Acute pancreatitis due to hypertriglyceridemia: Plasmapheresis versus medical treatment.

OBJECTIVE: Hypertriglyceridemia (HTG) is the third-most common cause of acute pancreatitis. Plasmapheresis is an extracorporeal treatment method used for treatment. This study aimed to investigate the efficacy of medical treatment and plasmapheresis in patients with acute pancreatitis due to HTG. METHODS: This was a retrospective cross-sectional study. The patients were divided into two groups according to the treatment they received as those who received only medical treatment and those who performed plasmapheresis with medical treatment. According to the treatment received by the patients; clinical, demographic, and laboratory data, Ranson scores, and bedside index of severity in acute pancreatitis (BISAP) scores, decrease in triglyceride levels in 24 h, length of hospital stay, and outcomes were recorded. RESULTS: Forty-seven patients were included in the study. The level of triglyceride decreases at the 24th h was 59.7% ±17.3% in those who received medical treatment and was 70.4% ±15.1% in those who received plasmapheresis (P = 0.032). Receiver operating characteristic curve analysis was performed to predict the need for plasmapheresis treatment, area under the curve (AUC) value of the triglyceride level was the highest (AUC: 0.822, 95% confidence interval: [0.703-0.940]; P < 0.001), the sensitivity and specificity were 83.3% and 72.4%, respectively, and the cut-off value of triglyceride was accepted as 3079.5 mg/dL. CONCLUSION: Plasma triglyceride levels and BISAP score on admission may help physicians to predict the need for plasmapheresis. Plasmapheresis helps to rapidly reduce triglyceride levels in patients with HTG-associated acute pancreatitis.

Immune alterations in subacute sclerosing panencephalitis reflect an incompetent response to eliminate the measles virus.

In subacute sclerosing panencephalitis (SSPE) the persistence of measles virus (MeV) may be related to the altered immune response. In this study, cytokine responses of lymphocytes and monocytes were evaluated in SSPE compared to controls with non-inflammatory (NICON) and inflammatory (ICON) diseases. Patients with SSPE (n = 120), 78 patients with ICON and 63 patients with NICON were included in this study. Phenotypes of peripheral blood mononuclear cells (PBMC) have been analyzed by flow cytometry. CD3 and CD28, and S. aureus Cowan strain I (SAC) stimulated and unstimulated cells were cultured and IL-2, IL-10, IFN-γ, IL-12p40, IL-12p70 and IL-23 were detected in supernatants by ELISA. MeV peptides were used for MeV-specific stimulation and IFN-γ secretion of PBMC was measured by ELISPOT. Spontaneous and stimulated secretions of IL-10 were lower in SSPE compared to both control groups. T cell stimulation induced lower IFN-γ production than ICON group, but higher IL-2 than NICON group in SSPE. Stimulated PBMC produced lower IL-12p70 in SSPE and had decreased CD46 on the cell surface, suggesting the interaction with the virus. IFN-γ responses against MeV peptides were not prominent and similar to NICON patients. The immune response did not reveal an inflammatory activity to eliminate the virus in SSPE patients. Even IL-10 production was diminished implicating that the response is self-limited in controlling the disease.

Coexistence of the POEMS syndrome with hepatitis B: a rare case report.

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) is a rare multisystemic disease of unknown pathogenesis. Proinflammatory and proangiogenic cytokines play important roles in its pathogenesis. POEMS syndrome is a rare cause of ascites. Until now, the coexistence of POEMS syndrome and hepatitis B has not been reported. In this case report, we present a 48-year-old male patient who presented with malaise, fatigue, diarrhea, and abdominal swelling. Organomegaly, endocrinopathy, ascites, skin changes, and polyneuropathy were identified, and we arrived at a diagnosis of POEMS syndrome. The patient was administered methylprednisolone 64 mg/day, lamivudine 100 mg/day, calcium 1.5 g/day, and calcitriol 0.5 µg/day. The patient's clinical manifestations had moderately resolved at the follow-up visits. At the end of 6 months of follow-up, his ascites was minimally reduced, and his neurologic manifestations had not lessened. The present case shows that accurate diagnosis is required for the management of patients with coexisting POEMS syndrome and hepatitis B.

Liver hepatotoxicity associated with pantoprazole: a rare case report.

