How confocal laser endomicroscopy can help us in diagnosing gastric lymphomas?

Primary gastric diffuse large cell lymphoma is one of the most common extranodal lymphomas of the gastrointestinal system. Diagnosing gastrointestinal lymphomas can be difficult, since there is no pathognomonic sign in endoscopy to distinguish it from other malignancies. In some cases biopsy can be non-diagnostic. Therefore, multiple endoscopic examinations and biopsies can be necessary. With using confocal endomicroscopy, histology of the tissue can be seen in vivo and a range of diseases can be identified by using this technique. We are presenting a case, which is diagnosed as primary gastric diffuse large cell lymphoma during the evaluation of erythema nodosum etiology. We want to emphasize the role of confocal laser endomicroscopy for in vivo diagnosis of gastric lymphoma and directing the endoscopist for sampling the diseased mucosa. Confocal endomicroscopy decreases non-diagnostic rates in endoscopic biopsy and can be performed successfully in cases of gastric lymphoma. Pit patterns of gastric lymphoma, ring cell gastric carcinoma and gastric adenocarcinoma are similar. To best of our knowledge, this case is the fifth case of confocal laser endomicroscopy aided in diagnosing gastric lymphomas (Tab. 1, Fig. 2, Ref. 13).

Prevalence of root dilacerations in Central Anatolian Turkish dental patients / Prevalencia de las dilaceraciones radiculares en pacientes dentales turcos de la región de Anatolia Central

OBJECTIVE: The aim of this study was to determine, retrospectively, the prevalence and distribution of the dilaceration of the root for each tooth-type in a sample of Central Anatolian Turkish population by using panoramic radiographs. METHOD: Panoramic radiograhs of 6912 patients (3860 women and 3052 men, mean age 29.04 years, range, 15 to 50 years) were examined for the presence of root dilacerations. Chi-square test was also used to compare the prevalence of dilacerations between male and female subjects and upper and lower jaws. RESULTS: Data showed that 1108 (16.0%) of these subjects had one or more teeth that were dilacerated and these were detected in 466 (15.2%) males and 642 (16.6%) females. Statistical analysis (χ² test) showed a significant difference in the prevalence of dilaceration among male and female patients. Mandibular third molars were dilacerated most often (3.76%), followed by mandibular second molars (1.81%). Dilaceration was found in 1.23% of maxillary second premolars and 1.23% of mandibular second molars. CONCLUSION: Root dilacerations are not uncommon among Turkish dental patients, and their early detection could be important in treatment problems associated with it. However, further larger scale studies are required to assess its prevalence in the general population in order to compare it with other ethnic groups.

OBJETIVO: El objetivo de este estudio fue determinar retrospectivamente la prevalencia y distribución de la dilaceración radicular para cada tipo de diente en una muestra poblacional turca de Anatolia Central, usando radiografías panorámicas. MÉTODO: Se examinaron las radiografías panorámicas de 6912 pacientes (3860 mujeres y 3052 hombres, edad promedio 29.04 años, rango 15 a 50 años) en busca de presencia de dilaceraciones de la raíz. También se usó la prueba de Chi-cuadrado para comparar la prevalencia de dilaceraciones entre los sujetos varones y hembras, y la mandíbula inferior y superior. RESULTADOS: Los datos mostraron que 1108 (16.0%) de estos sujetos tenían uno o más dientes dilacerados, detectados en 466 (15.2%) varones y 642 (16.6%) hembras. El análisis estadístico (prueba χ²) mostró una diferencia significativa en la prevalencia de dilaceración entre los pacientes varones y las hembras. Los terceros molares mandibulares se hallaban dilacerados con mayor frecuencia (3.76%), seguidos por los segundos molares mandibulares (1.81%). Se halló dilaceración en 1.23% de los segundos premolares maxilares y 1.23% de los segundos molares mandibulares. CONCLUSIÓN: Las dilaceraciones radiculares no son poco comunes entre los pacientes dentales turcos, y su detección temprana podría ser importante en el tratamiento de problemas asociados con ellas.

