Protein-losing gastroenteropathy complicated with asymptomatic primary biliary cholangitis, refractory to immunosuppressant, and improved by Helicobacter pylori eradication: a case report.

BACKGROUND: Protein-losing gastroenteropathy (PLGE) is a syndrome with a chief complaint of hypoalbuminemia, which occurs due to plasma protein leakage in the gastrointestinal tract, leading to general edema, ascites, and pleural effusions. CASE PRESENTATION: A 71-year-old woman visited another hospital for evaluation of hypoalbuminemia and systemic edema. She was hospitalized for a close inspection of hypoalbuminemia and was diagnosed with PLGE. Steroid and azathioprine therapy was prescribed; however, hypoalbuminemia did not improve, and the patient's condition worsened due to anasarca. As hospitalization was prolonged, the patient was transferred to our hospital. She was infected with Helicobacter pylori, and we performed H. pylori eradication. Following H. pylori eradication, her edema improved remarkably. CONCLUSION: We present the first case wherein H. pylori eradication successfully improved protein leakage in the lower gastrointestinal tract in a patient diagnosed with PLGE complicated with refractory to immunosuppressant treatment. H. pylori eradication should be considered in patients with PLGE complicated with H. pylori infection, without specific endoscopic finding or refractory to immunosuppressants.

A rare presentation of hypovolemic shock secondary to Whipple's disease.

Whipple's disease is a rare, multisystem infection caused by the Gram-positive Tropheryma whippelii organism. In addition to neurological and rheumatological manifestations, this disease can result in significant gastrointestinal symptoms such as malabsorption, diarrhea, and weight loss. Given the diagnostic challenge and rare occurrence, a high index of suspicion is critical to prevent morbidity and mortality from this otherwise highly infectious disease transmitted via the fecal-oral route. We present a very rare but near-fatal case of hypovolemic shock secondary to protein-losing enteropathy and gastrointestinal bleeding from small bowel T. whippelii infection. Furthermore, the epidemiology, clinical presentation, diagnosis, and management of Whipple's disease is reviewed.

Molecular diversity of the faecal microbiota of Toy Poodles in Japan.

The intestinal microbiota was revealed with the recent advances in molecular techniques, such as high-throughput sequencing analysis. As a result, the microbial changes are thought to influence the health of humans and animals and such changes are affected by several factors including diet, genetics, age, sex, and diseases. Similar studies are being conducted in dogs, and the knowledge of intestinal microbiota in dogs is expanding. Nonetheless, basic information on intestinal microbiota in dogs is less than that of humans. Our aim was to study toy poodles (n=21), a popular companion dog, in terms of basic characteristics of the faecal microbiota by 16S rRNA gene barcoding analysis. In the faecal microbiota, Firmicutes, Bacteroidetes, Proteobacteria, and Fusobacteria were the dominant phyla (over 93.4% of faecal microbiota) regardless of the attributes of the dogs. In family level, Enterobacteriaceae, Bacteroidaceae, and Lachnospiraceae were most prevalent. In case of a dog with protein-losing enteropathy, the diversity of faecal microbiota was different between before and after treatment. This study provides basic information for studying on faecal microbiota in toy poodles.

Isolation of Cokeromyces recurvatus from the gastrointestinal tract in a dog with protein-losing enteropathy.

The present case report describes the isolation of the fungus Cokeromyces recurvatus from the intestinal tract of a canine patient. Infection by this fungus is rare, having only been reported in 8 human beings and 1 cat. The fungus is not reported to exhibit tissue invasion. Cokeromyces recurvatus is most likely an opportunistic agent, and most cases described involve some degree of immunosuppression.

Protein-losing enteropathy in paracoccidioidomycosis identified by scintigraphy: report of three cases

Paracoccidioidomycosis (PCM) or South American Blastomycosis is a systemic fungal infection caused by a dimorphic fungus, Paracoccidioides brasiliensis. It represents the most important systemic mycosis in South America and with higher prevalence among male inhabitants of the rural area. PCM usually affects the lungs, and rarely the intestines. The authors report three cases of PCM, treated at the University Hospital of Universidade Federal de Mato Grosso do Sul whose scintigraphy with technetium-99 labeled human albumin revead intestinal protein loss.

Protein-losing enteropathy in paracoccidioidomycosis identified by scintigraphy: report of three cases.

Paracoccidioidomycosis (PCM) or South American Blastomycosis is a systemic fungal infection caused by a dimorphic fungus, Paracoccidioides brasiliensis. It represents the most important systemic mycosis in South America and with higher prevalence among male inhabitants of the rural area. PCM usually affects the lungs, and rarely the intestines. The authors report three cases of PCM, treated at the University Hospital of Universidade Federal de Mato Grosso do Sul whose scintigraphy with technetium-99 labeled human albumin revead intestinal protein loss.

Binding of intimin with Tir on the bacterial surface is prerequisite for the barrier disruption induced by enteropathogenic Escherichia coli.

Enteropathogenic Escherichia coli (EPEC) infects intestinal epithelial cells and perturbs the intestinal barrier that limits the paracellular movement of molecules. The disruption of the barrier is mediated by the effectors translocated into the host cells through the bacterial type III secretion system (TTSS). A previous report has described the importance of a bacterial outer membrane protein, intimin, in EPEC-mediated disruption of the barrier, and proposed that intimin, in concert with a host intimin receptor, controls the activity of the translocated barrier-disrupting effectors [P. Dean, B. Kenny, Intestinal barrier dysfunction by enteropathogenic Escherichia coli is mediated by two effector molecules and a bacterial surface protein, Mol. Microbiol. 54 (2004) 665-675]. In this study, we found that the importance of intimin is in its ability to bind a bacterial intimin receptor, Tir. Additionally, the impaired ability of an intimin-negative mutant was not restored by co-infection with intimin-expressing TTSS mutants. Collectively, the results in this study favor an alternative scenario explaining the importance of intimin, that the binding of intimin with Tir on the bacterial surface triggers or promotes the translocation of factors required for the efficient disruption of the barrier. Thus, the interaction of intimin with Tir may serve as a molecular switch that controls the delivery of virulence factors into the host cells.

