scholarly journals Case of severe liver damage in COVID-19

2021 ◽  
pp. 84-91
Author(s):  
E. Yu. Plotnikova ◽  
E. N. Baranova ◽  
M. S. Karyagina ◽  
O. A. Vorosova ◽  
K. A. Krasnov

The 2019 outbreak of coronavirus disease (COVID-19) caused by severe acute coronavirus 2 respiratory syndrome (SARS-CoV-2) has been a  global concern since December 2019. Although most patients with COVID-19  have mild clinical manifestations, in about 5% of these patients the disease eventually progresses to severe lung injury or even multiple organ dysfunction. This situation presents various problems for hepatology. In the context of liver damage in patients with COVID-19, several key problems need to be addressed. For example, it is important to determine whether a SARS-CoV-2 can directly enter the liver, especially when it appears that ACE2 is marginally expressed in hepatocytes. In addition, the mechanisms underlying liver dysfunction in patients with COVID-19 are multifactorial and are associated with hyperinflammation, dysregulated immune responses, abnormal coagulation, and drugs. The  article describes the  potential pathogenesis of  liver damage associated with COVID-19. Histopathological evidence suggests a marked disruption of the intrahepatic network of blood vessels secondary to systemic changes caused by a virus that can trigger a coagulation cascade and damage the endothelial layer of blood vessels. There is also a clinical case of polyethylene damage to the liver in a young man who led to death. Against the background of infection COVID-19 he developed massive thrombosis of the liver vessels, followed by the development of necrosis — fibrosis — cirrhosis — acute liver failure, which caused death.

2021 ◽  
Vol 8 (7) ◽  
pp. 978
Author(s):  
Shabarini Srikumar ◽  
Shridharan Perumal

The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a pandemic by the world health organization on March 11, 2020. The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations. SARS-CoV-2 causes direct activation of anti-viral immune responses and leads to the release of uncontrolled inflammatory mediators. These SARS-CoV-2-induced immune responses may lead to various other abnormalities like lymphopenia, thrombocytopenia and granulocyte and monocyte dysfunction, making the patient more prone to secondary infections by microorganisms, which may result in further further serious complications like septic shock, severe multiple organ dysfunction and eventually death. Therefore, mechanisms underlying immune abnormalities in patients with COVID-19 disease must be elucidated to guide clinical management of the disease. Rational management in combating the disease includes enhancing anti-viral immunity and inhibiting systemic inflammation, which is key to successful treatment.


2020 ◽  
Vol 76 (4) ◽  
pp. 9-15
Author(s):  
V.I. Petrov ◽  
◽  
A.V. Ponomareva ◽  
I.V. Ivakhnenko ◽  
O.V. Razvalyaeva ◽  
...  

Infection caused by the new coronavirus SARS-CoV-2 initially associated with respiratory damage and the development of respiratory symptoms. However, it was subsequently shown that COVID-19 can be considered as a systemic inflammatory process with multiple organ damage. One of the most frequent extra pulmonary manifestations of SARS-CoV-2 infection is liver damage. Several factors of influence on the liver in COVID-19 are currently being considered: viral immunological damage, hypoxia, systemic inflammatory process, drug toxicity and progression of existing liver diseases. This review is devoted to the analysis of available data on the mechanisms and clinical manifestations of liver damage in a new coronavirus infection.


2020 ◽  
Vol 5 (5) ◽  

Background and Objective: Rosai-Dorfman disease (RDD) are usually misdiagnosed because of rarity and nonspecific clinical and radiological features. The aim of our study is to explore the clinical and imaging characteristics of RDD to improve diagnostic accuracy. Methods: Clinical and imaging data in 10 patients with RDD were retrospectively analyzed. 7 patients were underwent CT scanning and 3 patients were underwent MR examination. Results: 8 (8/10) patients presented with painless enlarged lymph nodes (LNs) or mass. 3 cases were involved with LNs, 5 cases were involved with extra-nodal tissues, and the remaining 2 cases were involved with LNs and extra-nodal tissue simultaneously. In enhanced CT images, enlarged LNs displayed mild or moderate enhancement, and 2 cases showed heterogeneous ring-enhancement. MR features of 3 patients with extra-nodal RDD, 2 cases showed a mass located in the subcutaneous and anterior abdominal wall respectively, and 1 case showed an intracranial mass. Besides, all lesions showed high signal foci on DWI images, and were characterized by marked heterogeneous enhancement with blurred edge. The dural/fascia tail sign and dilated blood vessels could be seen around all the lesions on enhanced MRI. Radiological features of 2 cases with LN and extranodal tissue involved, one case presented with the swelling and thickening of pharyngeal lymphoid ring and nasopharynx, meanwhile with enlarged LNs in bilateral submandibular area, neck and abdominal cavity, and also companied with osteolytic lesion in right proximal humerus. All these LNs displayed mild and moderate enhancement on CT images. Another case showed enlarged LNs in bilateral neck accompanied with soft tissue mass in the sinuses. Conclusions: RDD occurred commonly in young and middle-aged men and presented with painless enlarged LNs or mass.RDD had a huge diversity of imaging findings, which varied with different location. The radiological features, such as small patches of high signal foci in the masses on DWI images, heterogeneous enhancement and blood vessels around the masses, are helpful in diagnosis of extranodal RDD.


