Hayretdin Koklu

Nutritional habits in functional dyspepsia and its subgroups: a comparative study

ABSTRACT Objective: Research data demonstrating nutritional habits of functional dyspepsia (FD) patients are very limited. This is the first study to evaluate nutritional habits in FD subgroups according to Rome III criteria. Our aim was to evaluate nutritional habits of FD patients and determine the food items that may provoke a dyspepsia symptom. Methods: A total of 168 adults with FD and 135 healthy control subjects participated in the study. FD subjects were divided into epigastric pain syndrome (EP-FD), postprandial distress syndrome (PS-FD), mixed (MX-FD) subgroups according to Rome Criteria III. Subjects completed a questionnaire that included a short-form food frequency questionnaire. Furthermore, subjects were asked to list the food items that were causing a dyspepsia symptom. Results: Functional dyspepsia subjects had a slightly higher BMI (26.1 ± 4.97 kg/m2) than control subjects (24.6 ± 4.08 kg/m2). The most common symptom triggering foods among all the FD groups were fried and fatty foods (27.1%), hot spices (26.4%), and carbonated drinks (21.8%). In FD subgroups, carbonated drinks were more likely to cause a symptom in PS-FD group (37.3%) than MX-FD (25.7%) and EP-FD (22.1%) groups. There was no difference in frequency of main meals and snacks among any of the groups. Conclusion: Fatty and spicy foods and carbonated drinks were the most common symptom triggering food items in FD group. In subgroups, carbonated drinks and legumes were more likely to cause a symptom in PS-FD. Removing these food items during the course of treatment might help alleviate the symptoms.

Multiple liver masses mimicking metastatic liver disease in an elderly patient

1Division of Gastroenterology, Department of Internal Medicine, Hacettepe University School of Medicine, Ankara, Turkey 2Division of Rheumatology, Department of Internal Medicine, Hacettepe University School of Medicine, Ankara, Turkey 3Department of Radiology, Hacettepe University School of Medicine, Ankara, Turkey 4Department of Nuclear Medicine, Hacettepe University School of Medicine, Ankara, Turkey 5Department of Pathology, Hacettepe University School of Medicine, Ankara, Turkey

Lamivudine Treatment Failure Risks in Chronic Hepatitis B Patients with Low Viral Load

Aim: To analyze the risk factors of lamivudine treatment failure (LTF) for the long-term use in patients with low viral load (LVL). Material and Methods: In this multicenter study, 548 antiviral naïve noncirrhotic adult patients with LVL (for HBeAg+ patients HBV DNA <109 copies/ml and for HBeAg- patients HBV DNA <107 copies/ml) were enrolled. As a control group, 46 lamivudine-initiated patients with high viral load (HVL) were included. Primary outcome was switching to or adding on another antiviral drug as a consequence of primary nonresponse, partial response, viral breakthrough or adverse events. Secondary outcomes included LTF rates at 1, 2, 3, 4 and 5 years and LTF-related viral and host factors. Results: Among 594 patients, 294 had to change lamivudine at the follow-up. Primary nonresponse, partial response, viral breakthrough or adverse events frequencies were 6.8, 1.6, 64.5 and 0.1%, respectively. Five-year LTF rates were 61.3 and 84.2% in patients with LVL and HVL, respectively. Among patients with LVL, patients with <100,000 copies/ml and ≥100,000 copies/ml had 54.8 and 67.3% LTF rates at the end of the 5th year, respectively. Logistic regression analysis of risk factors showed HBeAg+, hepatic activity index, HBV DNA, virological response at 6 months and duration of follow-up were independent predictors for LTF (p values were 0.001, 0.008, 0.003, 0.020 and 0.003, respectively). Conclusion: Similar to patients with HVL, first-line lamivudine therapy is not efficient for long-term use in patients with LVL. LTF risk is so high even in the absence of worse predictive factors.

