Hypomagnesemia Among Outpatient Long-Term Proton Pump Inhibitor Users.

Proton pump inhibitors (PPIs) are extensively prescribed drugs usually used for a long period. Recent reports linked PPI use with development of hypomagnesemia. However, there is still uncertainty regarding risk of hypomagnesemia in outpatients who were on long-term PPI use. Thus, we aimed to evaluate frequency of hypomagnesemia among a well-defined outpatient patient cohort with no other possible risk factors affecting serum magnesium levels. This was a case-control study carried out at the outpatient gastroenterology clinic of a University hospital. Patients who were on PPI therapy for at least 6 months without diuretic use and chronic kidney disease were included. Patients who were subjected to the same inclusion and exclusion criteria and not using PPI were included as control subjects. One hundred fifty-four patients and 84 control subjects were included. The mean duration of PPI use was 27.5 ± 2.5 months. Mean serum magnesium levels of PPI users and nonusers were 2.17 ± 0.20 mg/dL and 2.19 ± 0.15 mg/dL, respectively. None of the patient had a serum magnesium level below laboratory lower range of 1.7 mg/dL. Our results showed that for typical gastroenterology outpatient clinic patients with no other risk factors affecting serum magnesium levels, long-term PPI use did not affect serum magnesium levels.

Rectal or intramuscular diclofenac reduces the incidence of pancreatitis afterendoscopic retrograde cholangiopancreatography.

BACKGROUND/AIM: Acute pancreatitis is the most common adverse event of endoscopic retrograde cholangiopancreatography (ERCP). We aimed to evaluate the efficacy of intramuscular diclofenac sodium for prophylaxis of post-ERCP pancreatitis (PEP) in comparison to the rectal form. MATERIALS AND METHODS: One hundred and fifty consecutive patients who underwent ERCP were enrolled in this single-center, prospective, randomized controlled study. Patients were randomized into three groups. The first group received 75 mg of diclofenac sodium via intramuscular route and the second group received 100 mg of diclofenac sodium rectally 30-90 min before the procedure. The third group served as the control group. Patients were evaluated for post-ERCP pancreatitis with serum amylase levels and abdominal pain 24 h after the procedure. RESULTS: The overall incidence of PEP was 6% (n = 9) and 2% (n = 1) in the intramuscular (IM) and rectal groups, respectively, and 14% in the control group (P = 0.014). Nineteen (12.7%) patients developed post-ERCP abdominal pain (8% in IM, 10% in rectal, and 20% in control group; P = 0.154). Twenty-five (16.6%) patients developed post-ERCP hyperamylasemia (10% in IM, 12% in rectal, and 24% in control group; P = 0.03). CONCLUSION: Prophylaxis with diclofenac given rectally or intramuscularly is an effective option for the management of post-ERCP pancreatitis.

The effect of hypothyroidism on color contrast sensitivity: a prospective study.

BACKGROUND: Thyroid hormone has been shown to control retinal cone opsin expression, the protein of color vision, in adult rodents. OBJECTIVES: The aim of this study was to evaluate the effect of hypothyroidism on color contrast sensitivity in adult overt hypothyroid patients. METHODS: Thirty-eight overt hypothyroid (31 females, 7 males) subjects and 20 euthyroid (16 females, 4 males) controls were studied prospectively. Color vision examination was performed by Chromatest, a software program analyzing the tritan (blue-yellow) color contrast threshold (tritan CCT) and protan (red-green) color contrast threshold (protan CCT). Color contrast sensitivity analyses of hypothyroid subjects were performed on admission and after L-thyroxine treatment when biochemical euthyroidism was achieved. RESULTS: After a median period of 90 (90-210) days, 24 (19 females, 5 males) patients were euthyroid and eligible for a second color vision examination. Baseline tritan CCT and protan CCT values were significantly higher in the hypothyroid group compared to euthyroid controls, which clinically translates into impaired color contrast sensitivity (p < 0.001 and p < 0.001, respectively). There was a significant decrease in tritan CCT (p = 0.002) and protan CCT (p < 0.001) values in the hypothyroid group after euthyroidism was achieved, which denotes improvement in color contrast sensitivity. CONCLUSIONS: It is a novel finding of the current study that color contrast sensitivity is impaired in hypothyroidism and significantly improves after euthyroidism is achieved.

