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R K Maryniak

Publications and source records attributed to R K Maryniak.

14 recordsLinked to original sources
PubMed2006

3D ultrasound examination of the superficial lymph nodes--does it provide additional information?

PURPOSE: To compare the appearance of superficial lymph nodes on standard two-dimensional (2D) ultrasound examination and on three-dimensional (3D) ultrasound examination. MATERIALS AND METHODS: Fifty two lymph nodes (35 cervical, 16 axillary, 1 inguinal) in 52 patients were examined with ultrasound in 3D mode. In standard 2D grey-scale examination and on a C-plane of 3D mode (parallel to the surface of the probe), the shape of a lymph node and its hilum were assessed. Final histopathological diagnoses included 36 lymphomas, 11 reactive or inflammatory lymph nodes, 3 metastases and 2 plasmocytoma infiltrations. RESULTS: The appearance of hilums and lymph nodes as a whole changed on a C-plane of 3D mode (as compared with 2D presentation) in 28 % and 37 %, respectively. The differences in lymph node shape on 2D and 3D ultrasound were apparent in a comparable percentage of reactive lymph nodes (45 %) and lymphomatous lymph nodes (39 %). The differences in lymph node hilum shape on 2D and 3D ultrasound applied to 56 % of reactive lymph nodes and 20 % of lymphomatous lymph nodes. CONCLUSION: Three-dimensional imaging on a C-plane (parallel to the surface of the probe) may supply the examiner with different information concerning the shape of the lymph node and its hilum in comparison to standard 2D ultrasound. Changes in the shapes of hilum and lymph node occurred in reactive or inflamed lymph nodes as well as in lymphomas. Clinical significance of this fact demands further investigation.

Humans↗
PubMed2000

Immunomorphological studies and cytometric DNA ploidy in diagnostics of pheochromocytoma.

The aim of the study was to define features indicating malignancy in pheochromocytoma through analysis of clinical data, immunomorphological and nuclear DNA ploidy patterns with flow cytometry. The studied group consisted of 33 patients with hypertension and adrenal gland tumor. In all patients 24 hr measurements of adrenaline, noradrenaline, dopamine and their metabolites were taken and the content of these substances in the tumor tissue was measured. Morphologically most pheochromocytomas displayed alveolar pattern with polyhedral cells with clear cytoplasm. Nuclear pleomorphism was infrequent and mitotic figures were rare. In 5 tumors areas of ganglioneuromatous differentiation were present with neurofilament expression. Morphological features indicating malignancy were noted--vascular emboli of tumor cells, capsular infiltration and foci of necrosis. However, in the patient with metastases evident during operation, none of those features was found in the tumor sample. All pheochromocytomas expressed neuroendocrine markers (chromogranin A, synaptophysin and NSE) and most also vimentin. Reactivity of other markers was negligible. In DNA ploidy studies in 22/33 cases there was DNA diploid (normal) pattern. The patient with metastases belonged to this group. In 3 cases there were aneuploid tumor cells on histograms and in 8 increased number of tetraploid cells. The follow-up period of our patients was 1-43 months.

Adolescent↗
PubMed2000

Primary splenic B-cell lymphoma (marginal zone lymphoma). Clinicopathological evaluation of 10 cases.

SMZL has been included in the REAL classification of lymphoid neoplasms (1994) as an entity. It affects middle aged adults presenting with splenomegaly, mild lymphocytosis and in 40% of cases with the presence of monoclonal paraprotein. Our material includes 10 patients (6 women + 4 men). In all patients bone marrow biopsy was the initial material for histopathological examination. With characteristic intertrabecular nodular interstitial infiltrates of CD20+ small lymphocytes and corresponding clinical data (splenomegaly, lymphocytosis in peripheral blood and sporadic elevation of IgM levels) it was very suggestive of SMZL diagnosis. Splenectomy was the treatment of choice. The spleen showed micronodular white foci in all cases. Morphologically the pattern of white pulp involvement was observed with lymphoma infiltrates as well as small foci in the red pulp. The white pulp showed follicles surrounded by a wide marginal zone, resembling reactive splenic follicles. A corona-like rim consisted of medium size cells with abundant clear cytoplasm, resembling monocytoid B cells, often with plasmacytoid differentiation, or centrocyte-like cells. Smaller aggregates of these cells were present in the red pulp. Lymphoma cells were CD20+, bcl-2 and IgM+. In all cases monoclonal kappa light chains were found. Although SMZL is a disseminated lymphoma at diagnosis, its course is indolent and splenectomy is the treatment of choice. Clinical and histopathological differential diagnoses include hairy cell leukemia and secondary involvement of the spleen by infiltrates of nodal B-cell lymphomas.

