Introduction. The SARS-CoV-2 infection (COronaVIrus Disease 2019, COVID-19) usually progresses uncomplicated in an acute respiratory form but causes frequent severe illness in oncohaematological patients.

Aim — analysis of the management and efficacy of medical aid at a haematology clinic during the COVID-19 pandemic.

Patients. The clinic admitted 2,130 patients in April 20 — November 20, 2020, with 920 of them triaged into observatory wards. At the time of admission, 907 (98.5 %) patients were SARS-CoV-2 RNA-negative, with 13 hospitalised without nasopharyngeal swab tests. Patient nosology: 235 (25.5 %) lymphoma, 152 (16.5 %) multiple myeloma, 131 (14.2 %) acute leucaemia, 86 (9.3 %) haemophilia, 35 (4 %) Gaucher’s disease, 17 (1.8 %) Waldenstrom macroglobulinemia, 16 (1.7 %) aplastic anaemia, 153 (16.6 %) various surgical diseases, 81 (8.8 %) other haematological diseases and 14 (1.6 %) were bone marrow donors.

Results. Among the 920 patients admitted to the observatory, 139 (15 %) were severe and 653 (71 %) had a moderate condition. Fever was reported in 124 (13.5  %) patients at admission. Chest computed tomography (CT) was performed in 809 patients, with recent lung inflammation detected in 121 (15 %) cases. Twenty four (2.6 %) patients were revealed SARS-CoV-2-positive, with 20 diagnoses PCR-verified and four — in chest CT. Ten patients were diagnosed positive in routine examination or at a specialty unit as fever aggravated. Thus, a two-staged SARS-CoV-2 screening with PCR and chest CT allowed an extra 2.6 % detection of COVID-19 cases despite negative tests at admission.

Conclusion. The observatory management has reduced the likelihood of nosocomial COVID-19 and ensured a continued supply of specialty medical aid.

Introduction. The COVID-19 pandemic has challenged health professionals and patients suffering from haematological diseases with embarrassed diagnosis, treatment, surveillance, social distancing and other constraints.

Aim — addressing therapy for immune thrombocytopenia (ITP) during the COVID-19 pandemic in the light of own experience, as well as national and international professional medical community guidelines.

Main findings. A standard choice in COVID-19-negative ITP patients are conventional, e.g., glucocorticosteroid (GCS) and intravenous immunoglobulin therapies. An early transfer to thrombopoietin receptor agonists (rTPO) appears optimal as reducing the infection risk in GCS withdrawal and significantly improving the stable remission rate without supportive treatment. Combined ITP–COVID-19 patients should consider a prednisolone treatment of 20 mg/day, provided an absent active bleeding. The dose may increase to 1 mg/kg/day in no response after 3–5 days. ITP patients admitted for COVID-19 should start weight‐based LMWH thromboprophylaxis upon attaining a platelet count of ≥ 30 × 109 /L. Chronic ITP patients should carry on usual treatment with standard SARS-CoV-2 preventive and social distancing measures. We exemplify three contrasting clinical cases of COVID-19-comorbid thrombocytopenia and discuss the ITP differential diagnosis and therapy. Two patients received GCSs and rTPO agonists (romiplostim, eltrombopag), while GCSs alone provided for platelet response in the third case. All patients showed a good clinical and biological response. Issues in SARS-CoV-2 vaccination are discussed.

Introduction. Blood transfusion is a strong practice in traumatology, internal medicine, haematology, obstetrics and transplantation, which demands safety of haemotransfusion with estimating the red blood cell group antigens in donor and recipient blood. Routine immunotyping techniques usually provide for an antigen identification to weak subgroups, albeit with certain inherent limitations of serology tests that can be overcome in a genotyping approach.

Aim — performance assessment of serology and genotyping methods in the ABO, RH and KEL blood group identification.

Materials and methods. A total of 55,489 donor and 1,898 patient blood samples have been analysed. Ambiguous cases of chimerism, panagglutination and inconsistent results were tackled with genotyping. Serology tests were performed with gel cards. Whole blood DNA extraction was performed with Qiagen chemistry. Allele-specific PCR was used for the erythrocyte ABO, RH and KEL antigen genotyping with BAG Diagnostics commercial kits and a 2% agarose gel product detection. Sanger sequencing was used to complement genotyping.

Results. A combined use of serology tests and genotyping allowed a successful erythrocyte antigen-based blood group and Rh-status assignment in 26 donors and patients with ambiguous blood typing.

Conclusion. Genotyping coupled with serologic methods can be advised in a hampered blood group identification.

Introduction. Cytogenetic and genomic traits of tumour cells are considered the key mediating factors in multiple myeloma (MM). Selected chromosomal abnormalities are prognostic of therapeutic response and patient survival in MM.

Aim — to assess of the diversity and rate of chromosomal abnormalities in MM patients and their association with the disease course.

