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Open access

Marilena Stoian and Victor Stoica


Hepatocellular carcinoma (HCC), the third leading cause of cancer deaths worldwide, with incidence rising is expected to increase by another 81% by the year 2020, primarily due to the hepatitis C epidemic. The strongest risk factors for the development of HCC is a hepatitis B (HBV) and hepatitis C (HCV) virus infection, as well as cirrhosis of any cause. Other risk factors that have been reported include exposure to aflatoxin, alcohol, tobacco, obesity and diabetes. To detect potentially curable cases of hepatocellular carcinoma, outpatients with chronic liver disease who have been seen at the Dr. Ion Cantacuzino Hospital, since 10 years and examined periodically with real-time ultrasonography and measurement of serum alpha-fetoprotein.We analyzed the data on these patients for risk factors for hepatocellular carcinoma.

The risk of liver cancer in men was 1.33 times higher than in women; patients in their 60s had significantly higher rate ratios (6.46) than patients in their 40s; patients with liver cirrhosis diagnosed at enrollment had significantly higher rate ratios for liver cancer (1.93) than patients with chronic hepatitis. The high serum alpha-fetoprotein level at enrollment was also confirmed as a significant marker for a high risk, regardless of the stage of disease (chronic hepatitis or liver cirrhosis). The serum markers for hepatitis virus -- HBsAg, and anti-HCV - were significantly associated with the risk of liver cancer: the adjusted rate ratios for HBsAg, anti-HBc, and anti-HCV were estimated to be 6.92, 4.54, and 4.09, respectively. Hepatitis B surface antigen (rate ratio 6,92; 95% CI: 2.92 to 16.39) and hepatitis C antibody (rate ratio 4.09; 95% CI: 1.30 to 12.85) showed the most risk for carcinoma.

Further studies are required to clarify the roles of other risk factors, including drinking and smoking habits.

Open access

Cristina Buhoara and Mircea Penescu


Rapidly progressive glomerulonephritides are relatively rare but serious disorders of diverse etiology, which share some clinical features: rapid evolution, progressive to renal failure, often accompanied by oliguria or anuria. They are characterized histopathologically by an intense extracapillary proliferation, with the development of crescents (semilunar lesions) in over 50% of examined glomeruli. The following pathological entities are referred to as rapidly progressive glomerulonephritides: ANCA-positive pauci-immune vasculitides (microscopic polyangiitis, granulomatosis associated with microscopic polyangiitis, allergic granulomatosis associated with microscopic polyangiitis), extracapillary proliferative glomerulonephritides by immune complexes and glomerulonephritides by anti-glomerular basement membrane antibodies. Due to major histopathological and functional complications, their evolution to death or renal replacement therapy occurs within 6-2 months after the diagnosis, if they are not treated, but the evolution is favorably influenced by aggressive immunosuppression, whether or not associated with plasmapheresis.

Open access

Kenéz Emese-Katalin, Balló István, Gáspár Enikő and Biró Anna Julianna


Primary biliary cirrhosis is an autoimmune liver disease, characterized by the progressive destruction of the small intrahepatic bile duct epithelial cells and the presence of antimithocondrial antibodies (AMA). Ankylosing spondilitis is a systemic, inflammatory, progressive disease, which usually affects the joints of the spine and the sacroiliac joints. The association of these two is very rare, in literature we found only one single study published in 1994, which describes the occurrence of primary biliary cirrhosis accompanying ankylosing spondylitis in amale patient. The aim of our study is to present the case of our patient, who had ankylosing spondylitis and has developed primary biliary cirrhosis. Our patient has ankylosing spondylitis with peripheral joint involvement, so according to the guidelines we initiated treatment with Sulfasalazine. We know from the literature about the hepatotoxicity of Sulfasalazine in some cases, so within each follow-up examination we monitored the liver function tests, and we also performed complete blood counts. The treatment of ankylosing spondylitis is challenging in this case due to the hepatotoxicity of the medications. Besides Sulfasalazine, our patient continued the treatment for primary biliary cirrhosis (ursodeoxycholic acid with hepatoprotective drugs in higher doses).

Open access

Adina Cociorvei and Mădălina Ababei


Giant cell arteritis (GCA), or temporal arteritis, is the most common systemic vasculitis, and the greatest risk factor for developing GCA is aging. The disease almost never occurs before age 50, and its incidence rises steadily thereafter, peaking between ages 70 to 79, the risk of development being two times higher in women.

Polymialgia rheumatica (PMR) is an inflammatory rheumatic condition characterized clinically by aching and morning stiffness at the shoulders, hip girdle, and neck. PMR is almost exclusively a disease of adults over the age of 50, with a prevalence that increases progressively with advancing age. The peak incidence of PMR occurs between ages 70 and 80, the same as in the case ofGCA. PMRis 2-3 times more common in women than in men.

