48 research outputs found

    Churg-Strauss Syndrome Associated with Montelukast: Three Case Reports

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    Churg-Strauss Sendromu yeni adıyla Eozinofilik Granülomatosis ve Polianjiitis; astım, ateş, periferik kanda eozinofili, eozinofilik doku infiltrasyonu, küçük ve orta çaptaki damarların nekrotizan granülomatöz inflamasyonu ile karakterize multisistemik bir hastalıktır. ANCA ilişkili vaskülitler içinde sınıflandırılmaktadır. Lökotrien reseptör antagonistleri (montelukast, zafirlukast, pranlukast), inhaler glukokortikoidler, omalizumab, kokain ve klaritromisin gibi ilaçlarla ilişkili olduğu düşünülen Churg-Strauss Sendromu vakaları bildirilmiştir. Bu makalede montelukast ilişkili nadir görülen 3 CSS olgusu sunulmuşturChurg-Strauss syndrome (new name Eosinophilic granulomatosis and polyangiitis); asthma, fever, peripheral blood eosinophilia, eosinophilic tissue infiltration, small and medium sized arteries characterized by necrotizing granulomatous inflammation is a multisystemic disorder. Classified in ANCA associated vasculitis. The drugs such as leukotriene receptor antagonists (montelukast, zafirlukast, pranlukast), inhaled glucocorticoids, omalizumab, cocaine and clarithromycin is thought to be associated with Churg-Strauss Syndrome cases have been reported. Herein we presented a rare three CSS cases associated with montelukas

    Adult onset acid maltase deficiency

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    Glikojen depo hastalığı tip II (GDHII, Pompe hastalığı), lizozomal alfa-glukosidaz eksikliğine bağlı otosomal resesif bir, hastalıktır, infantil, juvenil ve adult olmak üzere üç farklı form tanımlanmıştır. Asit maltaz eksikliği olan otuz yaşında bayan hasta sunulmuştur. Lökosit asit maltaz seviyesi sıfır olan hastamızda semptomlar iskelet kasına sınırlıydı. Bu olgu nörolojik ve histopatolojik özellikleri ile tartışılmıştır.Glycogen storage disease type II (GSDII, Pompe's disease) is an autosomal recessive inherited deficiency of lysosomal alpha-glucosidase (GAA). Three different clinical forms as infantile, juvenile and adult form have been descibed. A thirty-year-old-female with adult form acid maltase deficiency is presented. Although the leucosyt acid maltase level was zero in our patient the symptoms were restricted to skeletal muscle. The neurological and histopathological findings of this case are discussed

    Angiogenesis and endothelial markers in primary CNS tumors

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    The neovascularization and endothelial antigenic changes of 47 different types of central nervous system tumors were analyzed • histochemically and immunohistochemically. The relation between the endothelial antigenic characteristics and the histological grading was also examined. Vascular endothelial proliferation was detected in the reticulum stain. Immunohistochemically, factor VIM related antigen (FVIIIR:Ag) and blood-group isoantigens (BGAg) were used as endothelial markers. In all the examined sections a diffuse, linear or slightly granular immunostaining pattern was observed in the endothelium for both antigens. The distribution and intensity of the antigens were nonspecific among the grades. [Turk J Cancer 1995;25(3):i11-9]The neovascularization and endothelial antigenic changes of 47 different types of central nervous system tumors were analyzed • histochemically and immunohistochemically. The relation between the endothelial antigenic characteristics and the histological grading was also examined. Vascular endothelial proliferation was detected in the reticulum stain. Immunohistochemically, factor VIM related antigen (FVIIIR:Ag) and blood-group isoantigens (BGAg) were used as endothelial markers. In all the examined sections a diffuse, linear or slightly granular immunostaining pattern was observed in the endothelium for both antigens. The distribution and intensity of the antigens were nonspecific among the grades. [Turk J Cancer 1995;25(3):i11-9

