Intake of Acetylsalicylic Acid and High Age Are Risk Factors for Iron Deficiency Anemia in Patients with Large Diaphragmatic Hernias.

INTRODUCTION: In 15% of patients with iron deficiency anemia, large diaphragmatic hernias are found as the cause of chronic iron loss. Conversely, iron deficiency anemia is present in 10-40% of diaphragmatic hernia patients. However, it is unclear why some patients with large diaphragmatic hernias develop anemia and others do not. METHODS: We retrospectively analyzed 116 patients with diaphragmatic hernias larger than 5 cm for the presence of anemia and the effect of surgery on this anemia, dividing these patients into 4 groups (group A: 21 patients with anemia/surgery, group B: 27 patients without anemia but with surgery, group C: 34 patients with anemia but without surgery, and group D: 34 patients without anemia/surgery). RESULTS: Women significantly predominated in the patient population (76%). Patients with iron deficiency anemia tended to be significantly older than patients without iron deficiency anemia (74.7 ± 12.2 vs. 69.6 ± 14.8 years, p = 0.08). The proportion of patients taking ASA was significantly higher in the anemia collective (41.8% vs. 9.8%, p < 0.001). Regression analysis further confirmed that higher age and ASA intake correlated significantly with lower hemoglobin in anemic patients. Performing hernia repair significantly decreased anemia rates and PPI use in the anemia patients, while both remained almost the same in the non-operated anemia patients. CONCLUSION: ASA use and advanced age are risk factors for the presence of iron deficiency anemia in patients with large diaphragmatic hernias. Surgical hernia repair is suitable to reduce anemia.

Paraesophageal hernia and iron deficiency anemia: Mechanisms, diagnostics and therapy.

There is ample clinical evidence suggesting that the presence of large axial or paraesophageal hernias may lead to iron deficiency anemia. So-called Cameron lesions, as well as other small mucosa erosions, in the sliding area of these diaphragmatic hernias lead to invisible chronic blood loss and consequently to iron depletion. While the spectrum of symptoms in these patients is large, anemia is often not the only indication and typically not the primary indication for surgical correction of diaphragmatic hernias. Drug treatment with proton pump inhibitors and iron substitution can alleviate anemia, but this is not always successful. To exclude other possible bleeding sources in the gastrointestinal tract, a comprehensive diagnostic program is necessary and reviewed in this manuscript. Additionally, we discuss controversies in the surgical management of paraesophageal hernias.

Prevalence of familial pancreatic cancer in Germany.

Based on several case-control studies, it has been estimated that familial aggregation and genetic susceptibility play a role in up to 10% of patients with pancreatic cancer, although conclusive epidemiologic data are still lacking. Therefore, we evaluated the prevalence of familial pancreatic cancer and differences to its sporadic form in a prospective multicenter trial. A total of 479 consecutive patients with newly diagnosed, histologically confirmed adenocarcinoma of the pancreas were prospectively evaluated regarding medical and family history, treatment and pathology of the tumour. A family history for pancreatic cancer was confirmed whenever possible by reviewing the tumour specimens and medical reports. Statistical analysis was performed by calculating odds ratios, regression analysis with a logit-model and the Kaplan-Meier method. Twenty-three of 479 (prevalence 4.8%, 95% CI 3.1-7.1) patients reported at least 1 first-degree relative with pancreatic cancer. The familial aggregation could be confirmed by histology in 5 of 23 patients (1.1%, 95% CI 0.3-2.4), by medical records in 9 of 23 patients (1.9%, 95% CI 0.9-3.5) and by standardized interviews of first-degree relatives in 17 of 23 patients (3.5%, 95% CI 2.1-5.6), respectively. There were no statistical significant differences between familial and sporadic pancreatic cancer cases regarding sex ratio, age of onset, presence of diabetes mellitus and pancreatitis, tumour histology and stage, prognosis after palliative or curative treatment as well as associated tumours in index patients and families, respectively. The prevalence of familial pancreatic cancer in Germany is at most 3.5% (range 1.1-3.5%) depending on the mode of confirmation of the pancreatic carcinoma in relatives. This prevalence is lower than so far postulated in the literature. There were no significant clinical differences between the familial and sporadic form of pancreatic cancer.

Gene amplification and protein overexpression of c-erb-b2 in Barrett carcinoma and its precursor lesions.

We examined 39 samples of metaplastic specialized epithelium (SE), 27 of low-grade dysplasia (LGD), 27 of high-grade dysplasia (HGD), and 46 of adenocarcinoma (CA) derived from Barrett esophagus for c-erb-b2 gene amplification using differential polymerase chain reaction and for overexpression of c-erb-b2 protein using immunohistochemical analysis. Amplification of the c-erb-b2 gene was as follows: SE, 0.0%; LGD, 0.0%; HGD, 11.1%; and CA, 13.6%; and protein overexpression was as follows: SE, 0.0%; LGD, 7.4%; HGD, 18.5%; and CA, 21.7%. In 8 (89%) of 9 samples, c-erb-b2 gene amplification correlated with protein overexpression. The reverse was true in 8 (47%) of 17 samples: c-erb-b2 protein overexpression was proved with simultaneous gene amplification. Amplification of c-erb-b2 is a late event in the carcinogenesis of Barrett esophagus. In contrast, protein overexpression appears more often and earlier Besides gene amplification, other mechanisms to induce protein overexpression must exist.