Invasive aspergillosis of gastrointestinal debut without apparent respiratory involvement in an immunocompetent host.

A 72-year-old female presented with abdominal pain and constipation and intestinal dilation was found. Abdominal computed tomography showed two areas of thickening and stenosis in the proximal jejunum and preterminal ileum, with an unknown etiology. Exploratory laparotomy was proposed but the patient suffered a sudden and progressive decrease in consciousness. Cranial computed tomography showed an ischemic area and a midline shift. Brain biopsies suggested infection by Aspergillus Fumigatus. Despite antifungal drugs, the patient had a progressive clinical deterioration and died. The autopsy concluded a systemic infection due to Aspergillus Fumigatus. Invasive aspergillosis is a serious fungal infection and usually occurs in immunocompromised patients. It mainly affects the lungs, followed by the gastrointestinal tract. The most frequent location in gastrointestinal involvement is the small bowel. Gastrointestinal involvement is more frequent in invasive disease. Although, there are case reports of isolated gastrointestinal aspergillosis, even in immunocompetent patients without risk factors. The prognosis is poor.

Enteroscopy in the diagnosis of melanoma metastases.

We present abdominal computed tomography and enteroscopy images of a 48-year-old male patient with a previous melanoma who presented with epigastric pain. The pain was not controlled with medical management. Abdominal computed tomography and a histological study of biopsies form enteroscopy confirmed the diagnosis of metastatic melanoma. The gastrointestinal involvement of melanoma is usually metastatic. Symptomatic gastrointestinal involvement occurs in less than 5% of melanomas, although postmortem analyses have reported up to 70%. The clinical presentation is variable and usually presents as abdominal pain. The diagnosis of small intestinal involvement of melanoma is a challenge due to its poor accessibility. The enteroscopy has a fundamental role as it allows a direct visualization and biopsies to be taken for histological study.

Enteroscopic diagnosis of intestinal malabsorption of a rare etiology: diaphragm disease.

We present the case of a 59-year-old patient with malabsorption syndrome which started with polyneuropathy. Capsule endoscopy and enteroscopy show villous denudation. Histological study confirms diaphragm disease of the small bowel. Diaphragm disease is a rare disease characterized by the presence of multiple thin diaphragms, such as septa, that narrow the intestinal lumen. The clinical features can be iron deficiency anemia, intestinal obstruction, change in bowel habits or acute abdomen secondary to perforation. It is usually generally with sustained use of high doses of non-steroidal anti-inflammatory drugs. The diagnosis usually requires the use of a capsule endoscopy or enteroscopy with biopsies.

Familial dysphagia: eosinophilic esophagitis.

We present a family with several cases of eosinophilic esophagitis. Some cases of eosinophilic esophagitis in the same family have been previously described. Patients with eosinophilic esophagitis present frequently atopy, and atopy has a strong family association due to complex interactions between genetic and environment. However, eosinophilic esophagitis has a stronger genetic component than other atopic diseases. Eosinophilic esophagitis has been linked to variations in genes like eotaxin-3, TSLP and its receptor and CAPN14, although the inheritance pattern has not yet well defined.

Hepatic hematoma after ERCP: two new case reports.

ERCP is an endoscopic procedure with a complication risk ranging from 2.5 to 8%. The most frequent complications are pancreatitis, cholangitis, hemorrhage or perforation. Hepatic hematoma after ERCP is a potentially serious, rare complication. Not many cases are reported in the literature. We present here two new cases of hepatic hematoma following ERCP along with a review of the literature and possible therapeutic options.

Prevalence of Primary Resistance of Helicobacter pylori to Clarithromycin and Levofloxacin in Southern Spain.