Neutrophil gelatinase-associated lipocalin in prediction of mortality in patients with hepatorenal syndrome: a prospective observational study.

BACKGROUND & AIMS: Hepatorenal syndrome (HRS) is a severe complication of cirrhosis which is characterized by renal dysfunction and associated with poor survival. Neutrophil gelatinase-associated lipocalin (NGAL) is a troponin-like biomarker for human acute kidney injury. We aimed to investigate levels of plasma and urine NGAL in HRS and predictive ability of these markers for all-cause mortality, in HRS, stable cirrhosis and control subjects. METHODS: A total of 64 patients with cirrhosis (8 patients with type 1 HRS, 22 with type 2 HRS, and 34 without HRS) and 23 control subjects were included in the study. Blood and urine samples were measured with Human NGAL sandwich ELISA. Patients were followed up prospectively. RESULTS: Patients with type 1 and type 2 HRS had significantly higher plasma and urine NGAL levels compared with stable cirrhosis and control subjects. Cox regression analysis showed that plasma NGAL and MELD-Na scores were independent predictors of mortality. ROC-curve analysis showed that the plot of the plasma NGAL, urine NGAL, MELD-Na and Child-Turcot-Pugh score could predict all-cause mortality in cirrhotic patients' area under the curve (AUC 0.819, 0.686, 0.807 and 0.795 respectively). CONCLUSIONS: NGAL could predict mortality in patients with HRS independent of other commonly used risk factors.

Glomerulonephritis associated with tuberculosis: a case report and literature review.

Rapidly progressive glomerulonephritis caused mycobacterium tuberculosis is rare; however, three case have been reported to date. Crescentic glomerulonephritis is a life-threatening disease and together with the presence of tuberculous infection is associated with a poor outcome if treatment is inadequate and delayed. We describe the case of a 31-year-old female patient with nephrotic syndrome and progressive renal failure secondary to pulmonary tuberculosis. Renal biopsy showed crescent formation in 14 out of 27 glomeruli, and there was diffuse linear staining of immunoglobulin G deposits. Treatment included corticosteroids in combination with antituberculosis drugs for 2 months, and resulted in a significant improvement in renal function, the disappearance of proteinuria and pulmonary symptoms. We also present a review of the pertinent literature and discuss the pathophysiology of tuberculosis-related acute postinfectious glomerulonephritis.

Heparin-induced thrombocytopenia in a hemodialysis patient treated with fondaparinux: nephrologists between two fires.

Heparin-induced thrombocytopenia (HIT) is caused by heparin exposure and presents with reduced platelet count. Patients undergoing hemodialysis (HD) treatment have increased risk of developing HIT due to prolonged exposure to unfractionated heparin or low-molecular weight heparin. We report a 79-year-old male patient with end-stage renal disease who developed type-II HIT during maintenance HD. Platelet count of the patient decreased gradually and antiplatelet factor IV antibody was found to be positive. The patient was treated with fondaparinux and continued heparin-free HD. Unfortunately, despite favorable initial response without any thrombotic episodes, the patient died due to severe sepsis complicated by gastrointestinal hemorrhage.

Blood neutrophil-to-lymphocyte ratio independently predicts survival in patients with liver cirrhosis.