Hepatotoxicity may occasionally develop over the course of treatment with proton pump inhibitors (PPIs). Although skin reactions, interstitial nephritis, pancytopenia, anaphylaxis, and generalized edema have been reported to be associated with PPIs, hepatotoxicity associated with oral pantoprazole is very rare. In this report, we present a case of hepatotoxicity in a 35-year-old man who received pantoprazole (40 mg/day) for acute gastritis. One week after discontinuation of pantoprazole, his liver function began to improve, and the patient gradually fully recovered. Although this toxicity occurs only infrequently, pantoprazole should be considered as a rare hepatotoxic agent in the literature.

Benign glycogenic acanthosis lesions of the esophagus.

BACKGROUND/AIMS: Glycogenic acanthosis is described as benign thickening of the esophageal squamous epithelium of unknown etiology. Although its etiology is unknown, it has been reported that glycogenic acanthosis may be related to gastroesophageal reflux and hiatal hernia. The aim of the present study was to review the patients who were diagnosed with glycogenic acanthosis on upper gastrointestinal endoscopy and to determine whether there is any association between glycogenic acanthosis and gastroesophageal reflux and hiatal hernia. MATERIAL AND METHODS: A total of 504 patients who underwent upper gastrointestinal endoscopy for evaluation of non-ulcer dyspepsia were reviewed retrospectively. RESULTS: Glycogenic acanthosis was detected in 143 (28.3%) of those 504 patients. Of the 143 patients, 82 (57.3%) were male and 61 (42.7%) were female. Patients with glycogenic acanthosis were aged 20-83 years. Gastroesophageal reflux was detected in 50 (34.9%) cases with glycogenic acanthosis, while hiatal hernia was detected in 30 (20.9%) cases. Gastroesophageal reflux was detected in 102 (28.2%) control subjects, while hiatal hernia was detected in 50 (13.8%). Hiatal hernia was significantly higher in glycogenic acanthosis patients than in controls subjects (p<0.05). Glycogenic acanthosis patients had higher gastroesophageal reflux than seen in controls subjects, but the difference between groups was not statistically significant (p>0.05). CONCLUSIONS: Our results suggest that glycogenic acanthosis is primarily an age-related disease. We demonstrated that glycogenic acanthosis may be associated with gastroesophageal reflux and hiatal hernia. Further studies are necessary to confirm these findings.

A rare cause of massive ascites: familial Mediterranean fever.

Familial Mediterranean fever is an autosomal recessive disease characterized by recurrent fever and peritoneal and pleural inflammation. It is an inherited disorder commonly found in Armenians, Turks, Arabs, Balkans, and Jews originating from North African countries. A small amount of peritoneal fluid collection can be observed during peritoneal attacks in patients with Familial Mediterranean fever, but chronic ascites has been described rarely in these patients. A 42-year-old female patient was admitted to our clinic in June 2010 with fever, severe abdominal pain and abdominal distention that had continued for one month. There was no family history of periodic fevers or abdominal pain. We could not find any cause for ascites, including tuberculosis. A diagnosis of Familial Mediterranean fever was suspected based on the clinical findings and her family history. She was screened for mutations causing Familial Mediterranean fever, and when found to be homozygous for M694V, treatment with colchicine was initiated. After treatment, the amount of ascites decreased, and relief of symptoms was confirmed during a follow-up. In conclusion, because Familial Mediterranean fever is common in our country, it should be considered in the differential diagnosis of patients with ascites of unknown etiology in populations where hereditary inflammatory disease is endemic.

The effect on serum myeloperoxidase activity and oxidative status of eradication treatment in patients Helicobacter pylori infected.

OBJECTIVES: Myeloperoxidase activity has been investigated after eradication of Helicobacter pylori (H. pylori) in infected patients in previous studies but the results are controversial. The aim of this study was to investigate effect on serum myeloperoxidase activity and oxidative status of eradication treatment in H. pylori-infected patients. DESIGN AND METHODS: Gastric biopsy specimens were obtained from 30 H. pylori infected patients. Serum myeloperoxidase activity was measured by enzyme-linked immunoassay. Oxidative status was determined using total antioxidant capacity (TAC) and total oxidant status (TOS) measurement and calculation of oxidative stress index (OSI). RESULTS: After 2 weeks of the eradication treatment, serum myeloperoxidase activity, TOS and OSI values were significantly lower (all; p<0.001), while TAC was significantly higher (p<0.001). CONCLUSIONS: Our results indicate that eradication treatment in H. pylori-infected patients may affect both oxidative stress and myeloperoxidase activity which is an important biomarker in pathogenesis of atherosclerosis.