Abdominal tuberculosis leading to portal vein thrombosis, mimicking peritoneal carcinomatosis and liver cirrhosis.

Abdominal tuberculosis is a rare infectious disease that can involve the peritoneum and lead to portal vein thrombosis and mimic peritoneal carcinomatosis. We report on a 43-year-old male patient with fatigue and progressive weight loss for two years. Ascites was the only pathologic finding in his physical examination and laboratory findings revealed only a mild anaemia with Ca-125 elevation. The ascitic fluid Adenosine deaminase (ADA) level was also elevated. Computed tomography revealed splenomegaly, a mesenteric mass measuring 3.5 cm and intra-abdominal lymphadenopathies at the hepatic hilum. Oesophagogastroduodenoscopy (EGD) revealed oesophageal varices which was also consistent with portal hypertension. Diagnostic laparotomy and biopsies obtained from the omentum and the lymph nodes revealed acid-fast staining tuberculosis bacilli.

Prevalence of root dilacerations in Central Anatolian Turkish dental patients.

OBJECTIVE: The aim of this study was to determine, retrospectively, the prevalence and distribution of the dilaceration of the root for each tooth-type in a sample of Central Anatolian Turkish population by using panoramic radiographs. METHOD: Panoramic radiograhs of 6912 patients (3860 women and 3052 men, mean age 29.04 years, range, 15 to 50 years) were examined for the presence of root dilacerations. Chi-square test was also used to compare the prevalence of dilacerations between male and female subjects and upper and lower jaws. RESULTS: Data showed that 1108 (16.0%) of these subjects had one or more teeth that were dilacerated and these were detected in 466 (15.2%) males and 642 (16.6%) females. Statistical analysis (chi2 test) showed a significant difference in the prevalence of dilaceration among male and female patients. Mandibular third molars were dilacerated most often (3.76%), followed by mandibular second molars (1.81%). Dilaceration was found in 1.23% of maxillary second premolars and 1.23% of mandibular second molars. CONCLUSION: Root dilacerations are not uncommon among Turkish dental patients, and their early detection could be important in treatment problems associated with it. However further larger scale studies are required to assess its prevalence in the general population in order to compare it with other ethnic groups.

Infection with Fasciola hepatica.

Fascioliasis, caused by the liver fluke Fasciola hepatica, is an infection that occurs worldwide, although humans are accidental hosts. F. hepatica infection comprises two stages, hepatic and biliary, with different signs and symptoms. Stool examination and ELISA can be used for the initial diagnosis. Radiographic techniques, such as computerised tomography and ultrasonography, as well as magnetic resonance imaging, are used widely for confirmation and follow-up of the disease. Invasive techniques, such as percutaneous cholangiography, endoscopic retrograde cholangiography and liver biopsy, may aid in the diagnosis but are not essential. Triclabendazole is recommended as the first-line agent for the treatment of F. hepatica infection, with bithionol as an alternative.

The importance of serial measurements of cytokine levels for the evaluation of their role in pathogenesis in familial Mediterraean fever.

Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterized by recurrent fever of unknown origin, renal amyloidosis, peritonitis, pleuritis and/or synovitis. There have been many studies to elucidate the etiopathogenesis of FMF. IL-6 is a cytokine that can induce the formation of serum amyloid A and C-reactive protein, both of which are important in development of amyloidosis. IL-6 was determined to be strongly associated in the etiopathogenesis of periodic fever in Chinese-pei dogs. The dogs with this syndrome experience periodic fever, arthritis, renal amyloidosis, a clinical picture very alike of human FMF. Here, we aimed to study mainly whether IL-6 had a similar etiopathogenetic role in human FMF as in Chinese-pei dogs syndrome. The median IL-6 blood levels were found to be higher in patients with acute (n=8) FMF attack (1.85 U/ml) compared to those (n=33) with asymptomatic ones (1.0 U/ml) (p=0.16). There are mainly two results: first; the study should be designed with a larger sample size of patients with acute attack in order to alleviate underestimation of significance, second; sampling time may give various results because of dynamic changes of cytokine levels during acute attack period.