2020 ◽  
Vol 21 (12) ◽  
pp. 1225-1236
Author(s):  
Silvio Terra Stefanello ◽  
Nelson Rodrigues de Carvalho ◽  
Simone Beder Reis ◽  
Felix Alexandre Antunes Soares ◽  
Rômulo Pillon Barcelos

Acetaminophen is a widely used analgesic for pain management, especially useful in chronic diseases, such as rheumatoid arthritis. However, easy access to this medicine has increased the occurrence of episodes of poisoning. Patients often develop severe liver damage, which may quickly lead to death. Consequently, numerous studies have been conducted to identify new biomarkers that allow the prediction of the degree of acetaminophen intoxication and thus intervene in a timely manner to save patients’ lives. This review highlights the main mechanisms of the induction and progression of liver damage arising from acetaminophen poisoning. In addition, we have discussed the possibility of using new clinical biomarkers for detecting acetaminophen poisoning.


2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110066
Author(s):  
Qinghong Meng ◽  
Na Li ◽  
Lianmei Yuan ◽  
Xiaona Gao

Aims To explore the causes of liver damage among children 12 years and younger in Weifang and to provide a theoretical basis for early diagnosis of liver damage in children. Methods Retrospective study of clinical data from pediatric patients (age ≤12 years) with liver damage in diagnosed at Weifang People's Hospital from June 2010 to May 2020. Results A total of 2632 children (1572 boys, 1060 girls) aged ≤12 years were diagnosed with liver damage including infectious liver damage (2100 cases), non-infectious liver damage (446 cases) and liver damage of unknown etiology (86 cases). The most common causes of infectious liver damage were viral infection (1515 cases), Mycoplasma pneumoniae infection (343 cases), and bacterial infection (197 cases). The most common causes of viral liver damage were Epstein–Barr virus, cytomegalovirus, and enterovirus. The most common causes of non-infectious liver damage were drug-induced liver damage, Kawasaki disease, and genetic metabolic diseases. There were 31 cases of severe liver damage. Conclusion There were many causes of liver damage among children in Weifang. Infections, and especially viral infections such as Epstein–Barr virus, were the most common causes of liver damage. Severe liver damage was primarily caused by drugs or poisons.


2020 ◽  
Vol 2020 (12) ◽  
Author(s):  
Stathis Tsiakas ◽  
Chrysanthi Skalioti ◽  
Paraskevi Kotsi ◽  
Ioannis Boletis ◽  
Smaragdi Marinaki

ABSTRACT Antiphospholipid syndrome (APS) is a systemic autoimmune disease defined by the presence of antiphospholipid antibodies in association with thrombotic events and/or obstetric complications. Renal involvement is not infrequent in both primary and secondary APS. Kidney manifestations comprise a wide range of clinical features, including hypertension, major renal vessel thrombosis or microvascular endothelial injury, also described as APS nephropathy. In the absence of a thrombotic event, clinical manifestations of APS are often non-specific. We recently encountered a case of primary APS in a young male with newly diagnosed hypertension and renal impairment. The diagnosis of APS was initially suspected by his kidney biopsy findings, when electron microscopy examination showed the features of chronic microangiopathy, and was later confirmed by a triple positive antiphospholipid antibody profile and multiple organ involvement.


1986 ◽  
Vol 5 (3) ◽  
pp. 201-206 ◽  
Author(s):  
R. B. Read ◽  
J. M. Tredger ◽  
R. Williams

