Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental occlusion of superior sagittal sinus was made in dogs according to ligation with thread at the posterior third portion of the sinus. Ventricular enlargement and histological changes in the cerebrum were studied in various stage after occulusion of the sinus. In the acute stage, no ventricular enlargement occured. However, in the chronic stage, nine dogs out of 12 dogs showed enlargement of the ventricle. Hitological examination revealed peeled ependymal layer from subependymal tissue, edematous findings in the periventricular tissue, perivascular gliofibrosis, perivascular hemorrhage, exanguination of plasm, and venous stasis in the ventricular wall and cerebral cortex in convexity. Extracellular space in the subependymal tissue, and the space between pial and glial membrane were widened remarkably. Two factors were raised by authors as the pathogenesis for ventricular enlargement. One factor was the hydrodynamic disturbance of CSF according to the CSF malabsorption into the superior sagittal sinus through arachnoid villi. The other one was the disturbance of venous circulation due to occlusion of the sinus.
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PMID:[Ventricular enlargement in experimental occlusion of superior sagittal sinus--in reference to histopathological findings (author's transl)]. 124 Jun 15

Severe obesity is associated with multiple comorbidities and is refractory to dietary management with or without behavioral or drug therapies. There are a number of surgical procedures for the treatment of morbid obesity, including purely gastric restrictive, a combination of malabsorption and gastric restriction or primary malabsorption. The purely gastric restrictive procedures, including vertical banded gastroplasty and laparoscopic adjustable silicone gastric banding, do not provide adequate weight loss. African-American patients do especially poorly after the banding procedure with the loss of only 11% of excess weight in one study. Gastric bypass (GBP) is associated with the loss of 66% of excess weight at 1 to 2 years after surgery, 60% at 5 years and 50% at 10 years. For unknown reasons, African-American patients lose significantly less weight than Caucasians after GBP. There is a risk of micronutrient deficiencies after GBP, including iron deficiency anemia in menstruating women, vitamin B12, and calcium deficiencies. Prophylactic supplementation of these nutrients is necessary. Recurrent vomiting after bariatric surgery may be associated with a severe polyneuropathy and must be aggressively treated with endoscopic dilatation before this complication is allowed to develop. The malabsorptive procedures include the partial biliopancreatic bypass (BPD) and BPD with duodenal switch (BPD/DS). The BPD appears to cause severe protein-calorie malnutrition in American patients; the BPD/DS may be associated with less malnutrition. Weight loss failure after GBP does not respond to tightening a dilated gastrojejunal stoma or reducing the size of the gastric pouch. These patients may require conversion to a malabsorptive distal GBP, similar to the BPD. However, because of the risk of severe protein-calorie malnutrition and calcium deficiency BPD should be reserved for patients with severe obesity comorbidity. The risk of death following bariatric surgery is between 1% and 2% in most series but is significantly higher in patients with respiratory insufficiency of obesity. In most patients, surgically induced weight loss will correct hypertension, type II diabetes mellitus, sleep apnea, obesity hypoventilation syndrome, gastroesophageal reflux, venous stasis disease, urinary incontinence, female sexual hormone dysfunction, pseudotumor cerebri, degenerative joint disease pains, as well as improved self-image and employability.
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PMID:Bariatric surgery for severe obesity. 1185 Dec 1

Mesenteric fibrosis (MF) constitutes an underrecognized sequela in patients with small intestinal neuroendocrine neoplasms (SI-NENs), often complicating the disease clinical course. The aim of the present systematic review, carried out by Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology, is to provide an update in evolving aspects of MF pathogenesis and its clinical management in SI-NENs. Complex and dynamic interactions are present in the microenvironment of tumor deposits in the mesentery. Serotonin, as well as the signaling pathways of certain growth factors play a pivotal, yet not fully elucidated role in the pathogenesis of MF. Clinically, MF often results in significant morbidity by causing either acute complications, such as intestinal obstruction and/or acute ischemia or more chronic conditions involving abdominal pain, venous stasis, malabsorption and malnutrition. Surgical resection in patients with locoregional disease only or symptomatic distant stage disease, as well as palliative minimally invasive interventions in advanced inoperable cases seem clinically meaningful, whereas currently available systemic and/or targeted treatments do not unequivocally affect the development of MF in SI-NENs. Increased awareness and improved understanding of the molecular pathogenesis of MF in SI-NENs may provide better diagnostic and predictive tools for its timely recognition and intervention and also facilitates the development of agents targeting MF.
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PMID:Pathogenesis and Clinical Management of Mesenteric Fibrosis in Small Intestinal Neuroendocine Neoplasms: A Systematic Review. 3252 77