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. Myeloproliferative disorders define a vast and heteregenous group of neoplastic entities, characterized by malignant proliferation of blood cells. These may affect multiple tissues, some of these malignancies involving organs in which there is lymphoid tissue. Case report. A 81-year-old female patient was admitted to the Department of Internal Medicine with moderate-to-intense spontaneous pain in the left hypochondrial and in the left abdominal flank, associated with generalized fatigue and loss of appetite. According to the personal medical history, the patient is known with type II diabetes mellitus, being under treatment with oral antidiabetics (metformin 1000 mg), and arterial hypertension under treatment with candesartan. Upon admission, the physical examination revealed cutaneous and mucosal pallor and marked physical weakness. Abdominal palpation revealed pain in the left hypochondrial and in the left abdominal flank, associated with firm and massive splenomegaly, descending towards the umbilicus. Abdominal ultrasound confirmed massive splenomegaly, associated with moderate hepatomegaly. Blood analysis revealed several modifications, indicative of hypochromic normocytic anemia, associated with lymphocytosis, thrombocytopenia and neutropenia. C-reactive protein (CRP) serum levels were in normal range upon admission. All of these modifications suggested a possible leukemogenous or lymphoid malignancy, which resulted in the patient's transfer towards the Department of Hematology, for further investigations. Conclusions. Massive splenomegaly, associated with anemia and thrombocytopenia in elderly patients, should always indicate a leukemogenous or lymphoid malignancy and a thorough differential diagnosis and collaboration between internists and hematologists is required.

Glomerulonephritis is a major cause of morbidity in systemic lupus erythematosus (SLE). In fact, immune complex formation and deposition in the kidney results in intraglomerular inflammation with recruitment of leukocytes and activation and proliferation of resident renal cells. Intense injury may destroy resident renal cells by necrosis or apoptosis resulting in fibrinoid necrosis. When injury is less intense, endocapillary cells respond by proliferating and production of extracellular matrix (proliferative lesions). Renal biopsy, examination of urine sediment and measurement of C3 levels (and to less anti-DNA titers) are essential for the management of lupus nephritis. Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thrombotic episodes in the arterial or venous circulation, in the presence of antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), anticardiolipin antibodies, and anti-β2glycoprotein-I antibodies (anti-β2GPI). Catastrophic APS (CAPS) is a very rare (---lt---1%) and extremely severe variant of APS. It is characterized by multiple systems and thrombotic organ involvement that occurs in a very short period (days to weeks). Renal involvement is a common feature in CAPS, the most frequent finding is thrombotic microangiopathy (TMA), but other chronic lesions of APSN can also be found.