PMR is two to three times more common than GCA and occurs in about 50% of patients with GCA. The percentage of patients with PMR who experience GCA at some point varies widely in reported series ranging from 5 to 30 percent. PMR can precede, accompany or follow GCA. The diagnostic in the case of PMR is made first of all on clinical features, in the patients in whom another disease to explain the findings is not present. For GCA we must follow the diagnostic algorithm presented below (figure 1) and keep in mind that a negative result for temporal artery biopsy does not exclude the diagnostic if clinical suspicion of GCA is high

We present the case of a 81 year-old male with signs and symptoms from both conditions, PMR and GCA.

Open access

Taraneh Faghihi Langroudi, Habib Haybar, Saeed Alipour Parsa, Mohamad Mahjoorian, Isa Khaheshi and Mohammadreza Naderian


Background. It is now suggested an association between non-alcoholic fatty liver disease (NAFLD) and the occurrence of coronary artery disease even in non-diabetic patients. We will determine the rate of NAFLD and its main determinants in non-diabetic patients undergoing coronary angiography.

Methods. This cross-sectional study was accomplished on 264 patients who were candidates for coronary angiography during the year 2016. Coronary angiography has been done to depict the presence or absence of coronary involvement, and the severity of coronary artery disease by determining the number of vessels involved and also the SYNTAX score. During 48 hours after coronary angiography, the patients underwent abdominal ultrasonography for detection of NAFLD.

Results. The overall prevalence of NAFLD in the patients was 72.3%. The prevalence of NAFLD in those with and without coronary involvement was 71.9% and 73.1% respectively, with no notable difference (p = 0.837). The mean SYNTAX score in the patients with and without NAFLD was 22.32 ± 11.10 and 21.75 ± 10.71 respectively with no difference (p = 0.702). According to the multivariable regression models, the presence of NAFLD could not predict the likelihood of coronary artery disease (OR = 0.879, p = 0.669) or its severity assessed by the SYNTAX score (beta = 0.046, p = 0.456). NAFLD grade was also not a determinant for coronary artery disease (OR = 1.139, p = 0.178) or its severity (beta = 0.058, p = 0.165).

Conclusion. It seems that the presence and grade of NAFLD may not be correlated with atherosclerotic involvement of coronary arteries and its severity in non-diabetic patients. Future large studies and trials could elucidate the independent role of fatty liver in nondiabetic non-alcoholic patients.

Open access

Paula Ionilă, Ruxandra Jurcuţ, Nicoleta Ferariu, Monica Roşca, Monica Chivulescu, Adriana Mursă, Sebastian Militaru, Alin A. Ionescu, Cristina Căldăraru, Ana G. Fruntelată, Silvia F. Goanţă, Simina Crişan, Adina Ionac, Ana-Maria Avram, Attila Frigy, Radu Sascău, Cătălina Arsenescu-Georgescu, Ioan M. Coman, Bogdan A. Popescu, Carmen Ginghină and Eduard Apetrei


Introduction. Hypertrophic cardiomyopathy (HCM) is a disease with increased left ventricular (LV) wall thickness not solely explained by abnormal loading conditions, with great heterogeneity regarding clinical expression and prognosis. The aim of the present study was to collect data on HCM patients from different centres across the country, in order to assess the general characteristics and therapeutic choices in this population.

Methods. Between December 2014 and April 2017, 210 patients from 11 Romanian Cardiology centres were enrolled in the National Registry of HCM. All patients had to fulfil the diagnosis criteria for HCM according to the European Society of Cardiology guidelines. Clinical, electrocardiographic, imaging and therapeutic characteristics were included in a predesigned online file.

Results. Median age at enrolment was 55 ± 15 years with male predominance (60%). 43.6% of the patients had obstructive HCM, 50% non-obstructive HCM, while 6.4% had an apical pattern. Maximal wall thickness was 20.3 ± 4.8 mm (limits 15-37 mm) while LV ejection fraction was 60 ± 8%. Heart failure symptoms dominated the clinical picture, mainly NYHA functional class II (51.4%). Most frequent arrhythmias were atrial fibrillation (28.1%) and non-sustained ventricular tachycardia (19.9%). Mean sudden cardiac death risk score (SCD-RS) was 3.0 ± 2.3%, with 10.4% of the patients with high risk of SCD. However, only 5.7% received an ICD. Patients were mainly treated with beta-blockers (72.9%), diuretics (28.1%) and oral anticoagulants (28.6%). Invasive treatment of LVOT obstruction was performed in a small number of patients: 22 received myomectomy and 13 septal ablation. Cardiac magnetic resonance was reported in only 14 patients (6.6%).

Conclusions. The Romanian registry of HCM illustrates patient characteristics at a national level as well as the gaps in management which need improvement – accessibility to high-end diagnostic tests and invasive methods of treatment.

