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  • Author: Anca Negovan x
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Cardiovascular and digestive diseases frequently share the same risk factors such as obesity, unhealthy diet, or several social behaviors, and the increasing prevalence of patients with overlapped cardiovascular and digestive symptoms is a challenging problem in the daily practice. Patients with gastro-esophageal reflux disease can exhibit various forms of chest pain that can be very similar to angina. Furthermore, antithrombotic therapies used for preventive or curative purposes in patients with cardiovascular diseases are frequently associated with gastrointestinal side effects including bleeding. At the same time, in patients with coronary stents presenting to the emergency department with chest pain, angina triggered by stent thrombosis or restenosis should be differentiated from angina-like symptoms caused by a gastrointestinal disease. The aim of this review was to present the complex inter-relation between gastroesophageal diseases and angina in patients on dual antiplatelet therapy following an acute coronary syndrome, with a particular emphasis on the role of anemia resulting from occult or manifest gastrointestinal bleeding, as a precipitating factor for triggering or aggravating angina.


Objective: To evaluate the impact of congestive heart failure and the most important clinical and pathological factors on severe upper digestive mucosal lesions.

Methods: The study included 749 patients referred for upper digestive endoscopy, divided into two groups: 140 subjects with congestive heart failure (study group) and 609 subjects without heart failure (control group).

Results: Severe endoscopic lesions quantified according to Lanza score (OR = 3.84, 95% IC: 2.62-5.62), active/inactive gastritis (OR = 2.07, 95% CI: 1.36-3.14), intestinal metaplasia and/or gastric atrophy (OR = 2.42, 95% CI: 1.67-3.52) were significant more frequent among patients with heart failure. Anemia (OR = 3.65, 95% IC: 2.48-5.37) and all investigated comorbidities, as well as alcohol consumption (OR = 1.60, 95% IC: 1.10-2.34) and smoking (OR = 1.76, 95% IC: 1.17-2.64) were more frequent in the study-group. Dividing the patients with cardiac insufficiency according to the severity of their endoscopic lesions, the male gender (OR = 2.76, 95% IC: 1.35–5.61) and daily low-dose aspirin consumption were found to be more frequent among patients with severe endoscopic lesions (OR = 7.71, 95% IC: 3.62–16.40), while anticoagulant therapy and alcohol consumption were borderline associated with mucosal lesions (p=0.08).

Conclusions: Male patients and aspirin consumers with heart failure, but not those with H. pylori infection seem to be more prone to develop upper digestive endoscopic lesions, while alcohol consumption or anticoagulant therapy could be other modifiable factors associated with severe endoscopic lesions in a congestive gastro-duodenal mucosa.


The aim of our study was to evaluate the association between variant genotype of angiotensinogen (AGT) c.-58A>C, lifestyle factors and clinical factors and corporeal extension of gastric inflammatory and preneoplastic lesions.

Methods: Our study included 209 subjects who underwent a complete set of gastric biopsies, followed by genotyping. They were included to study inflammatory gastric changes and preneoplastic lesions and were grouped according to the localization of changes.

Results: No significant statistical associations were noticed between AGT c.-58A>C genotypes and the corporeal extension of the inflammation or preneoplastic injury groups. Extending preneoplastic lesions to the gastric body was associated with smoking habits (p=0.01) and additionally, there was a significant association between nicotine consumption and the body extension of preneoplastic lesions (p=0.01). The use of acenocoumarol was frequently associated with the progression of histological lesions to preneoplastic lesions (p=0.01). Compared with the wild-type AA genotype, the combined genotypes AA+CC of AGT c.-58A>C were significantly associated with the progression of inflammatory gastric lesions’ according to the regular ingested doses of nonsteroidal anti-inflammatory drugs (NSAIDs).

Conclusion: The AGT c.-58A>C polymorphism is not associated with extension of the gastric lesions. In accordance with nicotine and alcohol consumption, the acenocoumarol co-treatment and multiple cardiac pathologies are associated with the corporeal progression of these injuries. The age below 70 years and NSAIDs treatment for the patients with heterozygous AC genotype and variant homozygous CC genotype for the mentioned SNP have been associated with the corporeal extension of gastric inflammation.


Background: Colon polyps are precursors of colorectal cancer (CRC), therefore their endoscopic detection is very important. A shift of in the localization of colorectal polyps toward the proximal colon has been recently observed in Western countries.