Aged↗
PubMed1995

[Hemangioma of bone and soft tissue in the midfoot--case report].

A case of in isolated arterovenous developmental disorder in 23 years old female is described. Bony changes were at the beginning obscured by skin and soft tissue changes. The diagnosis has been established on the basis of histopathological evaluation of the II metatarsal bone and soft tissue vascular changes removed at the operation.

Adult↗
PubMed1993

Primary malignant lymphoma of the uterine cervix. A clinicopathological evaluation of 3 cases.

Three cases of primary malignant lymphoma of the uterine cervix are presented; 1 in pre- and 2 in postmenopausal women. Two presented clinically with bleeding, one with pelvic discomfort. Histologically all were B cell lymphomas, two high, one low malignancy. Radiotherapy to the whole pelvis followed hysterectomy in 2 patients and in one wasthe primory modality. One of the patients was also treated with chemotherapy for dissemination within the abdomen and CNS. Two patients died, one is well at 38 months.

Adult↗
PubMed1991

[2 cases of Richter's syndrome].

Two cases of Richter's syndrome are reported (in a 62 and 64 years old man) consistent with the appearance of B cell lymphoma of high malignancy in the course of CLL (low malignancy B cell lymphoma). In one patient, after 8-, and in the other one--after 53 months since the diagnosis of CLL, there was rapid clinical deterioration with lymphadenopathy, hepato- splenomegaly, fever and progressive cachexia, anemia and thrombocytopenia and leukopenia, unrelated to treatment. Both patients died, 4 and 3 months respectively, since the appearance of these symptoms. In the first cases Richter's syndrome was diagnosed histopathologically from the autopsy material. In the liver, spleen, adrenals and bone marrow, in addition to the characteristic infiltrates of CLL (small lymphocytes) there were areas of large cell proliferation consistent with high malignancy lymphoma. In the other case, the infiltrates of large cell lymphoma were found in the gall bladder removed because of acute cholecystitis, and in the lymph node from the hepatic hilar area. Immunocytochemical studies performed on the biopsy material indicated that the neoplastic cells had markers of B lymphocytes and cytoplasmic IgM kappa, as lymphocytes of CLL. In patients with CLL, who display rapid clinical deterioration and general symptoms with cachexia, the possibility of Richter's syndrome should be considered, and appropriate morphological studies performed.

Gallbladder Neoplasms↗
PubMed1985

Transplant glomerulopathy: evolution of morphologically distinct changes.

The study was undertaken to redefine morphological appearance and clinical implications of the diagnosis of transplant glomerulopathy (TGP). Fifty-seven renal transplant biopsy specimens from thirty patients with the diagnosis of TGP were evaluated. Multiple repeat biopsies in several cases enabled us to follow the pattern of the evolution of the changes. Transplant dysfunction manifested itself 8 days to 13 years post-transplantation by proteinuria and/or elevated creatinine level. The earliest recognizable morphological change was the swelling of endothelial and mesangial cells. This stage was called evolving TGP. The intermediate stage was characterized by enlarged glomeruli with lobular simplification, spongy matrix, and glomerular basement membrane (GBM) deformities. The advanced stage of TGP showed pronounced GBM changes (reduplication, interposition). These light microscopic changes were associated with vascular rejection. Immunofluorescence showed significant glomerular deposition of IgM (83% of biopsies) and fibrinogen (66%). Electron microscopy at an early stage showed subendothelial widening with cellular debris and focal endothelial damage with fibrin deposition. In the advanced stage, complex GBM changes developed as a reparative response to the capillary wall injury. Effacement of foot processes was a constant finding at all stages. In follow-up, twenty-three allografts failed (77%), five patients are stable, and two died due to other causes. TGP has specific morphology with an attendant poor long-term prognosis for the allograft.

