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위산B12 helicobacter 몇가지 최근 논문들..
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B12 부족증의 주 원인은 atrophic gastritis라고 본다. 자가면역질환 혹은 헬리코박터균에 의해서 위산부족과 intrinsic factor부족(악성빈혈)을 야기하고 헬리코박터는 위장 자가면역질환의 원인이고 위산부족과 intrinsic factor부족으로 인해 B12부족이 되며 악성빈혈이 온다.(아래논문참조) 임신중 호모시스테인 수치가 높은 경우 B12부족이 원인인 경우가 많으며 헬리코박터로 인해서 온 경우이므로 임신전에 미리 위장 헬리코박터를 치료해야 한다. B12부족증은 celiac질환과 관련이 많다. (아래 논문참조) SAMe는 acetaminophen으로 인한 간독성을 보호해준다(아래 논문 참조) 흥분이 잘되는 아이들인 경우 세로토닌이 부족해지기 쉽고 따라서 B6(P5P)를 주었을 때 좋아지는 경향이 있다.(아래 논문참조) Vitamin B12 deficiency. New data on an old disease] Lechner K Fodinger M Grisold W Puspok A Sillaber C. Abteilung Hamatologie und Hamostaseologie Universitatsklinik fur Innere Medizin I Medizinische Universitat Wien Wien Osterreich. klaus.lechner@meduniwien.ac.at Cobalamin deficiency is a common finding. In the elderly the prevalence is 10-20% but only 5-10% of these are clinically symptomatic. Typical clinical symptoms include macrocytic anemia neuropsychiatric symptoms and glossitis. In many cases this triad is lacking however. The serum cobalamin assay is the best first line test but the results must be carefully interpreted since a normal level does not exclude deficiency. Markers of cobalamin activity such as serum homocysteine or methylmalonic acid may be helpful in this situation. The main cause of cobalamin deficiency is atrophic gastritis. It is either caused by an autoimmune process which leads to achlorhydria and severe intrinsic factor deficiency (""classical pernicious anemia"") or by atrophic gastritis from other causes in particular helicobacter pylori infection. In the latter cases the lack of gastric acid does not allow separation of cobalamin from proteins but intrinsic factor although low is sufficient for cobalamin protection (food cobalamin malabsorption). Helicobacter pylori eradication may cure some of these patients. While in food cobalamin malabsorption syndrome small doses of oral cobalamin are effective parenteral therapy or high oral doses are required for treatment of pernicious anemia. While almost all patients respond hematologically only half of the patients with neurological signs and a small minority of psychiatric patients respond to treatment. Patients with pernicious anemia and atrophic gastritis have a greatly increased long-term risk for gastric carcinoids. Helicobacter pylori infection and gastric autoimmune diseases: is there a link? Presotto F Sabini B Cecchetto A Plebani M De Lazzari F Pedini B Betterle C. Department of Medical and Surgical Sciences University of Padua School of Medicine Padua Italy. BACKGROUND: Helicobacter pylori is thought to be involved in atrophic body gastritis. We explored the prevalence of H. pylori infection in asymptomatic subjects with gastric parietal cell antibodies as well as in patients with pernicious anemia to evaluate a possible role of H. pylori gastric infection in gastric autoimmunity. PATIENTS AND METHODS: We studied 79 consecutive asymptomatic subjects with parietal cell antibodies 24 patients with pernicious anemia and 66 parietal cell antibody-negative controls. All patients underwent gastric biopsies for histology and detection of H. pylori. Red blood cell count and volume serum levels of gastrin pepsinogen I iron folic acid vitamin B12 and circulating antibodies to H. pylori and to intrinsic factor were also determined. RESULTS: We found an atrophic body gastritis in 14 of the 79 asymptomatic subjects with parietal cell antibodies (18%) and in 2 of the 66 controls (3%) (p =.01). Mean levels of gastrin were increased (p <.0001) while those of pepsinogen were reduced (p <.001) compared with controls. H. pylori was identified at the gastric level and/or circulating anti-H. pylori antibodies were detected in 46 parietal cell antibody-positive subjects (58%) compared with 26 controls (39%) (p =.03). In patients with pernicious anemia we found an atrophic body gastritis in 18 of 24 cases (75%) (p <.001 vs. controls). Mean levels of gastrin were markedly increased (p <.0001) and those of pepsinogen I decreased (p <.0001) relative to controls. Only five of these patients (21%) had evidence of H. pylori infection compared with 46 of the parietal cell antibody-positive subjects (58%) (p =.003) and 26 of the controls (39%). Considering all patients with gastric autoimmunity (i.e. with parietal cell antibodies and/or with pernicious anemia) H. pylori was found in 44 of 72 of those without atrophy (61%) but in 6 of 31 with gastric body atrophy (19%) (p <.001) indicating that H. pylori infection is greatly reduced when gastric acid secretion decreases. CONCLUSIONS: The frequent detection of H. pylori infection in subjects with early gastric autoimmunity indicated by the presence of parietal cell antibodies suggests that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level. S-Adenosylmethionine protects against acetaminophen-induced hepatotoxicity in mice. Song Z McClain CJ Chen T. Department of Medicine University of Louisville Medical Center Louisville KY 40292 USA. An overdose of acetaminophen (APAP) is the most frequent cause of fulminant liver failure in the United States. Increasing evidence demonstrates that oxidative stress plays an important etiologic role in APAP-induced liver injury. S-Adenosylmethionine (SAMe) is a key intermediate in the hepatic trans-sulfuration pathway and serves as a precursor for glutathione (GSH) as well as the methyl donor in most transmethylation reactions. In the present study we investigated effects of SAMe on liver injury induced by APAP administration in male C57BL/6 mice. Two related studies were performed. In the first experiment SAMe (1g/kg BW) was injected intraperitoneally 4 h before APAP (600 mg/kg BW) administration. In the second experiment SAMe was injected intraperitoneally 1 h after APAP administration. Our results showed that APAP administration induced changes typical of confluent centrilobular necrosis by histological examination and a marked elevation in serum alanine aminotransferase (ALT) activity. APAP administration induced significant decreases in both hepatic and blood SAMe concentrations. In addition APAP decreased intracellular (both cytosolic and mitochondrial) GSH concentrations along with increased lipid peroxidation in conjunction with mitochondrial dysfunction as documented by Ca2+-induced mitochondrial permeability transition. SAMe treatment (both before and after APAP) significantly attenuated the liver injury. Exogenous SAMe prevented the decrease in liver and blood SAMe concentrations. Moreover SAMe treatment attenuated both cytosolic and mitochondrial GSH depletion as well as mitochondrial dysfunction. We conclude that SAMe at least in part protects the liver from APAP-induced injury by preventing intracellular GSH depletion and mitochondrial dysfunction. Copyright 2004 S. Karger AG Basel The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children. Bhagavan HN Coleman M Coursin DB. The contents of serotonin (hydroxytryptamine) and pyridoxal phosphate (PLP) in the blood of 11 hyperactive children and 11 controls were determined on an outpatient basis. A significant decrease in serotonin content was found in blood samples from hyperactive patients as compared with controls. There were no differences in PLP content of blood between the two groups. Four children were selected for a study of the effects of pyridoxine hydrochloride (vitamin B6) on low serotonin levels. Oral doses of pyridoxine resulted in an appreciable increase in the serotonin content and a very large increase in the PLP content of blood in these hyperactive patients.

 
   
 
 
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