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Lege Artis Medicinae

FEBRUARY 15, 2015

[Inflammatory myofibroblastic tumor of abdominal wall arising from uterine myoma]


[INTRODUCTION - The inflammatory pseudotumor appears in various organs. It is well circumscribed, unencapsulated proliferation which simulates malignant tumor clinically as well as radiologically and morphologically. It’s etiology is unknown. The histology prooves inflammatory origin of this process: the nodular structure of the tumor-like mass is composed of fibroblasts, myofibroblasts, plasma cells and lympho­cytes. Recurrence may happen. CASE REPORT - Because of the rapidly expanding uterine myoma of a 40 years old woman laparotomy has been performed. In the lower two-thirds of abdominal wound the myoma penetrated into the abdominal wall. Here the abdominal wall lost it's normal structure, became bacon-like, homogenous in consistency and white-grey in colour. The myoma and the attached part of the abdominal wall was excised together. The part of myoma those in contact with abdominal wall contained proliferating myofibroblasts, fibroblasts and was infiltrated by plasma cells and lymphocytes. These findings could be seen in the abdominal wall too. The rapid proliferation which simulated malignant tumor has been diagnosed as inflammatory myofibroblastic tumor. The patient does well two years after the operation. CONCLUSION - It is important to know about the entity of inflammartory pseudotumor in differential diagnostic point of view, as it mimics malignant tumor. The structure is nodular, the histology is characteristic and the therapy is surgical. The follow up is very important because of possibility of probable recurrence. ]

Hypertension and nephrology

SEPTEMBER 20, 2014

[Signaling pathways in renal fibrosis]


[Myofibroblasts are the main effector cells of tissue fibrosis in chronic kidney disease. These cells are the main source of collagen rich extracellular matrix in the fibrous tissue. Recent hypotheses suggest that pericytes are the major progenitors of myofibroblasts. Platelet derived growth factor, transforming growth factor β and Wingless/Int signaling pathways play important role in pericyte activation. There are experimental evidences that blocking this pathways inhibits tissue fibrosis, therefore they might be targets for the development of antifibrotic drugs in the future.]

Clinical Neuroscience

MARCH 30, 2014


GIULIO Gabbiani

[The souvenirs of Hans Selye as a teacher of graduate and post graduate students are presented and discussed. The main aim of his teaching was to orient the student toward importance and originality of findings.]

Hypertension and nephrology

DECEMBER 30, 2012

[Molecular mechanisms leading to renal fibrosis: the origin of myofibroblasts]

HIMER Leonóra, SZIKSZ Erna, KOVÁCS S. Krisztián, ÓNODY Anna, Reusz Anna, REUSZ György, FEKETE Andrea, TULASSAY Tivadar, VANNAY Ádám

[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]

Hungarian Radiology

DECEMBER 27, 2010

[Inflammatory myofibroblastic tumor in rare abdominal localisation]

NAGY Tamás, GÁBOR Valéria, NAGY Csaba Balázs, PUSKÁS Tamás

[INTRODUCTION - Inflammatory myofibroblastic tumor is a rare entity. The etiology and pathomechanism of this tumor is still unknown. In most of the cases it behaves as a benign or locally recurrent tumor and does not metastasize, but because of its aggressive local growth it can be judged malignant. For an accurate diagnosis adequate imaging (CT, MR), invasive intervention which is usually surgical excision and pathologic or histological examination must be performed. CASE REPORT - A case of a 19 year old woman is presented who was diagnosed by a CT scan with a 4 cm tumor in the midline of the upper third of the abdominal cavity. After surgical excision the inflammatory myofibroblastic tumor was confirmed after the pathological inspection. CONCLUSION - Despite that inflammatory myofibroblastic tumor is infrequent in virtue of the clinical picture and imaging exams we have to take this disease into account. The misdiagnosis can lead to unnecessary invasive interventions and psychological effort for the patient which could be avoided by the cooperation of the different subspecialties and thoroughgoing medical examination.]

Hypertension and nephrology

FEBRUARY 28, 2011

[The importance of epithelial-mesenchymal transition in kidney fibrosis]


[Epithelial-mesenchymal transition (EMT) plays a central role in physiological and pathological processes of embryogenesis, carcinogenesis and tissue fibrosis. During EMT epithelial cells may transform to myofibroblasts, which are the effector cells of fibrosis. In our summary the process of EMT and its medical importance will be reviewed in relation to renal fibrosis. Regardless of the initiating cause the final common mechanism of organ fibrosis is similar in the different chronic renal diseases. It always involves major inflammatory responses, however the molecular mechanisms involved are still elusive. The EMT now takes centre stage as the point of convergence between inflammation and the progression of degenerative fibrotic diseases. Understanding the pathomechanism of EMT and the significance of signalling pathways involved in this process may lead to a new therapeutic approach in the treatment of chronic renal diseases.]