Open access

Romeo-Gabriel Mihăilă


Introduction. Our research strategy was aimed at evaluating the possible implication of the type of factor VIII product administered as substitution treatment to haemophilia A patients in the occurrence of inhibitors and their consequences on the management.

Methods. Scientific articles from July 2015 to July 2017 were searched using the PubMed and PubMed Central databases. The used search terms included “haemophilia A”, “inhibitors”, “plasma-derived factor VIII” and “recombinant factor VIII”.

Results. The risk factors for inhibitors occurrence may be patients-related (genetic and nongenetic) and treatment-related. The possibility of a correlation between the increased purity of factor VIII given as substitution treatment and the occurrence of inhibitors is discussed in the light of literature data. Plasma-derived factor VIII is less immunogenic, but not entirely safe from the point of view of the possibility of transmitting biological agents. It is obvious that there is not enough plasma-derived factor VIII for the planet’s needs. Recombinant factor VIII products have revolutionized the treatment of patients with haemophilia A over the past 3 decades by the disappearance of transfusion-related infections and their complications. They are safer in terms of pathogens and the new long-acting factor VIII products are based on recombinant DNA technology.

Conclusion. Plasma-derived or recombinant factor VIII products must co-exist on the market for the benefit of haemophilic patients. Future solutions could be: less immunogenic factor VIII products, nonfactor replacement strategies, or bispecific antibody that mimics the function of coagulation factor VIII.

Open access

Theodor Alexandru Voiosu, Andrada Viorela Gheorghe, Dan Adrian Bobeica, Andrei Mihai Voiosu and Radu Bogdan Mateescu


Tracheoesophageal fistula (TEF) is frequently congenital and requires surgical correction. TEF can also occur secondary to malignant esophageal tumors or benign diseases and these cases are managed by endoscopic means, such as closing the defect with metallic stents. Although esophageal injury can occur secondary to nonsteroidal anti-inflammatory drugs (NSAIDs), TEF secondary to chronic NSAIDs use has not been described in the literature.

We report the case of a male patient with refractory migraine and chronic use of NSAIDs, with a history of esophageal stenosis presenting with acute-onset total dysphagia. Upper gastrointestinal endoscopy and CT-scan revealed TEF located at 25 cm from the incisors. An esophageal stent was placed endoscopically, and 6 weeks a second stent was placed in a stent-in-stent manner to allow removal of both stents. Endoscopic control after the removal of the stents showed the persistence of the fistula, so a third stent was placed as a rescue therapy.

Against medical advice, the patient continued to use OTC painkillers and NSAIDs in large doses. Three months later, he was readmitted with total dysphagia and recent-onset dysphonia. CT scan revealed a new fistula above the already placed stent. A second metallic stent was endoscopically placed through the old stent to close the newly developed fistula. The patient was discharged on the third day with no complications and he remains well at 6 months follow-up.

Due to small cases studies, recurrent TEF remains a therapeutic challenge. Endoscopic therapy is usually an effective solution, but complex cases might require multiple treatment sessions.

Open access

Elisna Syahruddin, Aida Lufti Huswatun, Ari Prabowo, Jamal Zaini, Fariz Nurwidya, Achmad Hudoyo and Anwar Jusuf


Introduction. Combinations of gefitinib and radiotherapy have been observed to have synergistic and anti-proliferative effects on lung cancer in vitro. In the clinical setting, patients who presented with respiratory difficulties such as superior vena cava syndrome (SVCS), radiotherapy should be given immediately to address the emergency while waiting for the results of epidermal growth factor receptor (EGFR) mutation test. However, there has been no study that described the role of radio-therapy in Indonesian patients with EGFR-mutant lung adenocarcinoma.

Methods. This preliminary study aimed to evaluate the efficacy and toxicities of gefitinib and radiotherapy combination in lung adenocarcinoma patients in Persahabatan National Respiratory Referral Hospital, Jakarta, Indonesia. Subjects were consecutively recruited between January 2013 and December 2016.

Results. Thirty-one lung adenocarcinoma with EGFR mutations were enrolled. Most of them were male (51.61%) with a median age of 54.5 years old (range 38-70 years old). EGFR mutation characteristics were on exon 21 L858R point mutation (61.30%), exon 21 L861Q point mutation (16.12%) and exon 19 deletion (22.58%). Radiotherapy was given at doses between 30-60 Gy. Among these subjects, median progression-free survival (PFS) was 185 days (95%CI; 123.69 – 246.30), 1-year survival rate (1-yr) was 45.2%, and median overall survival (OS) was 300 days (95%CI; 130.94 – 469.06). There were no grade 3/4 hematological and nonhematological toxicities recorded. The most frequent grade 1 and 2 non-hematological toxicities were skin rash, diarrhea, and paronychia that might be related to tyrosine kinase inhibitor (TKI).

Conclusion. The combination of TKI with radiation may be considered in EGFR-mutant lung adenocarcinoma subjects.