Somatostatin antagonism prevents elemental diet-induced intestinal atrophy in the rat.

Somatostatin is a peptide with known antiproliferative effects on the intestine. The aim of the present work was to determine whether somatostatin (SST) antagonism reduces elemental diet-induced intestinal atrophy in the rat. Male Wistar rats were fed a standard diet and treated for seven days with either continuous infusion of saline or low and high doses of a putative somatostatin antagonist; another group was given a SST antagonist in a pulsatile high dose. All these groups received an elemental diet to induce gut mucosa atrophy. Rats were killed and samples were obtained for morphometric and proliferative measurements of the intestine and for SST and insulin-like growth factor-1 (IGF-1) level determination. The elemental diet decreased mucosal length and proliferation. Pulsatile administration of SST antagonist improved or prevented both effects, whereas continuous SST antagonist delivery prevented decreased crypt proliferation induced by the elemental diet. Somatostatin plasma levels were lowest in rats receiving pulsatile administration of SST antagonist. In conclusion, somatostatin antagonism increases proliferation in the intestinal mucosa, improving elemental diet-induced intestinal atrophy; however, morphological growth is not affected.

Somatostatin blockade improves the proliferative response but not intestinal morphological growth after small bowel resection in rats.

OBJECTIVE: To find out whether or not blockade of somatostatin improves intestinal adaptation after small bowel resection. DESIGN: Laboratory experiment. SETTING: Teaching hospital, Spain. SUBJECTS: Eighty adult Wistar rats. INTERVENTIONS: Animals underwent intestinal resection or sham operation (n = 40 each) and were treated with a somatostatin antagonist either intermittently or continuously in three different doses (n = 8 each). MAIN OUTCOME MEASURES: Bowel mucosal thickness, proliferation and concentrations of cAMP, somatostatin, insulin-like growth factor 1. RESULTS: Intestinal resection induced a proliferative and morphometric increase of the mucosa; however, the antagonist increased proliferation only in those animals given the highest dose. Intermittent doses induced a proliferative effect that was stronger than that in the three continuous groups. There was no relationship between trophic stimulus and insulin-like growth factor 1 or cAMP, but somatostatin concentrations increased after the intermittent course. CONCLUSIONS: Somatostatin receptor blockade with an antagonist does not cause in normal rats an intestinal morphological adaptation process or increase it after resection; however, it did promote a proliferative stimulus in the crypts.

[Pemphigus herpetiformis associated with neoplasm of the lung]. / Pénfigo herpetiforme asociado a neoplasia pulmonar.

We report a case of a 57 year-old male who developed atypical bullous disease and in whom an underlying carcinoma of the bronchus was found. The cutaneous eruption fulfilled the clinical, histological and immunological features of pemphigus herpetiformis. Reports of pemphigus herpetiformis and internal malignancy are extremely rare.