Clostridium perfringens bacteremia caused by choledocholithiasis in the absence of gallbladder stones.

A 67-years-old male presented with periumbilical abdominal pain, fever and jaundice. His anaerobic blood culture was positive for clostridium perfringens. Computed tomogram scan of the abdomen and abdominal ultrasound showed normal gallbladder and common bile duct (CBD). Subsequently magnetic resonance cholangiopancreaticogram showed choledocholithiasis. Endoscopic retrograde cholangiopancreaticogramwith sphincterotomy and CBD stone extraction was performed. The patient progressively improved with antibiotic therapy Choledocholithiasis should be considered as a source of clostridium perfringens bacteremia especially in the setting of elevated liver enzymes with cholestatic pattern.

Differences in outcomes between cholecalciferol and ergocalciferol supplementation in veterans with inflammatory bowel disease.

AIM: Vitamin D deficiency is a global health issue associated with increased health-care costs, and could play a role in the pathogenesis and management of inflammatory bowel disease. Prior studies show a high prevalence of vitamin D deficiency in veterans with inflammatory bowel disease. We aimed to examine the outcome differences in patients with inflammatory bowel disease, comparing treatment with ergocalciferol to cholecalciferol. METHODS: A retrospective review of electronic medical records of patients with inflammatory bowel disease at a Veterans Affairs Medical Facility in the Southeastern United States was carried out. Those with at least one serum 25(OH) vitamin D level were included. Initial and follow-up vitamin D values were recorded. The type of vitamin D supplementation, whether cholecalciferol or ergocalciferol, was documented. Costs in the year after measurement of vitamin D were divided into separate inpatient and outpatient categories. RESULTS: Veterans (n = 108) with ulcerative colitis or Crohn's disease and an available 25(OH) vitamin D level were studied. There were differences in follow-up vitamin D levels; those who received weekly ergocalciferol had higher subsequent levels than those who received cholecalciferol, especially at a second follow up, although differences did not achieve statistical significance. However, those who received vitamin D3 were less likely to use laboratory, pharmacy, radiology and fee-based services, and had lower laboratory and pharmacy costs. CONCLUSIONS: Our data suggest that cholecalciferol replacement might improve outcomes to a greater extent than ergocalciferol, and might be better in limiting health-care costs and expenses in patients with inflammatory bowel disease.

Vitamin D status in veterans with inflammatory bowel disease: relationship to health care costs and services.

Vitamin D deficiency is a global pandemic associated with increased health care costs and could play a role in the pathogenesis and management of inflammatory bowel disease. This study examined vitamin D status in veterans with ulcerative colitis (UC) and Crohn's disease (CD) and assessed its relationship to health care costs and service utilization. Veteran patients (n = 125) with UC or CD and with an available 25-hydroxyvitamin D level were studied. CD patients were more likely to be vitamin D insufficient than the UC group. Despite the higher vitamin D levels among UC patients, they were significantly more likely to utilize laboratory and pharmacy services compared with CD patients, whereas patients with CD had significantly higher radiology and pharmacy costs. Thus, it is likely that disease-specific characteristics rather than vitamin D status determine the costs of health care services in veterans with established inflammatory bowel disease.

Macronutrient absorption characteristics in humans with short bowel syndrome and jejunocolonic anastomosis: starch is the most important carbohydrate substrate, although pectin supplementation may modestly enhance short chain fatty acid production and fluid absorption.

BACKGROUND: Diet may play an important role in the management of patients with short bowel syndrome who have colon in continuity. However, macronutrient absorption has not been well characterized, and the most appropriate dietary constituents have not been well defined. OBJECTIVE: To define carbohydrate absorption characteristics in patients with short bowel syndrome and determine the potential role of pectin as a dietary substrate. METHODS: The authors studied the effect of a custom pectin-based supplement in 6 subjects (3 male/3 female) aged 29-67 years with jejunocolonic anastomosis, 4 of whom required long-term parental nutrition. Small intestinal absorption capacity, macronutrient and fluid balance, gastrointestinal transit time, and energy consumption were measured. RESULTS: Data showed that 53% nitrogen, 50% fat, and 32% total energy were malabsorbed. In contrast, the majority (92%) of total carbohydrate was utilized. Fecal short-chain fatty acids (SCFAs) were increased, an indication of increased fermentation. Although only 4% of starch was recovered in stool, it is indicative of considerable starch malabsorption, thus providing the main carbohydrate substrate, for colonic bacterial fermentation. In contrast, nonstarch polysaccharide was a relatively minor fermentation substrate with only 49% utilized. Eighty percent of the pectin was fermented. Supplementation was associated with increased total SCFAs, acetate, and propionate excretion. There was a trend observed toward greater fluid absorption (-5.9% ± 54.4% to 26.9% ± 25.2%) following pectin supplementation. Nonsignificant increases in gastric emptying time and orocolonic transit time were observed. CONCLUSION: Despite malabsorption, starch is the primary carbohydrate substrate for colonic bacterial fermentation in patients with short bowel syndrome, although soluble fiber intake also enhances colonic SCFA production.

PD-1 negatively regulates interleukin-12 expression by limiting STAT-1 phosphorylation in monocytes/macrophages during chronic hepatitis C virus infection.