Protein-losing enteropathy caused by Lawsonia intracellularis in a weanling foal.

A 5-month-old Morgan filly was presented to the Atlantic Veterinary College with a history of lethargy, fever, depression, anorexia, and dependent ventral edema. Diagnostic tests revealed severe inflammation, hypoproteinemia, and thickened small intestinal loops. Protein-losing enteropathy caused by Lawsonia intracellularis was diagnosed and treated successfully with erythromycin-rifampin.

Specific detection of Lawsonia intracellularis in porcine proliferative enteropathy inferred from fluorescent rRNA in situ hybridization.

Fluorescent in situ hybridization targeting 16S ribosomal RNA was used for specific detection of the obligate intracellular bacterium Lawsonia intracellularis in enterocytes from pigs affected by proliferative enteropathy. A specific oligonucleotide probe was designed and the specificity of the probe was determined by simultaneous comparison with indirect immunofluorescence assay for detection of L. intracellularis in formalin-fixed tissue samples from 15 pigs affected by porcine proliferative enteropathy. We used 10 tissue samples from pigs without proliferative mucosal changes as negative controls. The results showed that the oligonucleotide probe is specific for L. intracellularis and that fluorescent in situ hybridization targeting ribosomal RNA is a suitable and fast method for specific detection and histological recognition of L. intracellularis in formalin-fixed tissue.

[Characteristics of peritoneal exudate microflora in children with appendicular peritonitis]. / Kharakterystyka mikroflory eksudatu cherevnoï porozhnyny u ditei z perytonitom apendykuliarnoho henezu.

Bacteriological investigation of peritoneal exudate was conducted in 131 children with peritonitis. The greatest quantity of pathogenic and conventionally pathogenic Escherichias and bacteroids was revealed in March, April and September. In summer peritonitis was caused by pathogenic and conventionally pathogenic Escherichias in association with enterobacterias, staphylococci and other microorganisms.

Resolution of protein-losing hypertrophic lymphocytic gastritis with therapeutic eradication of Helicobacter pylori.

Lymphocytic gastritis (LG) is a recently described histological entity characterized by increased lymphocytes in the superficial gastric epithelium and foveolae. It includes a subgroup of patients with giant gastric folds and, often, a protein-losing state, a condition termed hypertrophic lymphocytic gastritis (HLG). Despite close endoscopic and clinical similarities to classical Menetrier's disease, the histopathological features of these two diseases are sufficiently distinct that they are regarded as separate entities. The etiology and pathogenesis of HLG are unknown, and the possible etiological role of Helicobacter pylori in particular is controversial. For this reason we report the case of a 48-yr-old female with HLG, hypoproteinemia, and H. pylori infection whose disease resolved clinically, endoscopically, and pathologically with therapeutic eradication of the H. pylori. H. pylori infection may be a treatable cause of at least some cases of HLG and should therefore be carefully sought in any patient with this condition.

Healing of protein losing hypertrophic gastropathy by eradication of Helicobacter pylori--is Helicobacter pylori a pathogenic factor in Ménétrier's disease?

Hypertrophic gastropathy--that is, Ménétrier's disease--was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylori gastritis in these patients. A case is described of a 28 year old woman with Ménétrier's disease associated with proved protein loss from the stomach. Treatment with cimetidine for more than three years had little benefit when colonisation by H pylori was detected. Density of H pylori colonisation and activity of gastritis, which was also present in the first biopsy specimens taken five years ago, were more pronounced in the body than in the antrum, which is in agreement with the characteristics of H pylori gastritis found in other cases with Ménétrier's disease. A 14 day antibacterial treatment course with 750 mg amoxicillin three times a day combined with 40 mg omeprazole three times a day was started in April 1991. This resulted in eradication of H pylori and the return to normal of giant folds and the mucosal histology. Serum protein concentrations returned to normal within six weeks and remained normal at two endoscopies during a two year follow up. This case report suggests that a subgroup of the patients with Ménétrier's disease may be healed by the eradication of H pylori.

[Exudative gastropathy associated with cytomegalovirus infection after allogenic bone marrow transplantation]. / Gastropathie exsudative à cytomégalovirus après greffe de moelle allogénique.

The authors report a case of protein losing gastropathy associated with cytomegalovirus. This form which is extremely rare in adults occurred alone after allogenic bone marrow transplantation and become apparent by a hypoalbuminaemia causing oedema of the lower limbs. Gastrocopy showed large red folds of approximately a centimetre covered in a whitish hypersecretion coating. Biopsy demonstrated active gastritis which appeared on a hypertrophic and hypersecretive gastritis. Outcome was favourable within 3 months without treatment.

Transient protein losing enteropathy associated with acute gastritis and campylobacter pylori.

Three children presented with acute protein losing enteropathy and were found to have acute gastritis associated with Campylobacter pylori infection. Recovery from protein losing enteropathy was accompanied by resolution of the gastritis and the disappearance of C pylori from the gastric mucosa. Their clinical course suggested that the C pylori had caused the gastritis and the protein losing enteropathy. The association between gastritis caused by C pylori and protein losing enteropathy in children has not to our knowledge been previously described.