Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1291077 (bloating)
 1,674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mixed retrospective-prospective study of 70 Chinese anorexic patients in Hong Kong shows that although they were similar to Western anorexics in most other ways, 41 (58.6%) of them did not exhibit any fear of fatness throughout their course of illness. Instead, these non-fat phobic patients used epigastric bloating (31.4%), no appetite/hunger (15.7%) or simply eating less (12.9%) as legitimating rationales for food refusal and emaciation. Compared to fat phobic anorexics, they were significantly slimmer pre-morbidly (P < 0.0001) and were less likely to exhibit bulimia (P = 0.001). The possible explanations for the absence of fat phobia and the interpretive dilemma this provokes are discussed from historical, pathoplastic and cultural anthropological perspectives. It is argued that anorexia nervosa may display phenomenological plurality in a Westernizing society, and its identity may be conceptualized without invoking the explanatory construct of fat phobia exclusively. As non-fat phobic anorexia nervosa displays no culturally peculiar features, it is not strictly speaking a Western culture-bound syndrome, but may evolve into its contemporary fat phobic vogue under the permeative impact of Westernization. Its careful evaluation may help clarify the aetiology and historical transformation of eating disorder, foster the development of a cross-culturally valid taxonomy of morbid states of self-starvation, and exemplify some of the crucial issues that need to be tackled in the cross-cultural study of mental disorders.
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PMID:Fat phobic and non-fat phobic anorexia nervosa: a comparative study of 70 Chinese patients in Hong Kong. 813 23

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.
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PMID:Gastrointestinal and nutritional aspects of eating disorders. 840 9

Autophagosomes are formed during autophagy, which is activated by hypoxia and starvation. Autophagy is important for mast cell degranulation. We hypothesized that autophagy is a key feature in the pathogenesis of systemic sclerosis (SSc). We examined SSc clinical features and mast cell density across the presence and severity of autophagy. Skin punch biopsy was performed on 33 SSc patients and 6 healthy controls (HC). Autophagy was evaluated by immunofluorescence on paraffin sections using LC3-FITC staining on these patients. The intensity of staining and mast cell density was examined across clinical features in 19 of the SSc patients. Presence of autophagosome formation was assessed by EM in 17 of the SSc patients and 4 HC. In our SSc study population, 29 of subjects were female and 23 were limited cutaneous. Twenty-nine of 33 SSc patients had autophagy by LC3-FITC staining. Intensity of staining decreased with longer duration of SSc (p = 0.09) and RP (p = 0.10). Bloating and distention differed across level of intensity staining (Wilcoxon signed-rank test, p = 0.05), with the greatest levels among those with moderate intensity. On EM, autophagosome formation was present in 16 of 17 SSc patients and no HC. All SSc patients had perivascular mast cells. Autophagy was present in 29 of 33 SSc patients, and none of our HC suggesting importance in pathogenesis. Autophagy staining was greater among those with shorter duration of SSc. Bloating and distention were higher in patients with moderate autophagy staining. Perivascular mast cells were present in all SSc patients. The role of autophagy in vasculopathy and mast cell activation in SSc warrants further studies.
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PMID:Autophagy is a key feature in the pathogenesis of systemic sclerosis. 2393 20

Anorexia nervosa (AN) is the third most common disorder, after obesity and asthma, in the population of adolescents between 13-18 years of age. Food intake reduction is associated with whole body dysfunction, affecting its physical, psychological and social spheres. As a result of starvation, dysfunction develops in virtually all systems and organs. However, most frequently patients with AN complain of digestive symptoms, such as a feeling of fullness after meals, pain in the upper abdomen, dysphagia, nausea, bloating and constipation. They can have mild functional character, but may also reflect serious complications, including diseases requiring urgent surgical intervention. In addition, gastric complaints may hinder nutritional management of AN. Care of AN patients requires cooperation of many specialists in the field of psychiatry, psychology, paediatrics, internal medicine and nutrition. However, it is often difficult to organize such a team. Therefore, we decided to approach the issues of gastrointestinal symptoms and complications in the course of AN, and the rules of nutritional therapy.
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PMID:Gastrointestinal complications and refeeding guidelines in patients with anorexia nervosa. 2858 33

Pancreatic ductal adenocarcinoma (PDA) is a deadly cancer that resists efforts to identify better chemotherapeutics. PDA is associated with chronic pancreatitis and acinar cell dedifferentiation. This reduces enzyme production by the exocrine pancreas, resulting in digestive insufficiencies. Malabsorption of partially digested food causes bloating, overfilled intestines, abdominal pain, excessive feces, steatorrhea, and malnutrition. These maladies affect quality of life and restrict treatment options for pancreatitis and PDA. Here, we characterize health benefits and risks of dietary pancreatic enzymes in three mouse models of PDA-KC, KCR8-16, and KIC. KC expresses oncogenic KrasG12D in pancreatic tissue whereas KCR8-16 also has deletions of the Rgs8 and Rgs16 genes. Rgs proteins inhibit the release of digestive enzymes evoked by G-protein-coupled-receptor agonists. KC and KCR8-16 mice developed dedifferentiated exocrine pancreata within 2 months of age and became malnourished, underweight, hypoglycemic, and hypothermic. KC mice adapted but KCR8-16 mice rapidly transitioned to starvation after mild metabolic challenges. Dietary pancreatic enzyme supplements reversed these symptoms in KC and KCR8-16 animals, and extended survival. Therefore, we tested the benefits of pancreatic enzymes in an aggressive mouse model of PDA (KIC). Median survival improved with dietary pancreatic enzyme supplements and was extended further when combined with warfarin and gemcitabine chemotherapy. However, dietary pancreatic enzymes stimulated tumor growth in the terminal stages of disease progression in KIC mice.
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PMID:Malnutrition in Pancreatic Ductal Adenocarcinoma (PDA): Dietary Pancreatic Enzymes Improve Short-Term Health but Stimulate Tumor Growth. 2924 57