BACKGROUND: The eradication of Helicobacter pylori (HP) using clarithromycin (CLA)-based triple therapy depends on the resistance of HP to antibiotics. The Maastricht III conference recommends the implementation of locoregional surveillance programmes for primary resistance of HP to CLA. In Andalusia, there are no previous data in this respect. The aim of this study was to determine the prevalence of the primary resistance of HP to CLA and levofloxacin (LF) in southern Spain. METHODS: Multicentre cross sectional study was carried out in 6 hospitals in Andalusia. Patients of both sexes numbering 401 were included (male 48%), aged 18-80 years and naïve to HP eradication. Resistance of HP to CLA (CLAr) and LF (LFr) was assessed by determining mutations by PCR: mutations of the 23S rRNA gene define CLAr and mutations of the gene gyrA define LFr. Four hundred one gastric samples were collected. CLAr was detected in 72 patients (17.9%) and LFr was detected in 56 patients (13.9%). Heteroresistance was detected for both antibiotics: CLA 37/72 (51.3%) and LF 28/56 (50%). Variability for CLAr was detected among the centres, ranging from 11.5% to 24.7% without statistical significance (p = 0.12). Female sex was related to CLAr. CONCLUSIONS: In Andalusia, there is a high rate of primary CLAr and LFr. CLA-based triple therapy should be avoided as the primary eradication regimen in this region. There is a wide variability in the rate of CLAr among centres.

Bone mineral density and serum levels of soluble tumor necrosis factors, estradiol, and osteoprotegerin in postmenopausal women with cirrhosis after viral hepatitis.

CONTEXT: Cirrhosis after viral hepatitis has been identified as a risk factor for osteoporosis in men. However, in postmenopausal women, most studies have evaluated the effect of primary biliary cirrhosis, but little is known about the effect of viral cirrhosis on bone mass [bone mineral density (BMD)] and bone metabolism. OBJECTIVE: Our objective was to assess the effect of viral cirrhosis on BMD and bone metabolism in postmenopausal women. DESIGN: We conducted a cross-sectional descriptive study. SETTING AND PATIENTS: We studied 84 postmenopausal female outpatients with viral cirrhosis and 96 healthy postmenopausal women from the general community. BMD was measured by dual-energy x-ray absorptiometry at lumbar spine (LS) and femoral neck (FN). RESULTS: The percentage with osteoporosis did not significantly differ between patients (LS, 43.1%; FN, 32.2%) and controls (LS, 41.2%; FN, 29.4%), and there was no difference in BMD (z-score) between groups. Serum concentrations of soluble TNF receptors, estradiol, and osteoprotegerin (OPG) were significantly higher in patients vs. controls (P < 0.001, P < 0.05, and P < 0.05, respectively). No significant difference was observed in urinary deoxypyridinoline. Serum OPG levels were positively correlated with soluble TNF receptors (r = 0.35; P < 0.02) and deoxypyridinoline (r = 0.37; P < 0.05). CONCLUSIONS: This study shows that bone mass and bone resorption rates do not differ between postmenopausal women with viral cirrhosis and healthy postmenopausal controls and suggests that viral cirrhosis does not appear to increase the risk of osteoporosis in these women. High serum estradiol and OPG concentrations may contribute to preventing the bone loss associated with viral cirrhosis in postmenopausal women.

Osteoporosis, mineral metabolism, and serum soluble tumor necrosis factor receptor p55 in viral cirrhosis.

Liver cirrhosis is a risk factor for osteoporosis. Nevertheless, little is known about the mechanisms of bone mass loss in patients with viral cirrhosis. TNFalpha is a potent bone-resorbing agent. Serum concentrations of soluble TNF receptor p55 (sTNFR-55) correlate with clinical activity in liver cirrhosis. Our aim was to evaluate the possible role of sTNFR-55 in the pathogenesis of osteoporosis in patients with viral cirrhosis and its relationship with bone turnover markers. We studied 40 consecutive patients with viral cirrhosis and no history of alcohol intake and 26 healthy volunteers. Bone mineral density (BMD) was measured by dual x-ray absorptiometry in the lumbar spine (LS) and femoral neck (FN). Patients with viral cirrhosis had reduced BMD (expressed as the z-score) in all sites [LS, -1.5 +/- 0.22 (P < 0.001); FN, -0.37 +/- 0.15 (P < 0.01)]. Serum concentrations of sTNFR-55 and urinary deoxypyridinoline, a biochemical marker of bone resorption, were significantly higher in patients with osteoporosis than in patients without osteoporosis (P < 0.001 and P < 0.05, respectively). Serum levels of sTNFR-55 correlated inversely with BMD in LS (r = -0.62; P < 0.005) and FN (r = -0.47; P < 0.05) and positively with urinary deoxypyridinoline (r = 0.72, P < 0.001). Our findings show that high serum concentrations of sTNFR-55 play a role in the pathogenesis of viral cirrhosis-associated bone mass loss and provide evidence of increased bone resorption related to the high serum sTNFR-55 levels.