An unusual cause of gastrointestinal bleeding in an elderly patient

QUESTION A 65-year-old male patient was referred to our clinic due to complaints of fatigue, intermittent melena, and hematochezia for 2 months. Chronic obstructive pulmonary disease, coronary heart disease, and peripheral arterial disease were noted in his medical history. The patient also had a history of aortofemoral bypass surgery during which an aortofemoral polyester vascular graft had been inserted. The surgery had been performed 2 years previously due to right common iliac artery occlusion. Laboratory test results were unremarkable except for anemia (hemoglobin: 8.7 g/dL [11.7-15.5]), leukocytosis (12.3×109/L [4.1-11.2]), and high C-reactive protein levels (24.3 mg/dL [0-0.8]). Upper gastrointestinal endoscopy was performed on the patient. The endoscopic view of the duodenum is shown in Figure 1.

An Unexpected Cause of Acute Enteritis in a Patient with Pure Red Cell Aplasia Parvovirus B19-Associated Acute Enteritis

An Unexpected Cause of Acute Enteritis in a Patient with Pure Red Cell Aplasia Parvovirus B19-Associated Acute Enteritis

Ulcerated colonic mass mimicking malignancy in an elderly patient: Letters to the Editor

was lower in PD patients than healthy controls, and replacement therapy can delay homocysteine-induced atherosclerosis, and might possess anti-oxidant and antiinflammatory activities, both dependent and independent of the hypothesized homocysteine-lowering activity. Second, as enzymatic reaction, which is dependent on vitamin B12, is the conversion of methylmalonic acid (MMA) to succinyl-CoA, vitamin B12 deficiency can cause increased serum MMA. Larnaout A et al. showed that MMA led to acute severe symmetrical basal ganglia necrosis in a post-mortem neuropathological study. Therefore, MMA also might be responsible for the development of acute parkinsonism in the present case. However, showing the reduction of dopamine transporter ligand-binding by dopamine transporter single-photon emission computed tomography or metaiodobenzylguanidine scintigraphy could be better to diagnose PD in these patients. In addition, serum vitamin B1, whose deficiency might have an affect on the development of PD, should be evaluated in such cases. In conclusion, parkinsonism and cognitive impairment might be due to vitamin B12 deficiency only. Therefore, before PD diagnosis, and levodopa treatment, clinicians should absolutely evaluate serum vitamin B12 levels, and adequate supplement therapy should be implemented in these patients.

Gastric mucosal metastasis of prostate cancer

A 65-year-old male patient who had been hospitalized in the ıntensive care unit for pneumonia presented with hematemesis and melena. He was diagnosed with metastatic adenocarcinoma of prostate (multiple bone and lung metastases), which was accompanied by diabetes mellitus, hypertension, and coronary heart disease. The hemoglobin levels decreased from 11.4 g/dL to 7.3 g/dL during follow-up. Upper endoscopy revealed widespread distribution of numerous umbilicated nodules with varying sizes (from 0.5 to 2 cm) on gastric mucosa (A, B, C). No hemostatic procedure was performed but the nodules were biopsied. The histopathological examination of the biopsy revealed infiltrative small- to medium-sized sheet-like neoplastic glands in the edematous antral mucosa that showed positive staining with prostate specific acid phosphatase (PSAP orig. mag. x200) in immunohistochemistry (D). The patient was diagnosed with gastric metastasis of prostate adenocarcinoma. He was followed-up uneventfully with red blood cell transfusions for GI bleeding. Unfortunately, he died due to septic shock and respiratory failure on the fourth week of hospitalization.