Hepatitis C virus (HCV) is remarkably efficient at evading host immunity to establish chronic infection. During chronic HCV infection, interleukin-12 (IL-12) produced by monocytes/macrophages (M/Mφ) is significantly suppressed. Programmed death-1 (PD-1), an inhibitory receptor on immune cells, plays a pivotal role in suppressing T-cell responses during chronic viral infection. To determine whether PD-1 regulates IL-12 production by M/Mφ during chronic HCV infection, we examined the expressions of PD-1, its ligand PDL-1, and their relationship with IL-12 production in M/Mφ from HCV-infected, HCV-resolved, and healthy subjects by flow cytometry. Toll-like receptor (TLR) -mediated IL-12 production by M/Mφ was selectively suppressed, while PD-1/PDL-1 expressions were up-regulated, in HCV-infected subjects compared with HCV-resolved or healthy subjects. Up-regulation of PD-1 was inversely associated with the degree of IL-12 inhibition in HCV infection. Interestingly, the reduced response of M/Mφ from HCV-infected individuals to TLR ligands appeared not to be the result of a lack of the ability to sense pathogen, but to an impaired activation of intracellular janus kinase/signal transducer and activator of transfection (STAT) pathway as represented by inhibited STAT-1 phosphorylation in M/Mφ from HCV-infected individuals compared with HCV-negative subjects. Successful HCV treatment with pegylated interferon/ribavirin or blocking PD-1/PDL-1 engagement ex vivo led to reduced PD-1 expression and improved IL-12 production as well as STAT-1 activation in M/Mφ from HCV-infected individuals. These results suggest that the PD-1 inhibitory pathway may negatively regulate IL-12 expression by limiting STAT-1 phosphorylation in M/Mφ during chronic HCV infection.

Programmed death-1 affects suppressor of cytokine signaling-1 expression in T cells during hepatitis C infection.

Chronic hepatitis C virus (HCV) infection is associated with T-cell exhaustion that is mediated through upregulation of the PD-1 negative regulatory pathway. PD-1 expression is induced by HCV core protein, which also induces upregulation of SOCS-1, a key modulator that controls the Jak/STAT pathway regulating cytokine expression. To determine whether these two negative regulatory pathways are linked during T-cell signaling, SOCS-1 expression was examined by blocking the PD-1 pathway in T cells stimulated with anti-CD3/CD28 in the presence of HCV core protein. T cells isolated from healthy subjects or HCV-infected individuals were treated with anti-PD-1 or anti-PDL-1 antibodies in the presence or absence of HCV core protein, and SOCS-1 gene expression was detected by RT-PCR or immunoblotting, while T-cell functions were assayed by flow cytometric analyses. Both PD-1 and SOCS-1 gene expression were upregulated in healthy T cells exposed to HCV core protein, and blocking the PD-1 pathway downregulated SOCS-1 gene expression in these cells. Additionally, T cells isolated from chronically HCV-infected subjects exhibited increased PD-1 and SOCS-1 expression compared to healthy subjects, and SOCS-1 expression in T cells isolated from HCV-infected subjects was also inhibited by blocking PD-1 signaling; this in turn enhanced the phosphorylation of STAT-1, and improved the impaired T-cell proliferation observed in the setting of HCV infection. These data demonstrate that PD-1 and SOCS-1 are linked in dysregulating T-cell signaling during HCV infection, and their cross-talk may coordinately inhibit T-cell signaling pathways that lead to T-cell exhaustion during chronic viral infection.

A wayward cyst.

CONTEXT: Pseudocysts are a common complication of acute and chronic pancreatitis. These are usually located within the pancreas but they can occur at other sites as well, including the mediastinum, neck, pelvis and rarely in the liver as in our case. The diagnosis of intrahepatic pancreatic pseudocyst relies on the demonstration of a high amylase level in the sampled cystic fluid in the absence of infection or neoplasm. CASE REPORT: A 60-year-old man with a history of chronic pancreatitis presents with a clinical and laboratory picture suggestive of acute exacerbation of his pancreatitis. A computed tomogram (CT) scan of the abdomen revealed a pancreatic pseudocyst and a cystic lesion involving both lobes of the liver. CT diagnostic aspiration of the intrahepatic cyst revealed high amylase level (greater than 20,000 U/L). The cyst was treated with percutaneous drainage with complete resolution of the cyst. CONCLUSION: In the setting of pancreatitis, intrahepatic pancreatic pseudocyst should be considered in the differential diagnosis of cystic lesion of the liver.

Oral rehydration solutions in non-cholera diarrhea: a review.

The use of oral rehydration solution (ORS) has revolutionized the management of acute diarrhea. The implementation of the standard World Health Organization ORS (WHO-ORS) has resulted in decreased mortality associated with acute diarrheal illnesses in children, although in general stool volume and diarrhea durations are not reduced. Decreased morbidity and mortality have occurred because of improved hydration status. Decreased morbidity has also been described in adults who used this therapy. Various modifications to the standard ORS have been derived. These modifications have included hypo-osmolar or hyperosmolar solutions, use of rice-based ORS, zinc supplementation, and the use of amino acids, including glycine, alanine, and glutamine. Some of these variations have been successful, some have not, and others are still under investigation. ORS has been used for travelers' diarrhea and to decrease intravenous (IV) fluid requirements in patients with short bowel syndrome (SBS) who require parenteral nutrition (PN). This paper reviews the standard WHO-ORS and its mechanism of action, followed by more contemporary reduced osmolarity ORS and rice-based ORS in non-cholera diarrhea. Various modifications to improve ORS are also discussed.