Search PubMed⌕ Search

Biomedical subjects

R Modigliani

Publications and source records attributed to R Modigliani.

At least 145 records · Page 8Linked to original sources
PubMed1976

[Nondeficiency chronic polyneuropathies in celiac disease in adults (2 cases with inflammatory neuromuscular vascularitis)].

The neurological and muscular complications seen in coeliac disease in adults are usually attributed to deficiency secondary to malabsorption. Amongst them, however, there exists a very rare cateogory, described by Cooke et al. (1966) taking the form of a chronic myeloneuropathy which cannot be explained in terms of the malabsorption syndrome. Our two cases of gluten intolerance enteropathy, confirmed by biopsy before and after diet, fell into this group of polyneuropathies. The patients, both women, suffered from an essentially sensory ataxic polyneuropathy with accessory motor component with pyramidal and posterior column signs. CSF findings showed a meningeal inflammatory reaction in one of the two cases. These neurological signs, appearing paradoxically during a digestive disease cured by diet, evolve chronically but become stabilised with corticosteroid therapy. Any vitamin deficiency may be excluded in the aetiology of these problems. Neuropathological study of neuromuscular biopsies in very fine serial sections confirmed the mild peripheral nervous involvement but revealed identical inflammatory lesions in the nerve and muscle which were remarkable by virtue of their very highly segmentally selective micro-vasculitis appearance. In these two cases, general, clinical and biological arguments, as well as the type of histological lesion, make it possible to exclude monoclonal gammapathies, malignant haemopathies, amyloidosis and the major collagen diseases. This micro-vasculitis, having transient forms with P.A.N. is no less distinctive, and may be integrated into the provisional group of "allergic angeitis", related to physiopathology of circulating immune complexes and very fashionable in theories as to the mechanism of gluten-sensitive enteropathies. The exact nature of the link between the latter and these types of polyneuropathy remains unknown.

Adult↗
PubMed1976

Effects of synthetic human gastrin I on movements on water, electrolytes, and glucose across the human small intestine.

The effect of graded doses (0.125, 0.500, 1.00 and 2.00 mug per kg per hr) of intravenous synthetic human gastrin I (SHG) on jejunal transport of water, electrolytes, and glucose from a glucose-saline solution (solution II) was studied in 12 healthy volunteers, using an intestinal perfusion technique with a proximal occluding balloon. SHG when infused at rates of 0.500 mug per kg per hr or greater significantly reduced water and electrolyte absorption; this effect was linearly related to the dose and reached 40 to 60% of basal absorption (and only 10% for glucose) with the highest dose; insorption of sodium and water were significantly decreased by SHG. In a further group of 9 subjects no effect of SHG (2 mug per kg per hr) was found on jejunal absorption from a mannitol-saline solution (solution I) and on ileal absorption from solutions I and II; in 5 additional subjects, SHG did not decrease jejunal transit time of intraluminal fluid. There was no increase in serum thyrocalcitonin during SHG infusion. It is proposed that SHG selectively depresses the glucose-stimulated sodium transport as suggested by the reduction of the rate of net sodium absorption per micromole of glucose absorbed during SHG infusion. Physiological and pathological implications of these findings are discussed, especially in the light of the circulating levels of immunoreactive gastrin achieved during SHG infusion.

Adult↗
PubMed1975

Pancreatic cholera (W.D.H.A. syndrome). Histochemical and ultrastructural studies.

Results of light and electron-microscopic studies of primary pancreatic tumor and of metastasis in a new case of Pancreatic Cholera (P.C.) are reported. The primary tumor but not the metastases, contained unusual, large cystic glandular formations, lined both by pancreatic-duct- and small-intestine-like epithelia and closely connected with the endocrine proliferation. A part from a few D-cells, the endocrine tumoral cells could not be identified by histochemical stainings. Their ultrastructural pattern, with small secretory granules (diameter less than 300 nm) and numerous cytoplasmic bunches of filaments, was very similar to that of gastric and duodenal D1-cells. Normal duodenal D1-cells have been said to produce gastric inhibitory peptide, a substance structurally and biologically similar to the vasoactive intestinal peptide actually secreted by the tumor. The normal histological appearance of gastric, gallbladder, jejunal, ileal, right and left colonic mucosae is consistent with the responsibility of the tumoral secretion in the impairment of gut functions in P.C.

Acute Kidney Injury↗
PubMed1975

Pancreatic cholera. Sudies on tumoral secretions and pathophysiology of diarrhea.

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.

Adult↗