OBJECTIVES: Neutrophil-to-lymphocyte ratio (NLR) is a novel inflammation index that has been shown to independently predict poor clinical outcomes. We aimed to evaluate the role of NLR in the prediction of long-term mortality in patients with stable liver cirrhosis. MATERIALS AND METHODS: This is a retrospective observational cohort study in which 145 stable cirrhotic patients without infection, hepatocellular carcinoma, and ongoing steroid therapy were enrolled between January 2009 and December 2011. The primary end point was survival during follow-up. NLR along with Child-Turcotte-Pugh (CTP), Model for End-Stage Liver Disease (MELD) scores, and Charlson comorbidity index were assessed for the prediction of mortality. RESULTS: There were 86 men and 59 women, mean age 58.9±13.4 years. The etiologies of liver cirrhosis included viral hepatitis (n=73), cryptogenic (50), alcoholic (12), and other (10). The mean follow-up duration was 27.8±6.8 months, during which 40 patients died. The mean NLRs were 2.08±0.99 and 4.39±3.0 in surviving and nonsurviving patients, respectively (P<0.001). Kaplan-Meier survival analysis was carried out according to the median NLR above and below 2.72. Patients with NLR of at least 2.72 had a significantly lower survival (log rank, P<0.001). NLR was found to be an independent predictor of mortality in all Cox Regression models (odds ratio 1.2; 95% confidence interval 1.2-1.3; P<0.001). Receiver operating characteristic analysis showed that cut-off values of 4.22, 3.07, and 2.96 for NLR predicted 12, 24, and 36-month mortality, respectively (AUC: 0.806, P=0.0029; 0.841, P<0.0001 and 0.783, P<0.0001, respectively). CONCLUSION: NLR is a predictor of mortality independent of CTP and MELD scores in patients with liver cirrhosis. NLR could predict mortality in the subgroup of patients with low MELD scores as well.

Brucella peritonitis in peritoneal dialysis: a case report and review of the literature.

Brucellosis is a zoonotic infection that humans contract usually by ingestion of unpasteurized milk and milk products or by direct contact with raw infected animal products. Infection is endemic in many countries, including Turkey. Being a systemic disease, brucellosis may affect almost any part of the body. The peritoneum is a site rarely involved in brucellosis. Most peritonitis episodes involving Brucella species have been spontaneous cases reported in cirrhotic patients with ascites. To our knowledge, the literature contains only 5 cases of Brucella peritonitis related to continuous ambulatory peritoneal dialysis. Here, we report Brucella peritonitis in a continuous ambulatory peritoneal dialysis patient, and we discuss the relevant literature.

Efficacy of ankaferd blood stopper application on non-variceal upper gastrointestinal bleeding.

AIM: To prospectively assess the hemostatic efficacy of the endoscopic topical use of ankaferd blood stopper (ABS) in active non-variceal upper gastrointestinal system (GIS) bleeding. METHODS: Endoscopy was performed on 220 patients under suspiciency of GIS bleeding. Patients with active non-variceal upper gastrointestinal bleeding (NVUGIB) with a spurting or oozing type were included. Firstly, 8-10 cc of isotonic saline was sprayed to bleeding lesions. Then, 8 cc of ABS was applied on lesions in which bleeding continued after isotonic saline application. The other endoscopic therapeutic methods were applied on the lesions in which the bleeding did not stop after ABS. RESULTS: Twenty-seven patients had an active NVUGIB with a spurting or oozing type and 193 patients were excluded from the study since they did not have non-variceal active bleeding. 8 cc of ABS was sprayed on to the lesions of 26 patients whose bleeding continued after isotonic saline and in 19 of them, bleeding stopped after ABS. Other endoscopic treatment methods were applied to the remaining patients and the bleeding was stopped with these interventions in 6 of 7 patients. CONCLUSION: ABS is an effective method on NVUGIB, particularly on young patients with no coagulopathy. ABS may be considered as part of a combination treatment with other endoscopic methods.

Dilated cardiomyopathy in a patient with antibody-negative Goodpasture's syndrome and pulmonary relapse.

