Conclusion Our two case reports in addition to literature review of 116 published cases may help offer insight into the clinical course of COVID-19 infection. Our two COVID-19 patients presented with neurological manifestations of GBS which were not preceded with any respiratory, gastrointestinal or other systemic infection. This leads us to raise the possibility of establish direct causal association between COVID-19 infection and GBS. Physicians should have high clinical suspicions when encounter GBS patient during the current COVID-19 pandemic and consider co-existence of COVID-19 infection that may warrant SARS-CoV-2 testing, isolation precautions, and specific treatment for Covid-19 infection.

Iron deficiency anemia is a common cause of anemia that develops when body stores of an iron drop too low to support normal red blood cell (RBC) production. Inadequate dietary iron, impaired iron absorption, bleeding, or loss of body iron in the urine may be the cause. Iron is a key part of red blood cells. Without iron, the blood cannot carry oxygen effectively. Our body normally gets iron through the diet. It also reuses iron from old red blood cells. A little is known about the association between iron deficiency anemia and neutropenia. Here we report a 44-year-old female who presented with iron deficiency anemia and found to have neutropenia recovered after she received intravenous (IV) iron therapy. However, she did not develop any serious infections during the neutropenia and responded to iron therapy.

Idiopathic thrombocytopenic purpura (ITP) is a disease in which the immune system attacks platelets and causes a decrease in their number, exposing the patient to bleeding risk. It is a diagnosis by exclusion. ITP usually presents as acute disease and is self-limiting in pediatric patients, while it tends to be chronic in adults. Eltrombopag is a thrombopoietin receptor agonist used as a second-line treatment for ITP. This drug is approved for use in adults as second-line therapy, but little is known about its use in the pediatric patient population. We report the case of a 14-year-old girl with chronic steroid-dependent ITP who responded well to eltrombopag and maintained treatment-free remission after stopping the drug.

Sickle cell anemia (SCA) is a hereditary hemoglobin (Hb) disorder associated with a very specific molecular lesion, which is the exchange of glutamic acid for valine in the sixth residue of the Hb beta chain, originating the S Hb. It is characterized by intermittent episodes of vascular occlusion and end-organ damage. Progressive organ damage may affect any organ with brain, eyes, pulmonary, hepatobiliary, spleen, genitourinary, and the musculoskeletal systems being the most commonly involved and reported. Other complications of the disease that have not been well described or studied include cranio-orbital syndromes, oropharyngeal syndromes, periodontal disease, and otologic syndromes. Considering the vaso-occlusive nature of sickle cell disease (SCD), the potential for auditory damage is not unexpected. However, the incidence of subjective hearing impairment among SCA is very low and and little is known about the relationship between SCA and hearing loss. Here we report a 43-year-old female with SCA who presented with sudden bilateral hearing loss and generalized body ache and admitted as a case of sensorineural deafness with vascular crisis; she received IV fluid and analgesia and improved after five days from the therapy.

Idiopathic thrombocytopenic purpura (ITP) is a disease in which the immune system attacks platelets and decreases their number, which increases the patient's risk of bleeding. ITP is diagnosed by exclusion and usually manifests as acute disease. It is self-limiting in pediatric patients, while it tends to be a chronic disease in adults. Treatment of ITP focuses on maintaining a sufficient platelet count to decrease the risk of bleeding rather than normalize the platelet count. Most patients respond to first-line treatments, such as steroids and intravenous immunoglobulin (IVIG). However, some cases can become steroid-dependent or unresponsive to first-line therapy, in which case, second-line therapy is required to control symptoms or the platelet count. Second-line therapy includes either rituximab or a thrombopoietin receptor agonist (eltrombopag, romiplostim). In a few cases, when second-line therapy alone is insufficient to control the disease, a combination of therapies is required to control the symptoms and platelet count. Here, we present a case of a 41-year-old man with refractory ITP who did not respond to first-line treatment with either steroids or IVIG or a combination of the two, and also did not respond to eltrombopag alone and required a combination of eltrombopag and rituximab to control his disease.

Idiopathic thrombocytopenic purpura (ITP) is a disease in which the immune system attacks platelets and causes decrease in its number exposing the patient to risk of bleeding. It is diagnosed by exclusion. Eltrombopag is a thrombopoietin receptor agonist which is used as second-line treatment for patients with ITP. The usual starting dose is 25 mg daily and maintenance dose is 75 mg daily. Little is known about the dose of eltrombopag in patients with sleeve gastrectomy since reduction in the amount of functioning gastrointestinal tract after gastric bypass surgery leads to decreased time to drug absorption and reduced drug bioavailability. Here we are reporting a 46-year-old female with ITP and sleeve gastrectomy who responded to low-dose eltrombopag 25 mg every other day, which is equivalent to 12.5 mg daily, and maintained adequate platelet counts on this dose.

Normal thyroid hormone level is essential to maintain the normal physiologic function of the human body. Disturbances of these hormone levels have variable clinical manifestations ranging from asymptomatic to severe illness. Resistance to thyroid hormone (RTH) is a syndrome characterized by reduced intracellular action of T3, the active thyroid hormone. It is a rare autosomal dominant condition and occurs mostly due to heterogeneous mutations in the thyroid hormone receptor. Other causes of RTH include thyroid hormone cell membrane transport defect and thyroid hormone metabolism defect. Affected individuals present with symptoms of both increased and decreased thyroid hormone action, depending on the tissue's predominant receptor isoform expression, the magnitude of hormonal resistance, and the effectiveness of compensatory mechanisms.Here, we share our experience in diagnosing a case of RTH confirmed with a genetic test and found to have sequence variant mutation that is not well described in the literature previously due to the absence of genetic conclusive evidence.