    A case with atypical reflex sympathetic dystrophy syndrome

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    Background and Design.- Reflex sympathetic dystrophy syndrome is a disorder characterized by pain, edema, discoloration and autonomic abnormalities. Its etiopathogenesis is not completely determined. A 31-year-old male was admitted to our department with complaints of edema, pain, motion limitation and skin color changes in his right foot and ankle of it that is started 3 months ago. He had a history of recurrent ulcers in the mouth for 3 years and working in cast iron factory for 19 years, and we learned that the same limb of him was exposed to a trauma. In neurological examination; paresis, hypoesthesia, allodynic and hyperpathic pain were detected in the right lower limb. Electrophysiological study showed mixt type polyneuropathy. Heavy metal intoxication, collagen tissue diseases, endocrinopathies and malignant conditions were excluded. Although there was a history of a mild trauma to that limb and we know that nerve injuries play a role in the etiopathogenesis of reflex sympathetic dystrophy syndrome, a question comes to the mind about whether polyneuropathies can cause this syndrome.Background and Design.- Reflex sympathetic dystrophy syndrome is a disorder characterized by pain, edema, discoloration and autonomic abnormalities. Its etiopathogenesis is not completely determined. A 31-year-old male was admitted to our department with complaints of edema, pain, motion limitation and skin color changes in his right foot and ankle of it that is started 3 months ago. He had a history of recurrent ulcers in the mouth for 3 years and working in cast iron factory for 19 years, and we learned that the same limb of him was exposed to a trauma. In neurological examination; paresis, hypoesthesia, allodynic and hyperpathic pain were detected in the right lower limb. Electrophysiological study showed mixt type polyneuropathy. Heavy metal intoxication, collagen tissue diseases, endocrinopathies and malignant conditions were excluded. Although there was a history of a mild trauma to that limb and we know that nerve injuries play a role in the etiopathogenesis of reflex sympathetic dystrophy syndrome, a question comes to the mind about whether polyneuropathies can cause this syndrome

    Simultaneous MALT-type lymphoma and early adenocarcinoma of the stomach: A case report

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    We report a rare case of a 52-year old man who was initially operated for early gastric adenocarcinoma but was found to have synchronous Iymphoma and in situ adenocarcinoma of the stomach on frozen sections, confirmed by postoperative pathological examination. The relationship between these two tumors and the most appropriate methods of diagnosis were discussed.We report a rare case of a 52-year old man who was initially operated for early gastric adenocarcinoma but was found to have synchronous Iymphoma and in situ adenocarcinoma of the stomach on frozen sections, confirmed by postoperative pathological examination. The relationship between these two tumors and the most appropriate methods of diagnosis were discussed

    Indomethacin Prevents Neuronal Apoptosis in Newborn Rats with Hypoxic-Ischemic Brain Injury

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    WOS: 000291330700015Objective: Cyclooxygenase pathway and prostaglandins play an important role in the pathogenesis and delayed mechanisms of hypoxic-ischemic brain injury. The aim of this study was to investigate the effect of different doses of indomethacin, a nonselective cyclooxygenase inhibitor, on neuronal apoptosis in rats with hypoxic-ischemic brain injury. Material and Methods: Seven-day-old rat pups with the Rice model of hypoxic-ischemic cerebral injury were randomly divided into five groups. Group 1 (n=15) pups were given physiologic saline, neither ligation nor hypoxia were performed. Group 2 (n=15) pups were treated with physiologic saline after hypoxic-ischemia. Group 3 (n=15) pups were treated with indomethacin at a dose of 2 mg/kg before hypoxic ischemia. Group 4 (n=15) pups were treated with three doses of indomethacin at a dose of 2 mg/kg every 12 h after hypoxic-ischemia. Group 5 (n=15) pups were treated with three doses of indomethacin, at a dose of 4mg/kg every 12 h after hypoxic ischemia. After 72 hours, the rats were decapitated and brain hemispheres were evaluated by the TUNEL (Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) staining method. Results: Indomethacin treatment, either before or after hypoxia, resulted in a significant reduction in the numbers of apoptotic cells in the rat brain when compared to those who were treated with physiologic saline after hypoxic-ischemia (P<0.001). Conclusion: Our results demonstrated that indomethacin administration, either before or after hypoxic-ischemia, reduces neuronal apoptosis; and we propose that indomethacin may be a potential choice of treatment for hypoxic-ischemic brain injury.Cukurova University Research FoundationCukurova UniversityThis study was supported by the Cukurova University Research Foundation

    Pseudo-Kaposi's sarcoma in Behçet's disease

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    Thrombosis in BehÇet's disease (BD) is not uncommon and venous occlussions affecting the venae cavae and their tributaries may result in during the course of the disease. Pseudo-Kaposi's sarcoma is characterized with a nodule or plaque which may lead to a painful ulceration. The development of the Mali's syndrome, an entity of Pseudo-Kaposi's sarcoma, usually follows stasis dermatitis and occurs on the lower extremities. In this report, we present a Pseudo-Kaposi's sarcoma case a 25-year-old male during the fourth year of the diagnosis with BD. The association of Pseudo Kaposi's sarcoma and BehÇet's disease has never- to our knowledge- been reported before.Thrombosis in BehÇet's disease (BD) is not uncommon and venous occlussions affecting the venae cavae and their tributaries may result in during the course of the disease. Pseudo-Kaposi's sarcoma is characterized with a nodule or plaque which may lead to a painful ulceration. The development of the Mali's syndrome, an entity of Pseudo-Kaposi's sarcoma, usually follows stasis dermatitis and occurs on the lower extremities. In this report, we present a Pseudo-Kaposi's sarcoma case a 25-year-old male during the fourth year of the diagnosis with BD. The association of Pseudo Kaposi's sarcoma and BehÇet's disease has never- to our knowledge- been reported before
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