Aim: The aim of this paper was to establish the most important clinical and endoscopic aspects of right colon polyps and to correlate them with their histopathological types, with an emphasis on sessile serrated adenomas/polyps (SSA/Ps).

Material and method: We perfomed a retrospective study on a series of consecutive patients who underwent colonoscopy in the Gastroenterology and Endoscopy Unit of the County Emergency Clinical Hospital of Tîrgu Mureș between January 1, 2010 – December 31, 2014, comparing the results with those of patients who underwent colonoscopy between January 1, 2005 – December 31, 2009. In all cases with abnormal aspects at endoscopy, multiple biopsies were taken for histopathological examination. Only cases where the diagnosis of colon polyp was confirmed by the Histopathology Department were included in the study.

Results: In the 2010–2014 period there were 871 patients diagnosed with colon polyps (1,038 polyps), with a mean age of 62.28 years. The most frequent histopathological form was tubular adenoma in 55.97% of cases (n = 581). SSA/Ps were found in 66 patients (75 polyps). Considering all polyps, the most frequent localization was in the sigmoid colon in 32.36% of cases (n = 336), but for SSA/Ps the most common localization was the ascending colon in 24% of cases (n = 18), followed by the sigmoid colon in 21.33% of cases (n = 16). Compared with patients investigated between 2005 and 2009, we found an increasing localization in the right colon, from 10.43% (n = 67) in 2005–2009 to 15.41% (n = 160) in 2010–2014. SSA/Ps were found in the right colon in 5.97% of cases (n = 4) in the first period compared with 11.25% of cases (n = 18) in the second period.

Conclusions: In the last years we found an increasing localization of colon polyps in the right colon. These findings underscore the importance of high quality colonoscopy to maximize protection against colorectal cancer.


Genetic factors may play a role in prediction of gastrointestinal side effects of aspirin, one of the most used drugs worldwide. We aim to determine a possible correlation between AGT A-20C (rs5050) gene polymorphism and gastro-duodenal ulcer in patients taking low-dose aspirin, adjusted for clinical and histological characteristics.

Results. We enrolled 211 patients stratified according to AGT A-20C genotype: 122 AA, 83 AC and 6 CC patients. There were no significant differences regarding demographical and clinical parameters, except for the frequency of ulcers (4%, 8.4% respective 50%, p=0.03), endoscopic bleeding signs (12.3%, 14.5% respective 50%, p=0.0001) and the frequency of gastritis in biopsy (63.9%, 54.2% respective 16.7%, p=0.03) in genotype groups. When we compared ulcer and non-ulcer group, variant homozygous CC genotype carried an increased risk for ulcer (OR:9.66, 95% CI: 1.46-63.7, p=0.04) than AA group, as well as variant C allele compared with normal A allele (OR: 2.12, 95% CI: 1.07-4.63, p=0.04). On multivariate analysis, variant homozygous CC genotype AGT A-20C showed an OR: 12.32 (95% CI:1.40 -108.13, p=0.02) for ulcer, while H. pylori infection (OR:2.40, 95% CI:1.18 -6.54, p=0.04) and concurrent use of non-steroidal anti-inflammatory drugs (NSAIDs) (OR:1.31, 95% CI:1.07 - 2.27, p=0.05) remained predictors for ulcer in aspirin consumers.

Conclusions. Variant C allele and variant homozygous CC genotype AGT A-20C, infection with H. pylori and NSAIDs co-treatment are risk factors for gastro-duodenal ulcer in low-dose aspirin consumers. The variant homozygous CC genotype AGT A-20C patients treated with LDA are more prone to have reactive gastropathy and bleeding ulcers in a population with a high prevalence of H. pylori infection


Background: The additional benefits of certain frequently used chronic drugs such as statins or aspirin are investigated for their possible effect of influencing various types of cancer, including gastric cancer. The possible role of statins in the occurrence of pre-neoplastic gastric lesions has not been investigated.

Aim: The study aims to determine the influence of chronic statin therapy on premalignant gastric lesions (glandular atrophy, intestinal metaplasia and dysplasia), adjusted with the most important aggressive environmental factors of the gastric mucosa (Helicobacter pylori [H. pylori] infection, low-dose aspirin [acetylsalicylic acid, ASA], biliary reflux, smoking, alcohol consumption).