An unusual neurological complication in a patient with ulcerative colitis

A 60-year-old female was admitted to our clinic with fever, headache, weakness, and confusion. Her past medical history was unremarkable other than ulcerative colitis (UC), and she received 4 g/day mesalamine, 100 mg/day azathioprine, and 25 mg/day prednisolone on admission. Because of UC activation 1 month previously, azathioprine and prednisolone were initiated at initial doses of 50 and 40 mg/day, respectively. The prednisolone dose was decreased by 5 mg weekly, whereas the azathioprine dose was increased to 100 mg in the second week. Physical examination revealed that her body temperature was 38.4°C. She had right hemiparesis, neck stiffness, and confusion. Laboratory test results were as follows: hemoglobin level, 10.9 g/ dL (11.7–15.5 g/dL); white blood cell (WBC) count, 2×103/μL (4.1–11.2×103/μL); platelet count, 125×103/ μL (159–388×103/μL); neutrophil count, 1.7×103/μL (1.8–6.4×103/μL), and C-reactive protein level, 15.8 mg/ dL (0–0.3 mg/dL). Liver enzyme and creatinine levels were normal. Magnetic resonance imaging (MRI) findings of the patient were consistent with meningitis. Lumbar puncture was performed, and cell count of the cerebrospinal fluid (CSF) was 600/mm3 WBCs, with 40% neutrophil and abundant erythrocytes. Gram-positive rods were detected in the Gram stain of CSF. Meropenem plus ampicillin was administered to the patient for a central nervous system (CNS) infection. Azathioprine was discontinued, and the prednisolone dose was gradually reduced (5 mg/1–4 day) because of the infection. The control cranial MRI in the second week revealed a left thalamo-mesencephalic abscess (Figure 1). Listeria monocytogenes (LM) was identified in the CSF culture. Meropenem was switched to gentamicin, and gentamicin plus ampicillin was continued for 1 month. The patient clinically improved, and the control cranial MRI in the sixth week showed a marked improvement of the abscess (Figure 2). She was discharged from the hospital with continuing treatment of 4 g/day mesalamine for UC. Turk J Gastroenterol 2017; 28: 137-9

A rare cause of severe gastrointestinal bleeding in a thrombocytopenic patient with acute myeloid leukemia.

A 24-year-old female who had been diagnosed with acute myeloid leukemia (AML) 1 month prior was admitted to our clinic with acute-onset substernal chest pain, hematemesis, and melena. She had completed her second cycle of chemotherapy (Cytosine arabinoside/ idarubicin.) 2 weeks ago. Apart from AML, her past medical history was unremarkable. Her physical examination was normal, except for melena in her digital rectal examination. Laboratory test results were as follows: hemoglobin level: 7.7 g/dL (11.7–15.5 g/dL), white blood cell count: 0.2×109/L (4.1×109–11.2×109/L), platelet count: 14×109/L (159×109–388×109/L), creatinine level: 0.62 mg/dL (0.5–0.9 mg/dL), alanine transaminase level: 19 U/L (0–33 U/L), aspartate transaminase level: 25 U/L (0–31 U/L), and international normalized ratio: 0.9 (0.8–1.2). Her hemoglobin level decreased in repeated measurements, leading to the development of tachycardia and hypotension. Upper gastrointestinal endoscopy was performed after red blood cell and platelet transfusions. Endoscopy showed a double lumen in the middle portion of the esophagus separated by a mucosal bridge that was coated with a hematoma (Figure 1).

Esophageal food impaction with an unexpected meal in an elderly woman: Letters to the Editor

ener because of dysphagia resulting from a previous cerebral infarction. She was served easy-to-swallow food and drugs including MgO tablets (500 mg/day) for constipation. Two weeks after admission, follow-up plain computed tomography incidentally showed a tablet-shaped foreign body in the colon, while the size of the aortic dissection had not significantly changed (Fig. 1a). We recovered an undisintegrated, ocher-colored tablet approximately 7 mm in length in the stool (Fig. 1b). Elemental analysis under scanning electron microscopy with energy-dispersive X-ray spectrometry identified a MgO tablet (Fig. 1c–e). Food thickeners have been reported to decrease the dissolution rate and affect the laxative activity of MgO tablets in mice. Food thickeners have also been shown to potentially inhibit MgO disintegration in vitro. As the patient had no obvious gastrointestinal problems, we assume that the food thickener was responsible for the lack of disintegration of the MgO tablet. Food thickeners have been shown to delay the rate of disintegration of various other drugs, including acetaminophen, valproic acid, carbamazepine and voglibose, affecting drug pharmacokinetics in both rodents and humans. However, to the best of our knowledge, this is the first report beyond a small number of abstracts to describe precise identification of an undistintegrated tablet in a patient taking a food thickener. Such effects of food thickeners are partly attributable to the structure of the polymer matrix in polysaccharide thickeners, and also depend on the concentrations of the specific components (e.g. polysaccharide or gum). The present case, together with previous reports, suggests that clinicians should be aware that food thickeners can impede the disintegration of some drug formulations.