Two common genetic thrombotic risk factors: factor V Leiden and prothrombin G20210A in adult Turkish patients with thrombosis.

The prevalence of genetic risk factors for thrombosis varies greatly in different parts of the world, both in patients with thrombosis and in the general population. Factor V Leiden (FVL) and prothrombin G20210A (PT G20210A) mutations are the most common genetic defects leading to thrombosis. We have previously reported that those two thrombotic risk alleles are frequently found in Turkish children with thrombosis. The aim of the present study was to investigate the frequency of FVL and PT G20210A and their clinical manifestations in adult Turkish patients with thrombosis. Between January 1997 and February 2000, 146 patients with documented thrombosis were investigated in our center for the presence of the FVL and PT G20210A mutations. Forty-five of 146 patients with thrombosis (30.8%) were detected to have FVL mutation. Among those cases with the FVL mutation, seven (4.8%) had homozygote and 38 (26%) had heterozygote mutation. The PT G20210A mutation was detected in 10 of the 146 patients with thrombosis (6.8%). Another six cases (4.1%) had both FVL and PT G20210A mutations. The overall frequency of these two common risk alleles in our adult population with thrombosis was 41.6%. Our findings reveal that FVL and PT G20210A mutations are significant genetic risk factors contributing to the pathophysiology of thrombosis in the Turkish population.

Antiphospholipid syndrome presenting as portopulmonary hypertension.

The association of pulmonary hypertension with portal hypertension, also called portopulmonary hypertension, is a well-described condition. The pathogenesis of this association remains unclear. We describe a 34-year-old female patient with "primary antiphospholipid syndrome" and portopulmonary hypertension. Our finding supports that in situ microthrombosis associated with the presence of anticardiolipin antibodies could be the pathophysiologic explanation for both portal and pulmonary hypertension.

Disappearance of "pseudocholangiocarcinoma sign" in a patient with portal hypertension due to complete thrombosis of left portal vein and main portal vein web after web dilatation and transjugular intrahepatic portosystemic shunt.

The main portal vein web is probably a consequence of portal vein thrombosis, which is a very rare cause of portal hypertension. Principal manifestations are related to the degree of portal hypertension. In the literature, no data has been found for the treatment modality of portal vein web. We report, herein, the clinical and laboratory findings of a 38-year-old woman with angiographically proven incomplete main portal vein web and complete thrombotic occlusion of the left portal vein causing pseudocholangiocarcinoma sign (PCCS) on the common bile duct. She was treated by transjugular intrahepatic portosystemic shunt (TIPS) and membrane dilatation, which resulted in complete disappearance of collaterals and PCCS. It appears that TIPS and balloon dilatation of the portal vein web via transjugular approach was effective in decreasing portal pressure and its consequences.

Gastrointestinal manifestations of Behcet's disease.

Behcet's disease (BD) is a multisystem, chronic, relapsing vasculitis of unknown origin that affects nearly all organs and systems. While recurrent oral ulcerations are a "sine qua non" of BD, the frequency of extra-oral parts of the gastrointestinal involvement varies widely in different countries. The most frequent extra-oral sites of gastrointestinal involvement are the ileocecal region and the colon. The liver (except with Budd-Chiari syndrome), pancreas, and spleen are rarely involved. The symptoms associated with these extra-oral manifestations of BD are abdominal pain, nausea, vomiting, diarrhea with or without blood, and constipation. The lesions typically are resistant to medical treatment and frequently recur with surgical treatment. We review the literature regarding the gastrointestinal and hepatobiliary systems in BD. Also, we present a patient who had BD complicated with radiologically-proven hepatic veins involvement (Budd-Chiari syndrome) and complete occlusion of hepatic portion of inferior vena cava and who had a good response to colchicine and penicillin treatment.

