Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Craniopharyngioma is a rare, benign, suprasellar brain tumor associated with a significant number of endocrine and metabolic impairments. Growth hormone deficiency, caused by the tumor itself or by its subsequent surgical treatment, is the most common hormone deficiency in these patients and replacement is frequently necessary. Hypothalamic obesity observed after surgery treatment, whether combined with radiotherapy or not, presents with increased abdominal fat and altered lipid profiles and is likely caused by both disruption of the mechanisms controlling satiety, hunger and energy balance and impairment of sensitivity to leptin, insulin and ghrelin axis. It is well known that hyperlipemia is associated with acute pancreatitis, both as a precipitant and as an epiphenomenon. Moreover, the increased incidence of acute pancreatitis during growth hormone therapy is possibly due to increased enzyme production (e.g., amylase, lipase and elastase). We report the case of a 13-year-old girl affected by craniopharyngioma on growth hormone replacement treatment who developed acute pancreatitis. We suggest including routine evaluation of lipid profile during follow-up of all children on growth hormone treatment, especially those affected by hypopituitarism secondary to craniopharyngioma, given pancreatic adverse effects of growth hormone replacement therapy and associated metabolic impairment due to hypothalamic obesity.
 ...
PMID:Acute pancreatitis in a girl with panhypopituitarism due to craniopharyngioma on growth hormone treatment. A combination of risk factors. 1950 96

Acute pancreatitis (AP) is an inflammatory disease characterized by steady, acute abdominal pain of varying severity, often radiating from the epigastrium to the back. Its presentation ranges from a self-limiting mild disorder to a more severe and fulminant disease. Severe acute pancreatitis accounts for 30% of all deaths related to pancreatitis. The incidence of AP is increasing progressively with a corresponding increase in the incidence of its risk factors. Alcohol abuse and gallstone migration are the established risk factors for development of AP. In recent years, genetic factors and obesity have also been identified as risk factors responsible for the development of AP. The pathophysiology of AP involves acute inflammation of the acinar cells. Excessive acinar cell injury leads to a condition called systemic inflammatory response syndrome (SIRS). Protracted SIRS is responsible for most of the life-threatening complications associated with AP. Most common AP-related complications include pulmonary, renal, cardiovascular, and central nervous system dysfunction. Thus prompt and accurate diagnosis of AP is of paramount importance. The medical management of AP includes controlling pain, providing adequate nutritional support, and monitoring complications. Endoscopic retrograde cholangiopancreatography and surgery have also shown to reduce the mortality and morbidity associated with AP. Drugs such as resveratrol and rosiglitazone are being investigated as potential candidates for the treatment of AP.
 ...
PMID:Acute pancreatitis: a literature review. 1956 40

Obesity is associated with increased severity of acute pancreatitis (AP). We recently developed a model of AP induced by administration of interleukin (IL)-12+IL-18, two cytokines that are elevated in patients with AP. In this model, severe AP develops in obese leptin-deficient ob/ob mice compared to lean littermates. In the present report, we evaluated the pancreatic response of diet-induced obesity (DIO) mice to IL-12+IL-18. Body weight loss and adipose tissue necrosis were more severe and prolonged in cytokine-injected DIO compared to lean mice. Edematous AP developed in lean mice, whereas DIO mice developed necrotizing AP. Obese DIO mice developed more severe hypocalcemia, increased liver damage and a heightened acute-phase response compared to lean mice, although leukopenia and thrombocytopenia were of comparable severity in lean and DIO mice. Serum levels of IL-6, IL-10, and IL-22 were significantly higher in DIO compared to lean mice, whereas interferon-gamma and tumor necrosis factor-alpha did not differ between the two groups. In conclusion, obesity induced by high-fat diet is associated with increased disease severity and duration in the model of AP induced by administration of IL-12+IL-18.
Obesity (Silver Spring) 2010 Mar
PMID:Effect of diet-induced obesity on acute pancreatitis induced by administration of interleukin-12 plus interleukin-18 in mice. 1969 61