Materials and methods. The study enrolled 134 MM patients with pre-treatment bone marrow FISH assay screening for chromosomal abnormalities: t(11;14), t(4;14), t(14;16), t(14;20), t(6;14), hyperdiploidy, del13q14/-13, del17p13/TP53, amp1q21, t(8q24)/cMYC. The studied criteria at the MM onset were: hemogram, lactate dehydrogenase (LDH) activity, calcium, β2-microglobulin and creatinine concentrations, punctate cytology, bone marrow trephine biopsy and/or soft tissue biopsy histology, bone X-ray, immunochemical variant of MM, disease staging. A median follow-up was 20 months (3.2–77.4).

Results. The primary chromosomal abnormality rate was 82.9  %, among them t(14q32)/IGH  — 29.1  %, multiple trisomies — 46.3 % and their combination — 7.5 %. The rates of particular t(14q32)/IGH): t(11;14) — 16.4 %, t(4;14) — 12.7 %, t(14;16) and t(14;20) — 3.7 and 2.2 %, respectively. The secondary chromosomal abnormality rate was 69.4 %, among them del13q14/-13 — 40.3 %, amp1q21 — 39.6 %, t(8q24)/cMYC — 17.2 %, del17p13/TP53 — 12.7 %, del1p32 — 2.2 %. Analyses of the primary–secondary abnormality combinations showed that del13q14/-13 is more frequently combined with t(4;14) and less frequently with trisomies (p < 0.05). Amp1q21 occurs more frequently with t(4;14) and less — with t(11;14) (p<0.05). Patients with t(4;14) more frequently (p < 0.05) had anemia at a hemoglobin level<100 g/L, and the presence of amp1q21 and del17p13/TP53-enhanced serum LDH activity (p < 0.05). Abnormality t(8q24)/cMYC more often co-occurred with higher serum β2-microglobulin concentrations (p < 0.05). A three-year overall survival (OS) in del17p13/TP53-positive patients was 35.5 vs. 71.3 % in the negative (p = 0.002) and 50.8 vs. 67 % — in t(8q24)/cMYC-positive and negative patients, respectively (p = 0.001). Patients without amp1q21, with one, with two or more additional 1q21 copies had a five-year OS 79.4, 67.3 and 20.9 %, respectively (p = 0.0016), and a two-year progression-free survival (PFS) 83, 50 and 0 %, respectively (p = 0.005).

Conclusion. We establish a negative impact of del17p13/TP53 and t(8q24)/cMYC on patients’ OS in MM, as well as unfavourable effect of amp1q21 on OS and PFS in the presence of two or more additional copies of 1q21 loci.

Introduction. Primary myelofibrosis (PMF) is a clonal disease violating the cell composition, histological topography and stroma in bone marrow (BM). Allogeneic haematopoietic stem cell transplantation (allo-HSCT) is a curative therapy in PMF.

Aim — description of change in the haematopoietic tissue cell composition and stroma, as well as in trabecular bone in allo-HSCT patients with fibrotic PMF.

Materials and methods. We studies 24 trephine biopsy samples from nine PMF patients with allo-HSCT at the intervals: I — 1 month prior to, II — past 1–3 months and III — past 4–6 months from allo-HSCT. BM trephine biopsy slides were prepared in a standard histological assay with haematoxylin—eosin and additional staining with Gomori’s silver and Masson’s trichrome. Morphological change was evaluated in reticulin and collagen stroma, bone trabeculae, cellularity and topography of haematopoietic tissue.

Results. The BM trephine biopsies of interval I were morphologically distinguished in three types by haematopoietic cellularity, stromal and trabecular sclerotic change. Post-transplant intervals II and III (3–6 months after allo-HSCT) did not reveal these types but showed an evident myelofibrosis and osteosclerosis reduction and signs of a restoring bone remodelling cycle. Myelopoietic lineages recovered in stages: the erythroid germ restored in three, granulocytic — in six months, and megakaryocytic cellularity did not fully recover in six months. Myelopoietic cellularity recovery outpaced blood recovery, which may be due to induced myelodysplasia or disruption of stromal niches.

Conclusion. Allo-HSCT leads to the disappearance of PMF-pathognomonic BM morphology reflecting a histological remission. The reduction of myelofibrosis and osteosclerosis and normalisation of the trabecular bone remodelling cycle in post-transplant periods indicates an impact of cell microenvironment on PMF pathogenesis and warrants research into the composition and histological topography of cell microenvironment in PMF.

Introduction. Among the most common congenital coagulopathies are haemophilia and Von Willebrand disease. These illnesses are often mimicked by orphan hereditary coagulopathies, including combined coagulation factor V and VIII deficiency.

Aim — description of a clinical presentation, hampered diagnosis and choice of haemostatic therapy in a surgical patient with combined blood coagulation factor V and VIII deficiency.

Main findings. We describe a clinical case of congenital combined factor V and VIII deficiency and detail the aetiology, frequency, localisation and intensity of haemorrhages. Comorbidity and surgical indications are demonstrated to require an inter-specialty medical involvement.