Basement Membrane↗
PubMed1985

Recurrence of diabetic nodular glomerulosclerosis in a renal transplant.

A 36-year-old woman with a 26-year history of insulin-dependent diabetes mellitus developed chronic renal failure in 1974 and was started on dialysis. She received a kidney transplant from her HLA-identical brother. Her HLA typing showed the following antigens: A1, A28, B8, B12 (44), BW4, BW6 DR3, and DR4. Nephrectomy performed prior to transplantation showed advanced diffuse diabetic glomerulosclerosis. Her postoperative course was relatively uncomplicated, but within the next seven years she gradually developed symptoms of deteriorating renal function and hypertension. Two years later, a renal arteriogram showed 90% stenosis of the main renal artery. Biopsy of the kidney was obtained during surgical repair of this lesion and showed diffuse nodular diabetic glomerulosclerosis. Since the B8/DR3 form of diabetes is reported to have a predilection for diabetic microangiopathy and vascular complications, we are speculating that the patient's antigenic composition might have enhanced the recurrence of the diabetic lesions in the transplanted kidney.

Adult↗
PubMed1984

Membranous glomerulopathy following kidney transplantation. Association with renal vein thrombosis in two of nine cases.

The association of renal vein thrombosis and membranous glomerulopathy in native kidneys has been well documented. However, this association has only occasionally been described following renal transplantation. A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. A diagnosis of membranous glomerulopathy was made in 7 patients. Two further cases were added on the basis of biopsy findings--1 patient had a protein excretion of 1.7 g/24 hr, the other had microscopic hematuria and red cell casts in the urine. Renal venography was performed in 4 cases. The decision to perform venography was based on clinical criteria (thrombophlebitis or marked edema of the leg on the side of the allograft), and/or histological criteria (associated interstitial edema and venous congestion). Renal vein thrombosis was present in 2 patients. Three of the 9 patients had membranous glomerulopathy as the cause of their end-stage renal disease; 2 of these patients had received kidneys from living-related donors. Four of the patients were classified as having de novo membranous glomerulopathy on the basis of having a different cause for their end-stage renal disease. Two patients were classified as having unspecified membranous glomerulopathy; both of these patients had had chronic glomerulonephritis, but there was lack of characterization of the original glomerular disease. Seven of the 9 patients continued to have stable allograft function 1-12 months after the diagnosis of membranous glomerulopathy was made in the renal allograft. The remaining 2 patients both had associated renal vein thrombosis; 1 had progressive deterioration of renal function and returned to dialysis 24 months after the diagnosis of membranous glomerulopathy had been made, while the other died of unrelated causes 27 months after the diagnosis had been made.

Adult↗
PubMed1984

Proteinuria following transplantation. Correlation with histopathology and outcome.

A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. Twenty-one patients had received kidneys from living-related donors, the remaining 56 from cadaveric donors. The cause of proteinuria in these 77 patients was as follows: transplant glomerulopathy (30), allograft glomerulonephritis (22), chronic rejection (21), renal vein thrombosis (2), diabetic glomerulosclerosis (1), and hypertensive nephrosclerosis (1). Of the 22 patients who developed glomerulonephritis in the transplanted kidney, 6 had recurrent disease (3--membranous glomerulopathy, 2--focal sclerosis and hyalinosis, 1--membranoproliferative glomerulonephritis); 6 developed de novo glomerulonephritis; and in 10 the type of glomerulonephritis could not be classified as recurrent or as de novo because of lack of characterization of the original kidney disease. Renal vein thrombosis occurred in association with other lesions in an additional 5 cases (3--chronic rejection; 2--membranous glomerulopathy). In follow-up only 23.4% (18 of 77) of the patients maintained prolonged graft function; the majority of grafts being lost within one year of the development of persistent, heavy proteinuria. Of the 18 patients who retained their grafts, 8 had glomerulonephritis, 5 transplant glomerulopathy, and 5 chronic rejection. This study confirms the poor prognosis that has been reported with the development of nephrotic-range proteinuria in renal allograft recipients.

Graft Survival↗