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1.
Braz J Med Biol Res ; 36(7): 879-86, 2003 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-12845374

RESUMO

The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirty-three of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.


Assuntos
Anemia Hemolítica/complicações , Hemólise , Pancreatite/etiologia , Doença Aguda , Amilases/sangue , Animais , Modelos Animais de Doenças , Lipase/sangue , Pancreatite/sangue , Pancreatite/patologia , Fator de Ativação de Plaquetas/análise , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/análise
2.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;36(7): 879-886, July 2003. ilus, tab, graf
Artigo em Inglês | LILACS | ID: lil-340680

RESUMO

The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20 percent. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20 percent (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20 percent ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70 percent) of 50 rats, moderate hemolysis in seven (14 percent), and no hemolysis in eight (16 percent). Thirty-three of 35 (94.2 percent) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8 percent) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-alpha and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80 percent of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines


Assuntos
Animais , Ratos , Anemia Hemolítica , Hemólise , Pancreatite , Doença Aguda , Amilases , Modelos Animais de Doenças , Lipase , Pancreatite , Fator de Ativação de Plaquetas , Ratos Wistar , Índice de Gravidade de Doença , Fator de Necrose Tumoral alfa
3.
Braz J Med Biol Res ; 36(6): 747-51, 2003 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-12792704

RESUMO

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.


Assuntos
Dispepsia/microbiologia , Infecções por Helicobacter/complicações , Helicobacter pylori/isolamento & purificação , Adulto , Análise de Variância , Antígenos de Bactérias/análise , Proteínas de Bactérias/análise , Dispepsia/patologia , Feminino , Gastrinas/análise , Infecções por Helicobacter/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase , Estatísticas não Paramétricas , Fator de Necrose Tumoral alfa/análise , Turquia
4.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;36(6): 747-751, June 2003. tab
Artigo em Inglês | LILACS | ID: lil-340662

RESUMO

The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6 percent), motility disorder-like (ML), 281 (31.2 percent), and the combination (C) of these symptoms, 298 (33.1 percent). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-alpha (TNF-alpha) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-alpha and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Dispepsia , Infecções por Helicobacter , Helicobacter pylori , Análise de Variância , Dispepsia , Gastrinas , Infecções por Helicobacter , Reação em Cadeia da Polimerase , Receptores da Colecistocinina , Estatísticas não Paramétricas , Fator de Necrose Tumoral alfa , Turquia
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