Method: The study included 566 patients with cardiovascular diseases who underwent an upper endoscopy: 222 patients with chronic statin therapy (atorvastatin 20–80 mg/day or rosuvastatin 5–20 mg/day for at least 6 months) and 344 patients without statin intake. A complete set of biopsies from the gastric antrum and corpus were routinely processed and examined, and demographical, clinical, and pathological variables were recorded.

Results: Active H. pylori infection in gastric biopsies (p = 0.45), biliary reflux (p = 0.74), alcohol consumption (p = 0.43), or prior ulcer disease (p = 0.07; OR: 0.59; 95% CI: 0.33–1.04) were not associated with an increased risk for premalignant lesions, neither in the statin, nor the no-statin group. Smoking was associated with premalignant lesions in both groups (p = 0.01; OR: 2.24; 95% CI: 1.12–4.47; and p = 0.04; OR: 1.72; 95% CI: 1.01–2.94, respectively), while chronic use of ASA had no influence (p = 0.24, respective p = 0.35). In multivariate regression models, chronic treatment with statins had a protective effect (p = 0.006; OR: 0.59; 95% CI: 0.4–0.8), while smoking (p = 0.01; OR: 1.99; 95% CI: 1.17–3.39) and age >50 years (p <0.01, OR: 3.09; 95% CI: 1.84–5.21) were predictors for pre-neoplastic lesions. H. pylori infection, gender, alcohol consumption, biliary reflux, or prior ulcer disease were not associated with premalignant lesions (p >0.05). Conclusions: In the studied population, chronic statin treatment seems to be associated with a decreased risk for premalignant gastric lesions, while age over 50 years and smoking, regardless of gender or ASA consumption, remain the most important risk factors for premalignant gastric lesions.


A 62 year-old caucasian male was admitted in our pulmonary hypertension expert center with initial diagnosis of pulmonary veno-occlusive disease for validation and specific treatment approach. Routine examinations revealed no apparent cause of pulmonary hypertension. Patient was referred for a thorax contrast enhanced multi-slice computed tomography which revealed extensive bilateral thrombi in pulmonary lower lobe arteries, pleading for chronic post embolic lesions. A right heart catheterization and pulmonary angiography confirmed the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH). Following the local regulations, the patient underwent thrombophilia screening including molecular genetic testing, with positive findings for heterozygous for VCORK1 -1639G>A gene single nucleotide polymorphism, PAI-1 4G/5G and factor II G20210A gene. With heterozygous genetic profile of 3 mutations he has a genetic predisposition for developing a thrombophilic disease which could be involved in the etiology of CTEPH. Familial screening was extended to descendants; the unique son was tested with positive results for the same three genes. Supportive pulmonary hypertension drug therapy was initiated together with patient self-monitoring management of oral anticoagulation therapy. For optimal control of targeted anticoagulation due to a very high risk of thrombotic state the patient used a point-of-care device (CoaguChek®XS System, Roche Diagnostics) for coagulation self-monitoring.


Introduction: Extrahepatic portal vein thrombosis (EPVT) is the most frequent cause that leads to portal hypertension in non-cirrhotic patients. This condition is related to systemic and local risk factors (such as inflammatory lesions, injuries to portal venous system by surgery, vascular procedures).

Case presentation: A case of extended extrahepatic portal vein thrombosis and simultaneous thrombosis of left common iliac vein and inferior vena cava, appeared after abdominal surgery in a hypertensive, diabetic, 50 y.o. man is presented. An acute episode of abdominal pain was interpreted as an emergency and a surgical (initially laparoscopic and then open) procedure was planned in order to perform an appendectomy. Discharge diagnosis was hemoperitoneum secondary to iatrogenic rupture of sigmoid mesocolon provoked by trocar manipulation. Repeated imaging studies performed later revealed the thrombosis of portal vein with extension into right portal branch associated with superior mesenteric thrombosis and free-floating thrombus into left common iliac vein extended towards inferior vena cava. Surgical manoeuvres are considered as triggers of these thrombotic events. After 4 weeks of parenteral anticoagulation a partial recanalization of thrombi was identified, without bleedings.

Conclusions: Acute EPVT needs a carefully management. Case is linked to abdominal surgery and requires prolonged anticoagulation related to simultaneous portal and iliac vein thrombosis. Associated conditions (hypertension and diabetes mellitus) must have an appropriate approach. After our knowledge this is the first case published in literature.