A prospective randomized trial from Turkey comparing octreotide versus injection sclerotherapy in acute variceal bleeding.

BACKGROUNDS/AIMS: Bleeding from gastroesophageal varices continues to be a life threatening complication of chronic liver diseases and portal hypertension. The purpose of this randomized prospective study is to compare the efficacy of octreotide administration and emergency injection sclerotherapy for the control of actively bleeding esophageal varices and prevention of early rebleeding in patients with cirrhosis. METHODOLOGY: A total of 66 episodes of endoscopically proven active variceal bleeding in 52 patients were included in this study. Following admission to the hospital, the patients were resuscitated with blood and plasma, and fiberoptic endoscopy was performed within 2 hours. Thirty-six bleeds in 28 patients and 30 bleeds in 24 patients were randomized to endoscopic variceal sclerotherapy (1% polidocanol) and to octreotide infusion (at 50 micrograms/h for 12 hours following the initial 50 micrograms i.v. bolus), respectively. RESULTS: Bleeding was initially controlled within 6 hours in 75% of episodes by endoscopic variceal sclerotherapy and in 73.3 by octreotide infusion (P > 0.05). There were no significant differences between the 2 groups in early rebleeding (within 72 hours of randomization) (22% vs. 22.7%), blood transfusion (4.2 +/- 1.8 units vs. 4.8 +/- 2.9 units), or hospital mortality (3.6% vs. 3.3%). Treatment failed in 9 episodes (25%) in the sclerotherapy group and in 8 episodes (26.7%) in the octreotide group. CONCLUSIONS: We consider that Octreotide would appear to be as effective as sclerotherapy in both the early control of variceal hemorrhage and in the prevention of early recurrent bleeding and should therefore be considered the treatment of choice in those centers where 24-hour endoscopy is not available. Furthermore, even in hospitals that do have a 24-hour endoscopy service there is good evidence that octreotide therapy should be commenced as soon as a patient enters hospital with a suspected variceal bleed to achieve rapid homeostasis. When initial hemostasis is achieved, elective endoscopic therapies can be undertaken with greater success.

The role of natural anticoagulant deficiencies and factor V Leiden in the development of idiopathic portal vein thrombosis.

One of the causes of portal hypertension is portal vein thrombosis (PVT). The aim of this study was to determine whether natural anticoagulant deficiencies, activated protein C resistance (APCR), and factor V Leiden play a role in the development of PVT, leading to cavernous transformation of the portal vein (CTPV). Twenty-three patients with idiopathic CTPV (group 1) seen at Hacettepe University Hospital during the past 12 years were identified and prospectively studied. These 23 patients underwent a detailed hematological evaluation including measurement of protein S, protein C, antithrombin III, activated protein C resistance (APCR), and factor V Leiden gene mutation. Additionally, all patients were tested for anticardiolipin antibodies (ACA), IgG, IgM, and lupus anticoagulant (LA). Natural anticoagulants and APCR were measured using available commercial kits, and factor V Leiden mutation (R506Q) was detected by Mnl I digestion of an amplified factor V DNA fragment. All parameters were measured at least 6 months after the diagnosis of CTPV was established. No patient was on anticoagulant or antiaggregant treatment while tested. The findings in these 23 patients were compared with those in 20 healthy control subjects (group 2), in whom all tests mentioned above were also performed. In 23 patients (group 1), who had no recognizable factor for portal vein thrombosis, considerably natural anticoagulant deficiencies and factor V Leiden mutation positivity were found when we compare them to those healthy controls (group 2). The protein C levels of six patients (26%), the protein S levels of 10 patients (43.5%), and the antithrombin III levels of five patients (26%) were lower than in control subjects. Two patients were found to have combined protein S and antithrombin III deficiency, and one had combined protein S and C deficiency and APCR. APCR was detected in seven of the 23 patients, and six of these seven patients were found to have R506Q factor V Leiden mutations. In group 1, ACA IgG levels were higher in four patients (17%) and ACA IgM level was higher in one (4%) compared with the control group. LA was positive in only one patient in group 1. Natural anticoagulant deficiencies and factor V Leiden mutation are strongly associated with PVT. The natural anticoagulant deficiencies and APCR (almost totally caused by R506Q mutation) produce a favorable medium for thrombus generation. PVT seems to be related to the natural anticoagulant deficiencies and factor V Leiden R506Q mutation. A combination of these defects increases the incidence of PVT and these factors should be evaluated carefully in patients with idiopathic CTPV.

