RESUMO
BACKGROUND: Peptic ulcer has multifactorial aetiology, including genetic factors. We have identified a family with pepsinogen Group A levels higher than normal, with a high prevalence of ulcer disease and a low prevalence of Helicobacter pylori infection. AIMS: Performing linkage analysis in the identified family PATIENTS AND METHODS: We examined the segregation of pepsinogens with microsatellite dinucleotide repeat DNA markers along chromosome 11 (D11S480, PYGM) for pepsinogen Group A and along chromosome 6 [D6S105, D6S 1610, TRMI) for pepsinogen Group C. RESULTS: In markers examined along chromosome 11, linkage analysis provided no evidence for significant causal mutation but, controlling for some risk factors we observed that the probability of falling ill, increases. The linkage analysis along chromosome 6 for pepsinogen Group C did not show a uniform genetic profile. CONCLUSIONS: This study evaluates the hypothesis of peptic ulcer inheritance at least in a small group of patients without the common risk factors.
Assuntos
Cromossomos Humanos Par 11/genética , DNA/análise , Infecções por Helicobacter/microbiologia , Helicobacter pylori , Pepsinogênio A/sangue , Úlcera Péptica/genética , Anticorpos Antibacterianos/análise , Cromossomos Humanos Par 6/genética , Feminino , Ligação Genética/genética , Predisposição Genética para Doença , Infecções por Helicobacter/sangue , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/genética , Helicobacter pylori/imunologia , Humanos , Incidência , Itália/epidemiologia , Masculino , Linhagem , Pepsinogênio A/genética , Pepsinogênio C/sangue , Pepsinogênio C/genética , Úlcera Péptica/sangue , Úlcera Péptica/epidemiologia , Úlcera Péptica/microbiologia , Reação em Cadeia da PolimeraseRESUMO
Mixed saliva of the patient with cirrhosis of the liver contains often large quantities of immune globulins. IgA and M transport is facilitated, but whereas IgA globulins are present in all cases, the IgM appear in the saliva only where plasma concentration is greater than 200 mg %. Owing to a simple passive diffusion mechanism, the IgG reach high saliva levels in all subjects studied.
Assuntos
Imunoglobulinas/análise , Cirrose Hepática Alcoólica/imunologia , Saliva/imunologia , Humanos , Imunoglobulina A/análise , Imunoglobulina G/análise , Imunoglobulina M/análiseRESUMO
The Authors, after having examined the factors responsible for the hyperprolactinemia in the cirrhotic, confirm the lack of a relationship between the increase in the prolactinic reserve and gynecomastia and between the amount of the prolactinic reserve and the degree of liver disorder. While hyperestrinism and the false transmitters lost most of their pathogenetic importance, other factors such as GABA, the Serotonin and the VIP, offered a new pathogenetic prospective. The prolactin reserve was studied in 63 patients affected by cirrhosis and in 25 affected by fibrosis and hepatic fibrosteatosis, pointing out an increase in the prolactin reserve in 61% of cirrhotic patients and an absence of pathological reports in patients affected by fibrotic hepatopathies. These data confirm the low pathogenetic responsability to be strictly ascribed to ethanol and the preminent role of liver cirrhosis and portal hypertension in the prolactin turnover.
Assuntos
Fígado Gorduroso Alcoólico/sangue , Ginecomastia/etiologia , Cirrose Hepática Alcoólica/sangue , Prolactina/sangue , Fígado Gorduroso Alcoólico/complicações , Humanos , Hipertensão Portal/etiologia , Cirrose Hepática Alcoólica/complicações , Masculino , Pessoa de Meia-Idade , Hormônios Liberadores de Hormônios Hipofisários/sangue , Prolactina/metabolismo , Serotonina/sangue , Ácido gama-Aminobutírico/sangueRESUMO
Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.