Background. Post-COVID-19 systemic inflammatory syndrome is considered to be an aquired immunological disorder, which may develop in some individuals after the remission of infection with SARS-CoV-2 and defined by inflammatory clinical manifestations (fever, arthralgias, cutaneous and mucosal pallor, physical weakness) and modified biological parametres (normochromic normocytic anaemia, increased serum levels of C reactive protein and rheumatoid factor), with no proof of an infectious process, to which corticotherapy may be a suitable therapeutic strategy. Case report. A 43 year old male was admited in the Department of Internal Medicine for high fever (39,4°C), moderate polyarthralgias and physical weakness, with a negative test result of SARS-CoV-2 RT-PCR. The patient had been previously diagnosed with a moderate-to-severe form of COVID-19, a month prior to the current admission. The patient also experienced transitory dry cough for a month, with no other relevant clinical abnormalities. Upon physical examination, cutaneous and scleral pallor was observed and lung auscultation revealed hardened vesicular murmur bilaterally. Blood analysis revealed normochromic normocytic anaemia and increased serum levels of rheumatoid factor and of C reactive protein, which suggested a nonspecific inflammatory syndrome. Although blood cultures and other microbiological tests were negative for an infectious process, a chest X-ray was performed, which detected the presence of a nodular formation in the superior left lung lobe. Several differential diagnoses were taken into consideration, including pulmonary sarcoidosis and granulomatosis with polyangiitis, both of which were excluded, clinically and biologically. A thoracic computed tomography (CT) was later performed, which revealed the presence of a tumoral nodule in the left lung, associated with multiple mediastinal and supraclavicular lymphadenopathies, indicative of lung cancer. However, lung cancer was also excluded upon the histopathological examination of paratracheal lymphnodes, which detected multiple areas of parenchymal necrosis surrounded by dense inflammatory infiltrates, formed predominantly by histiocytes. All of these findings resulted in the diagnosis of a post-COVID-19 rheumatoid syndrome, the only therapeutic strategy being the administration of high doses of intravenous and oral methylprednisolone, which improved the patient’s health. Conclusion. Post-COVID-19 immunological disturbances should be taken into consideration in patients who experience repetitive clinical and biological inflammatory manifestations after the remission of the infection with SARS-CoV-2, which may be improved through high dose corticosteroid therapy.
Non-alcoholic fatty liver disease (NAFLD) constitutes a common pathological condition of the liver, the prevalence of which is currently increasing in western countries. NAFLD is frequently diagnosed in males and its incidence is higher in individuals with type 2 diabetes mellitus and obesity. Hence, the disease is considered to be the hepatic manifestation of the metabolic syndrome. A multitude of interconnected risk factors have been described over the years – genetic, hormonal and nutritional, which play important roles in the development of NAFLD. Insulin resistance is considered to be the central pathophysiological condition that promotes the disease in diabetic patients, whereas dyslipidemia and cardiovascular comorbidities (arterial hypertension, ischaemic heart disease) are frequently associated conditions. Although there are currently numerous pathophysiological mechanisms involved in NAFLD that are still unknown or poorly understood, there has been some advancements concerning the pathogenesis of the disease and its progression towards its severe form, known as non-alcoholic steatohepatitis (NASH). In the absence of a clear diagnosis and carefully controlled treatment, NAFLD/NASH may evolve towards liver cirrhosis, liver failure or hepatocellular carcinoma. However, the disease may also generate systemic effects, including the development of chronic kidney disease (CKD). The diagnosis of NAFLD/NASH is based both on its clinical manifestations, revealed by a carefully conducted patient history and physical examination of the patient, and on other investigations; histopathological findings upon liver biopsy, liver ultrasonography and the use of transient elastography (or FibroScan) are some of the most important investigations in NAFLD/NASH. The understanding of the most important risk factors and pathogenic mechanisms of the disease is fundamental for the elaboration of the most efficient treatment, to prevent chronic liver disease or the development of hepatocellular carcinoma.
Postinfectious glomerulonephritis is associated with bacterial, viral, fungal, and parasitic infectious agents and histologically appears most often as acute diffuse endocapillary or proliferative glomerulonephritis secondary infection with: group A streptococcus, streptococcus viridans, staphilococus aureus, diploccocus pneumoniae, Brucella melitensis, Salmonella typhi, Yershinia enterocolitica, Plasmodium falciparum, meningococcus, Mycoplasma, Klebsiella, varicella, variola, mumps. Less commonly, it appears as diffuse crescentic glomerulonephritis and a lot of infectious causes are incriminated like: streptococcus, legionella, varicella, Treponema pallidum or as focal crescentic glomerulonephritis: streptococcus A. It rarely appears as mesangiocapillary glomerulonephritis secondary infection with: streptococcus viridans, hepatitis C virus; diffuse or focal mesangial proliferative glomerulonephritis: hepatitis B virus, salmonella, adenovirus, influenza virus, salmonella; focal segmental, necrotizing and sclerosing glomerulonephritis: bacterial endocarditis; membranous glomerulonephritis: hepatitis B virus, syphilis, filarial, Mycobacterium, plasmodium falciparum; focal proliferative: Mycoplasma; mesangiolytic glomerulonephritis :Echo virus. Poststreptococcal glomerulonephritis (PSGN) is caused by prior infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The clinical presentation of PSGN varies from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury. The prognosis is generally favorable, especially in children, but in some cases, the long-term prognosis is not benign. Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patients.
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