Coronavirus disease 2019 (COVID-19) is currently considered a complex systemic infectious and inflammatory disease, determined by the infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), and the cause of one of the most important epidemiological phenomena in the last century – the COVID-19 pandemic. This infectious-inflammatory disease may generate a wide range of clinical manifestations and biological modifications, explained by the ubiquitous nature of the SARS-CoV-2 receptors, represented by the angiotensin-converting enzyme-2 (ACE-2), and by the host’s violent immune and proinflammatory reaction to the viral infection. These manifestations include immunological disturbances, which, according to certain clinical findings, may persist post-infection, in the form of a presumed systemic inflammatory entity, defined by several clinical concepts with a common pathological significance: post-COVID-19 multisystem (or systemic) inflammatory syndrome, post-COVID syndrome or long-COVID. Although the pathophysiological mechanisms of the post-COVID-19 syndrome are elusive at the present moment, there are currently several studies that describe a systemic inflammatory or autoimmune phenomenon following the remission of the COVID-19 infection in some patients, which suggests the existence of molecular and cellular immune abnormalities, most probably due to the host’s initial violent immune response to the viral infection, in the form of three overlapping entities: secondary hemophagocytic lymph histiocytosis (HLH), macrophage activation syndrome (MAS) and cytokine release syndrome (CRS). Thus, this is reminiscent of different classic autoimmune diseases, in which various infections are risk factors in developing the autoimmune process.

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.

The concept of “hyperferritinemic syndrome” defines a complex pathophysiological and clinical entity, characterized by a systemic hyperinflammatory state, generally associated with elevated levels of proinflammatory cytokines (hypercytokinemia) and high serum levels of ferritin (hyperferritinemia), traditionally recognized as an iron-binding plasma protein involved in the storage of iron in a biologically available form for different physiological cellular processes. Recent studies have shown that ferritin has other important functions as well, operating both as a proinflammatory mediator and as a immunosupressive agent, its elevated levels in the serum being detected in various conditions associated with inflammatory states, such as infectious diseases, autoimmune and autoinflammatory disorders and, in some cases, in malignancies. Catastrophic antiphospholipid syndrome (cAPS), systemic juvenile idiopathic arthritis (sJIA) and adult-onset Still’s disease (AOSD) and acquired forms of hemophagocytic lymphohistiocytosis (HLH), which includes macrophage activation syndrome (MAS), have been associated with hyperinflammatory states and dramatic elevations of serum ferritin, generating hyperferritinemic syndromes. Severe forms of coronavirus disease-2019 (COVID-19), in which MAS may frequently develop, has also been linked to the development of a hyperferritinemic syndrome. This review offers several insights into the physiological and pathophysiological roles of ferritin in several (hyper-)inflammatory diseases, but also into the causal entities, the underlying pathophysiological mechanisms, clinical manifestations and diagnostic features of somewhat obscure, yet potentially fatal pathological conditions, reunited under the concept of hyperferritinemic syndromes.

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

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.