Four cases with chronic intestinal pseudo-obstruction due to hollow visceral myopathy.

BACKGROUND/AIMS: Chronic intestinal pseudo-obstruction is a rare clinical syndrome characterized by symptoms and signs of intestinal obstruction without any organic lesion obstructing the intestine. Visceral myopathy is one of the etiological causes and full thickness intestinal biopsy is essential for reaching a diagnosis. In this article we describe 4 cases of hollow visceral myopathy; our aim is to stress the importance of full thickness biopsy. METHODOLOGY: Four cases of hollow visceral myopathy are studied herein. All the patients had recurrent abdominal pain and constipation. The onset of symptoms was early in life or in the second to third decade. A diagnosis was established in all cases by full thickness intestinal biopsy obtained during laparotomy. Associated disorders were noted in 2 cases. One patient had Axenfelt syndrome, non-descended testicles and primary hypogonadism, and another had a diagnosis of Kleinfelter syndrome. RESULTS: All of the 4 cases were diagnosed to be suffering from hollow visceral myopathy by full thickness intestinal biopsy and 2 had additional disorders as well. CONCLUSIONS: Patients with chronic intestinal pseudo-obstruction should be carefully evaluated as to whether there is an associated disorder and the diagnosis may be delayed unless full thickness intestinal biopsy is obtained.

Arterial thrombosis leading to intestinal infarction in a patient with Behçet's disease associated with protein C deficiency.

Behçet's disease may be a possible cause of both occlusive and aneurysmal arterial involvement as well as recurrent venous thrombosis. A case of Behçet's disease complicated with vascular involvement leading to intestinal infarction is presented. A 41-yr-old man suffering from Behçet's disease for 15 yr presented with a 2-day history of severe abdominal pain and bloody diarrhea. Intestinal infarction secondary to thrombosis of the superior mesenteric artery had been diagnosed during surgical exploration 3 yr previously. He was started on anticoagulation with nutritional support. The patient was readmitted with severe diarrhea and malabsorption symptoms 3 yr after intestinal resection. A thrombus located in the posterior wall of the infrarenal portion of aorta was detected by aortography and ultrasonography. Although thrombosis is a relatively common complication of Behçet's disease caused by vasculitis, protein C deficiency, which is a pertinent laboratory finding in this case, might be a secondary factor in the thrombotic event. This is the first case reported of mesenteric artery thrombosis leading to bowel infarction and abdominal aorta thrombosis associated with protein C deficiency.

Does hepatic vein outflow obstruction contribute to the pathogenesis of hepatocellular carcinoma?

