Longitudinal course of depressive symptoms and anxiety after aneurysmal subarachnoid hemorrhage.

BACKGROUND: Symptoms of anxiety and depression are present in almost half of the patients who survive an aneurysmal subarachnoid hemorrhage (aSAH), but the long-term course is unknown. AIM: To study the longitudinal course and predictors of symptoms of anxiety and depression after aSAH. DESIGN: Prospective longitudinal study with test occasions at 3 months (baseline), 1 year (T2) and 2-5 years (T3) post-aSAH. SETTING: SAH outpatient clinic. POPULATION: One hundred forty-three patients visiting the outpatient clinic. METHODS: Patients visiting our outpatient clinic 3 months after aSAH and living independently in the community completed the Beck Depression Inventory-II-NL and the State-Trait Anxiety Inventory at 3 months (T1), one year (T2) and 2-5 years (T3). Potential predictors were collected at T1. RESULTS: Complete datasets from 93 patients were analyzed. Depressive symptoms were present in 39% (T1), 41% (T2) and 54% (T3) of patients, symptoms of anxiety in 52% (T1), 48% (T2) and 53% (T3). Of patients with depressive symptoms at T1, 72% still had symptoms at T3, compared to 67% for anxiety. Disability on the Glasgow Outcome Scale (GOS), passive coping (UCL-PR) and depressive symptoms at T1 were significantly independent variables explaining 52% of the variance of depressive symptoms at T2. GOS and UCL-PR at T1 were variables explaining 25% of the variance of depressive symptoms at T3. Depressive symptoms and anxiety at T1 were predictive variables for anxiety at T2 (explained variance 43%) and UCL-PR for anxiety at T3 (explained variance 21%). CONCLUSIONS: The prevalence of symptoms of depression and anxiety remained high during the first 2-5 years after aSAH. Passive coping at 3 months after aSAH was the most consistent predictor of symptoms of anxiety and depression in the long term. CLINICAL REHABILITATION IMPACT: Since many patients who are initially free of symptoms of depression and anxiety develop such symptoms over time, we advocate screening for these symptoms and coping strategies to identify these patients and apply targeted therapy.

Colonization with cagA-positive Helicobacter pylori strains in intestinal metaplasia of the esophagus and the esophagogastric junction.

OBJECTIVES: Recent studies indicate that colonization with cagA-positive Helicobacter pylori (H. pylori) strains may protect against gastroesophageal reflux disease (GERD) and its complications, but the role of cagA in the etiology of Barrett's esophagus has so far been poorly investigated. The pathogenesis of intestinal metaplasia (IM) at an endoscopically normal esophagogastric junction (EGJ) is still unclear, and the role of the H. pylori virulence factor cagA in it has not been investigated. The aim of our study was to assess the relationship between H. pylori and cagA-positive H. pylori in particular and IM at an endoscopically normal EGJ and Barrett's esophagus. METHODS: Serum samples were obtained from 62 patients without IM, 43 patients with IM at an endoscopically normal junction, and 51 patients with Barrett's esophagus. IM was defined as presence of goblet cells with positive staining with Alcian blue. The prevalence of H. pylori and cagA was investigated by assessment of IgG antibody levels as determined by ELISA. RESULTS: The overall H. pylori prevalence was 59% (92/156), and the cagA prevalence was 29% (46/156). Although 63% (39/62) of IM negative subjects and 74% (32/43) of those with IM at the junction were H. pylori positive, only 41% (21/51) of Barrett's patients tested positive. The differences between the IM negative and the Barrett's group (p = 0.02) and between IM at the junction and Barrett's were significant (p = 0.002). The relative cagA prevalence (percentage with cagA positivity and H. pylori positivity) was 56% (22/39) in patients who were IM negative, 59% (19/32) in those with IM at the junction, and 24% (5/21) in those with Barrett's. The prevalence of anti-CagA was significantly lower in patients with Barrett's esophagus compared with patients who were IM negative (p = 0.002) and those who had IM at the junction (p < 0.001). No difference in cagA prevalence was seen between the latter groups. CONCLUSIONS: These findings are in line with the concept that H. pylori and cagA-positive strains in particular protect against the development of Barrett's esophagus. In contrast, our findings do not support the theory that IM at an endoscopically normal esophagogastric junction is associated with H. pylori or cagA-positive strains. IM at the junction and Barrett's esophagus seem to have different etiologies.