Heterotopic pancreas of the gallbladder associated with chronic cholecystitis and high levels of amylasuria.

CONTEXT: Heterotopic pancreas of the gallbladder is an extremely rare entity, especially when pancreatic tissue appears histologically with an exclusively exocrine structure. CASE REPORT: We report the case of a 35-year-old man who presented with symptoms of acalculous gallbladder disease with high levels of amylasuria. Immunohistochemical analysis of the surgical specimen of the cholecystectomy revealed pancreatic tissue at the gallbladder wall. CONCLUSIONS: Heterotopic pancreatic tissue is a rare pathological finding in the gallbladder. It requires consideration and sensitization in the differential diagnosis of acalculous gallbladder disease, which can explain hyperamylasuria in cases of unknown origin.

The proteolysis-inducing factor: in search of its clinical relevance in patients with metastatic gastric/esophageal cancer.

The proteolysis-inducing factor is a putative mediator of cancer-associated weight loss. The goal of this study was to examine for the first time: (i) its prevalence in patients with metastatic gastric/esophageal cancer; and (ii) whether it possibly correlated with weight loss and anorexia and whether it predicted tumor response and patient survival. This study recruited 41 patients as part of a phase II therapeutic, chemotherapy protocol for patients with metastatic gastric/esophageal cancer. Patient eligibility criteria were designed to select a group of patients who would tolerate treatment with the drugs capecitabine and oxaliplatin. Urine for assaying the proteolysis-inducing factor was obtained at registration and then 6 weeks later. Patients completed the FACT-E questionnaire every 6 weeks and had their weights checked at the same interval. Patients were followed prospectively for tumor response and patient survival. Twenty-three (56%) patients had the proteolysis-inducing factor in their urine at registration, and 18 (64%) had it at 6 weeks. There was no statistically significant correlation between the presence of the proteolysis-inducing factor and weight loss or between its presence and anorexia. Moreover, there was no evidence that the presence of the proteolysis-inducing factor in urine was able to predict tumor response or patient survival. The proteolysis-inducing factor in urine does not appear to be tied to weight loss, anorexia, tumor response, or patient survival in the clinical setting of metastatic gastric/esophageal cancer.

Urinary peptide levels in women with eating disorders. A pilot study.

The aim of this study was to evaluate whether the urinary excretion of low molecular weight peptides is increased in women with a history of anorexia nervosa/self starvation. The study group consisted of 12 women aged 20-38 years who were treated in a specialised day care unit for eating disorders in Stockholm between January and December 1998; the controls were eight women with primary bulimia treated in the same unit (A) and ten healthy women without any eating disorder (B). The chromatographically measured urinary peptide levels in the study group were significantly higher than those in control group A (and B when one highly influential individual with very low peptide excretion in the study group was excluded from the analyses). These findings offer some support to the speculative hypothesis that eating disorder symptoms may be linked to increased levels of neuroactive peptides, although it is necessary to define the peptides further before any definite conclusion can be drawn. Furthermore, the study group was characterised by many interpersonal differences in eating behaviour that could explain the increased urinary peptide levels.

Interleukin-6-deficient mice refractory to IgA dysregulation but not anorexia induction by vomitoxin (deoxynivalenol) ingestion.

Dietary exposure to the trichothecene vomitoxin (VT) causes feed refusal and elevates IgA production in the mouse. Based on the observations that IL-6 can cause anorexia and promote IgA production and that gene expression of this cytokine is increased in vivo and ex vivo on VT exposure, we hypothesized that IL-6 is an essential cytokine in VT-induced feed refusal and IgA dysregulation. To test this hypothesis, the effects of dietary VT on feed intake, weight gain, serum IgA levels and kidney mesangial IgA deposition in an IL-6-"knockout" mouse (B6129-IL6(tmi Kopf)) were compared to those in both a corresponding "wildtype" (B6129F2) and a previously characterized "sentinel" strain (B6C3F1) that possess the intact gene for this cytokine. IL-6 deficiency did not alter the capacity of VT to cause feed refusal or impair weight gain. VT-fed B6129F2 and B6C3F1 mice had significantly higher serum IgA concentrations than did their corresponding controls fed clean diet, whereas significant differences were not observed between IL-6 KO mice fed VT or control diets. Kidneys taken from VT-fed wild-type and sentinel mice had significantly increased mesangial IgA deposition as compared to controls. While slight increases in mesangial IgA were observed in VT-fed IL-6 KO mice, mean fluorescence intensities were significantly less than that found in the corresponding wild-type and sentinel strains. IL-6 KO mice appeared to be less prone to the development of microscopic haematuria following VT exposure than were the corresponding wild-type and sentinel strains. In total, the results suggested that IL-6-deficient mice were refractory to VT-induced dysregulation of IgA production and development of IgA nephropathy, whereas chronic VT-mediated nutritional effects related to feed intake and weight gain were unaffected.

Chronic TNF infusion causes anorexia but not accelerated nitrogen loss.

It has been proposed that many of the physiologic and metabolic changes that occur during critical illness and malignancy are mediated by the cytokine tumor necrosis factor alpha/cachectin (TNF). To test this hypothesis, a study of the metabolic responses that occurred during 5 days of continuous intravenous (I.V.) infusion of TNF both in rats and tumor-bearing humans was conducted. TNF administration was associated with anorexia, fluid retention, acute phase responses, and negative nitrogen balance. In both species, changes in nitrogen balance were related to the onset of anorexia and not to the development of hypermetabolism and accelerated net tissue breakdown. TNF may represent the primary afferent stimulus inducing many of the metabolic changes that occur during critical illness, but it is not solely responsible for the accelerated net proteolysis that occurs in these patients.