Hepatocellular carcinoma (HCC) is one of the more common malignant diseases in the world. Here we have investigated role of hepatic venous outflow obstruction in the development of HCC. During a 10-year period from November 1986 to December 1996, 1,748 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction, or inferior vena cava obstruction without Behçet's disease (BD) and 512 patients with Behçet's disease were examined at Hacettepe University Hospital. The presence of and the effect of hepatic venous obstruction on the subsequent development of HCC was assessed. In each case, hepatic vein thrombosis was assessed by hepatic venography and by digital subtraction angiography (DSA), computed tomography (CT), ultrasonography (US), and liver biopsy. Coagulation factors, including protein C, protein S, anti-thrombin III, and routine laboratory studies assessing the coagulability of blood were also investigated. The role of hepatic venous outflow obstruction on the subsequent development of HCC was determined by periodic laboratory investigations that included alpha-fetoprotein (AFP), ultrasonography, and when indicated liver biopsy. During the same time period all patients diagnosed as having HCC were investigated to identify all potential etiologic factors responsible for the HCC. Fifty-five (10.7%) of the 512 patients with BD were found to have one or more large vein thromboses. Sixteen of these 55 (29%) patients had hepatic vein thrombosis. During the follow-up period HCC developed in 2 of these 16 patients (12.5%), 34 and 21 months after a diagnosis of hepatic vein thrombosis was established. Forty patients from a total of 1,748 patients with clinical evidence of portal hypertension and cirrhosis, but without BD, were found to have evidence of hepatic vein thrombosis. Twenty-one of these 40 patients had an identifiable underlying disorder responsible for their hepatic vein thrombosis. Despite a full clinical and laboratory investigation in the other 19 patients, the etiologic factor responsible for the hepatic vein thrombosis remained obscure. Only one of these 19 patients, who also had portal vein thrombosis, developed HCC during a 9-year follow-up. Thus, a total of three of the 56 (5.36%) of cases of hepatic vein thrombosis developed an HCC. All of the hepatic tumors were of the multicentric, nodular, rapidly growing type. Despite the presence of hepatic vein thrombosis, there was no clear-cut histologic evidence for cirrhosis. Our experience suggests that hepatic vein thrombosis may be a contributing factor responsible for HCC development. Moreover, we advise that individuals with hepatic vein thrombosis should be assessed periodically for the development of HCC.

Superior vena cava thrombosis and obstructive sleep apnea in a patient with familial Mediterranean fever.

Familial Mediterranean fever (FMF), a paroxysmal, self-limited, inflammatory disease of unknown etiology, may result in thrombotic complications after the development of nephrotic syndrome due to amyloidosis. It has been suggested that there is increased thrombogenic activity in the blood of patients with FMF who did not develop nephrotic syndrome. We describe a patient with FMF who presented with thrombosis in the superior vena cava (SVC) in the absence of nephrotic syndrome, and discuss the contributory role of increased procoagulant activity detected in this disorder. Moreover, the patient was proved to have obstructive sleep apnea (OSA) which we believe was secondary to SVC thrombosis that lead to soft tissue edema in the upper airways. To our knowledge, this is the second reported case in the literature in which OSA occurred secondary to the SVC thrombosis.

Determination of hepatic zinc content in chronic liver disease due to hepatitis B virus.

BACKGROUND/AIMS: Zinc is an essential, mostly intracellular, trace element which participates in many physiologic mechanisms. Some liver functions like urea formation require the presence of zinc; thus the determination of hepatic zinc content may contribute to the understanding of probable zinc-related clinical consequences of chronic liver disease. In this study, we aimed to determine the hepatic zinc concentrations in patients with chronic liver disease due to the Hepatitis B virus and to ascertain the relationship between the severity of liver disease and hepatic zinc content, if one in fact exists. METHODOLOGY: A total of 99 HBsAg positive subjects were included in the study. We performed a liver biopsy on all subjects. Hepatic zinc concentrations were determined by atomic absorption spectrophotometry. RESULTS: The liver biopsies were normal in 25 subjects. There were 33 chronic active hepatitis (CAH), 34 cirrhosis and 7 chronic persistent hepatitis (CPH) patients in the study group. In the control group, CAH, cirrhosis and CPH groups, the mean liver zinc concentrations were 3.83 +/- 1.86, 1.86 +/- 0.92, 1.14 +/- 0.68 and 3.74 +/- 1.81 mumol/g dry weight, respectively. Hepatic zinc in the CAH and cirrhosis groups were lower than that of the control group (p < 0.05). We also found that liver zinc in the cirrhosis group was lower than in the CAH group (p < 0.05). CONCLUSION: According to these results, as the severity of liver damage increases, the hepatic zinc concentration decreases. Therefore, it can be suggested that zinc supplementation may improve hepatic encephalopathy by increasing the efficiency of the urea cycle.