Unexplained iron deficiency anemia: does Helicobacter pylori have a role to play?

BACKGROUND AND AIM: Testing for Helicobacter pylori (Hp) infection is recommended for work-up of unexplained iron deficiency anemia (IDA), although the evidence supporting this recommendation is scant. The aim of this study was to investigate the association between Hp infection and unexplained iron deficiency (ID) or IDA in the older adult population without significant upper gastrointestinal source of blood loss. METHODS: Retrospective single-center cohort study; 523 out of 1253 consecutive patients who underwent esophagogastroduodenoscopy with no significant upper and/or lower gastrointestinal source for blood loss or risk factors for IDA. Comparisons were made between the Hp-positive and Hp-negative groups using Fisher exact test, chi-square test and Student's t-test. Univariate and multiple logistic regression analyses were used to identify significant risk factors associated with ID and IDA. RESULTS: One hundred and three subjects (19.7%) had Hp infection and 420 (80.3%) were negative for Hp. Sixty-eight (22.1%) out of 307 subjects with available serum iron profile had unexplained ID and 28 (5.4%) out of 510 subjects with available hemoglobin profile had unexplained IDA. No association was found between ID/IDA and Hp infection in univariate and multiple logistic regression analyses. CONCLUSION: We found no association between unexplained ID or IDA and Hp infection in older adult population without peptic ulcer disease or significant upper gastrointestinal source of blood loss.

Increasing hippocampal acetylcholine levels enhance behavioral performance in an animal model of diencephalic amnesia.

Pyrithiamine-induced thiamine deficiency (PTD) was used to produce a rodent model of Wernicke-Korsakoff syndrome that results in acute neurological disturbances, thalamic lesions, and learning and memory impairments. There is also cholinergic septohippocampal dysfunction in the PTD model. Systemic (Experiment 1) and intrahippocampal (Experiment 2) injections of the acetylcholinesterase inhibitor physostigmine were administered to determine if increasing acetylcholine levels would eliminate the behavioral impairment produced by PTD. Prior to spontaneous alternation testing, rats received injections of either physostigmine (systemic=0.075 mg/kg; intrahippocampal=20, 40 ng/muL) or saline. In Experiment 2, intrahippocampal injections of physostigmine significantly enhanced alternation rates in the PTD-treated rats. In addition, although intrahippocampal infusions of 40 ng of physostigmine increased the available amount of ACh in both pair-fed (PF) and PTD rats, it did so to a greater extent in PF rats. The increase in ACh levels induced by the direct hippocampal application of physostigmine in the PTD model likely increased activation of the extended limbic system, which was dysfunctional, and therefore led to recovery of function on the spontaneous alternation task. In contrast, the lack of behavioral improvement by intrahippocampal physostigmine infusion in the PF rats, despite a greater rise in hippocampal ACh levels, supports the theory that there is an optimal range of cholinergic tone for optimal behavioral and hippocampal function.