The Goodpasture's syndrome, also known as anti-GBM disease, is an uncommon disease, responsible for 20% of all cases of rapidly progressive glomerulonephritis. Anti-GBM antibodies are directed against non-collagenous domain (NC-1) of the alpha-3 chain of type IV collagen. When conventional ELISA assays are used, these antibodies can be detected in almost all the patients. Nevertheless, some reports have described antibody-negative relapsing disease. Some aggravating factors, namely, smoking, pulmonary infection and hypervolemia, may expose embedded antigenic target and may be responsible for the relapse. In addition, these antibody-negative relapses also respond to standard treatment, which comprises of plasma exchange, pulse steroids and cyclophosphamide. Herein, we report a patient who presented at the Selcuk University Meram School of Medicine, Meram, Konya, Turkey, with the pulmonary-renal syndrome. He was also found to have idiopathic dilated cardiomyopathy (DCM). To our knowledge, this is the first report describing co-existence of DCM and anti-GBM disease. There is growing evidence showing strong relation of both DCM and anti-GBM disease with HLA. Although not proven, this might have occurred in our patient. In our opinion, volume overload was facilitated by anuria and DCM and led to an antibody-negative pulmonary relapse. The relapse was treated just as the first episode and the patient improved satisfactorily.

When urine is no longer beneficial: renal artery embolisation in severe nephrotic syndrome secondary to amyloidosis.

Renal artery embolisation (RAE) is an interventional radiology procedure which is used to embolise small branches of renal artery. It is mainly used for urologic purposes, i.e., vascular malformations, angiomyolipomas and renal tumours not amenable to surgical resection. Bilateral RAE can be performed via using absolute ethanol, polyvinyl alcohol or microparticles. After RAE, patients may experience post-embolisation syndrome which is usually self-limited. Use of this procedure for refractory nephrotic syndrome has been rarely defined in the literature to date. Here, we describe a patient who had nephrotic syndrome due to secondary systemic amyloidosis. The patient presented with severe proteinuria (33 g per day), hypoalbuminaemia and anasarca oedema. We applied bilateral RAE with microparticles. We did not observe any complications associated with the procedure. Protein excretion, laboratory values and clinical signs returned to normal.

Colchicine treatment in autosomal dominant polycystic kidney disease: many points in common.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the inherited renal cystic diseases and constitutes 10% of the end stage kidney disease population. ADPKD is caused by PKD1 and PKD2 gene mutations in 85% and 15% of the cases respectively. Its high prevalence and negative impact on health outcomes fostered efforts to explain pathophysiologic pathways of cyst formation in kidneys. Among these are increased apoptosis, unopposed proliferation of tubule cells, impaired polarization and planar cell polarity, impaired cAMP pathway, cilier dysfunction, activated mTOR pathway, increased tumor necrosis factor-alpha (TNF-alpha) production. Many drugs have been tried in an attempt to halt cystogenesis in some point. Despite success to some extent in experimental studies, none reached clinical armamentarium yet. Colchicine, originally extracted from Colchicum autunale, is an anti-inflammatory drug that has been in continuous use for more than 3000 years. It has been used successfully to prevent attacks of familial mediterranien fever and amyloidosis, to treat gout and pseudogout attacks for a few decades. Colchicine principally is a microtubule inhibitor, thus prevents cell migration, division, and polarization. It also has anti-apoptotic, anti-proliferative and anti-inflammatory effects and down-regulates (TNF-alpha) receptors. As can easily be seen, many of the effects of colchicine have pathophysiologic counterparts in ADPKD. Thus, we hypothesized that colchicine would be beneficial to prevent or at least delay cyst formation in ADPKD patients. Indirect evidence also support our hypothesis, in which taxol and paclitaxel, other two microtubule inhibitors, were shown to delay cyst formation in experimental models of ADPKD. To our opinion, despite its narrow therapeutic index, widespread experience makes colchicine a suitable candidate for prolonged clinical use, should experimental studies show any benefit in ADPKD.