1 To determine reasons for the continuing mortality in patients taking a paracetamol overdose, the presentation, drug ingestion history, patient background, use of antidote ( N-acetylcysteine and methionine), clinical course and outcome were determined in 247 patients treated at King's College Hospital in 1982 and 1983. Patients (147) were referred from other centres because of severe liver damage and 100 were local patients seen in the accident and emergency department. 2 Survival in the local patients was 100% and, for those with severe liver damage, 49 and 63% (1982 and 1983 values). Delay in initial presentation to hospital was a major factor in determination of an adverse outcome, with a median delay of 30 h in the referred patients and 8 h in the local cases. Such a delay precluded administration of antidote to the majority of patients in the referred group, but in 11 cases where antidote could have been given a full course was not provided and all 11 patients died. Included among these were four patients in whom the serum paracetamol concentration was in the ‘non-toxic’ range. 3 One patient with a chronic alcohol-drinking history (> 200 g/day) received N-acetylcysteine at 12 h but died from liver failure. However, in the complete series prior alcohol consumption was not associated with a significantly worse prognosis and simultaneous ingestion of alcohol with paracetamol had no effect on outcome. 4 The concomitant ingestion of dextropropoxyphene caused an early and marked impairment of consciousness unrelated to any hepatotoxicity but, in three cases where dextropropoxyphene combinations were used, death occurred subsequently from liver failure.


Author(s):  
Rajesh Kumar ◽  
Seetha Harilal ◽  
Sabitha M ◽  
Leena K Pappachan ◽  
P R Roshni ◽  
...  

: SARS-CoV-2, the novel coronavirus and the causative organism of Covid-19 pandemic wreaked havoc worldwide producing asymptomatic to symptomatic cases leading to significant morbidity and mortality even after infection. Most of the countries reported a mortality rate of 2-3 % majorly due to cardiorespiratory failures. Recent studies highlighted the neurological involvement playing a key role in cardiorespiratory failures and other symptoms such as headache, anosmia, and ageusia observed in Covid-19 patients. Studies suggests SARS-CoV-2 entry via olfactory epithelium (OE) and the expression of type 2 transmembrane serine protease (TMPRSS2) in addition to angiotensin converting enzyme 2 (ACE2) can facilitate SARS-CoV-2 neurotropism. The virus can either travel via peripheral blood vessel causing endothelial dysfunction, triggering coagulation cascade and multiple organ dysfunction or reach the systemic circulation and take a different route to the blood brain barrier (BBB), disrupting the BBB causing neuroinflammation or neuronal excitotoxicity resulting in the development of encephalitis, encephalopathy, seizures, and strokes. SARS-CoV-2 invasion on brain stem is believed to be responsible for the cardiorespiratory failures observed in Covid-19 patients. Apart from viral invasion via hematogenous route, SARS-CoV-2 neural invasion via PNS nerve terminal, resulting in viral replication and retrograde transportation to soma leading to invasion of the CNS including the brain producing neurological manifestations of the disease either in the initial stages or during the course of the disease and even in a long period post infection in many cases. The ACE2 receptors are expressed in the brain and glial cells and SARS-CoV-2 acts via neuronal as well as non-neuronal pathway. But the exact cell types involved and how they can trigger inflammatory pathways need further in-depth study for the development of targeted therapy.


2020 ◽  
Author(s):  
Alexandra Theisen ◽  
Paroma Bose ◽  
Christina Knight ◽  
Melissa Oliver

Abstract Background: Systemic lupus erythematosus (SLE) is an autoimmune disease with various clinical manifestations involving multiple organ systems. Neuropsychiatric manifestations of SLE has been associated with increased morbidity and mortality, thus it is important to recognize and diagnosis the disease entity and treat early. When neuropsychiatric symptoms are involved, typically there are many other systemic features to aid in the diagnosis of SLE. Many autoantibodies have been discovered and are used to help diagnose SLE. The antibody present in most cases of pediatric SLE, as well as in many other rheumatic diseases, is the nonspecific antinuclear antibody (ANA), making it a commonly used screening tool by primary care physicians when evaluating a patient with a possible rheumatic disorder. However, a small subset of SLE patients, 1-5%, present with a negative ANA, and it is important to keep SLE on the differential diagnosis in specific instances when a thorough infectious and neurological workup has been completed and proven to be inconclusive. Case Presentation: This case involves a Hispanic adolescent female with a negative ANA who presented with diffuse cerebral edema secondary to leukoencephalopathy due to SLE with central nervous system involvement. She had an extensive workup while inpatient involving metabolism, infectious disease, rheumatology, and neurology prior to obtaining the diagnosis of SLE. She was treated with both cyclophosphamide and rituximab and showed improvement. Conclusions: A review of the literature revealed 8 cases with SLE presenting with or developing diffuse cerebral edema and/or leukoencephalopathy. Our patient’s case differs in that she was also ANA negative despite other autoantibody positivity. While she did have low complements and transient leukopenia, she did not present with other signs of organ involvement, which made the diagnosis of SLE with neuropsychiatric involvement quite challenging. We discuss the importance of keeping SLE on the differential despite a negative ANA in complex cases without any other cause and to consider initial screening with not only the ANA but also dsDNA and complements to avoid missed diagnoses.


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