The incidence of acute pancreatitis, an inflammation of the pancreas, is increasing worldwide. Pancreatic injury is mild in 80%-90% of patients who recover without complications. The remaining patients may develop a severe disease with local complications such as acinar cell necrosis, abscess and remote organ injury including lung injury. The early prediction of the severity of the disease is an important goal for physicians in management of patients with acute pancreatitis in order to optimize the therapy and to prevent organ dysfunction and local complications. For that purpose, multiple clinical scale scores have been applied to patients with acute pancreatitis. Recently, a new problem has emerged: the increased severity of the disease in obese patients. However, the mechanisms by which obesity increases the severity of acute pancreatitis are unclear. Several hypotheses have been suggested: (1) obese patients have an increased inflammation within the pancreas; (2) obese patients have an increased accumulation of fat within and around the pancreas where necrosis is often located; (3) increase in both peri- and intra-pancreatic fat and inflammatory cells explain the high incidence of pancreatic inflammation and necrosis in obese patients; (4) hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators; and (5) ventilation/perfusion mismatch leading to hypoxia associated with a low pancreatic flow might reduce the pancreatic oxygenation and further enhance pancreatic injury. Recent experimental investigations also show an increased mortality and morbidity in obese rodents with acute pancreatitis and the implication of the adipokines leptin and adiponectin. Such models are important to investigate whether the inflammatory response of the disease is enhanced by obesity. It is exciting to speculate that manipulation of the adipokine milieu has the potential to influence the severity of acute pancreatitis.
 ...
PMID:Experimental evidence of obesity as a risk factor for severe acute pancreatitis. 1990 32

Obesity and lipid metabolism are associated with the severity of acute pancreatitis. Fat necrosis appears in the severe acute pancreatitis as a consequence of the release of lipolytic enzymes, but its potential role on the progression of the disease is unclear. In this study, we have examined the role of white adipose tissue as a source of inflammatory mediators that can promote systemic inflammation during experimental taurocholate-induced acute pancreatitis in rats. The inflammatory status and the expression of TNFalpha, iNOS, adiponectin and IL-10 were determined in necrotic and non-necrotic areas of adipose tissue. Samples of adipose tissue were also used to induce the activation of macrophages in vitro. Finally, the release of TNFalpha to mesenterial vessels surrounded by necrotic or non-necrotic fat was evaluated in ex vivo perfused mesenterium. A strong inflammatory infiltrate was observed in the border between necrotic and non-necrotic areas of adipose tissue. In these areas, high expression of TNFalpha and iNOS and a reduced expression of IL-10 were observed, while adiponectin showed only a moderate increase. Necrotic fat strongly activates peritoneal macrophages in vitro. Mesenterial areas with fat necrosis release to the vascular vessels significantly increased amounts of TNFalpha when compared to vessels without necrosis. Altogether, these results indicate that adipose tissue inflammation is a process secondary to acute pancreatitis but also contributes to the generation of mediators potentially involved in the induction of the systemic inflammatory response. In particular, the areas of fat necrosis are important sources of inflammatory mediators.
 ...
PMID:Release of inflammatory mediators by adipose tissue during acute pancreatitis. 2021 59

Four adult, full-sibling slender-tailed meerkats (Suricata suricatta) were diagnosed with acute pancreatitis. The incident case presented with lethargy, anorexia, abdominal guarding, and a cranial abdominal mass. Serum was grossly lipemic, with elevated cholesterol and triglyceride concentrations and increased amylase and lipase activity. An exploratory laparotomy confirmed chylous peritonitis and included excision of a saponified spleno-duodenal mass, a partial pancreatectomy, and a splenectomy. Histopathology revealed severe, multifocal, subacute necrotizing and granulomatous pancreatitis. Within 13 days of the incident case, the second meerkat was identified with essentially identical clinical, surgical, and histologic findings. During subsequent physical examinations of apparently unaffected cohorts (n=12), physical and hematologic findings suggestive of pancreatitis were identified in the two remaining siblings of the first two cases. The definitive cause for these four cases is undetermined; however, common risk factors identified were obesity and hyperlipidemia, a change to a higher-fat diet, and genetic predisposition. To assess its usefulness in the diagnosis of meerkat pancreatitis, serum canine and feline pancreatic lipase immunoreactivity (cPLI and fPLI) concentrations were measured in serum samples (n=61) from two unrelated meerkat populations. Although these assays are highly sensitive and specific for the diagnosis of pancreatitis in domestic carnivores, similar correlation was not apparent for meerkats. In addition, hyperlipidemia was inconsistently present in many meerkats, with no apparent correlation to the development of clinical illness. Based on these observations, sensitive and specific diagnostic tests for pancreatitis in meerkats are currently unavailable.
 ...
PMID:Acute pancreatitis in slender-tailed meerkats (Suricata suricatta). 2059 19

Acute pancreatitis (AP) is an important cause of morbidity and mortality worldwide and the annual incidence appears to be increasing. It presents as a mild self-limiting illness in 80% of patients. However, one-fifth of these develop a severe complicated life-threatening disease requiring intensive and prolonged therapeutic intervention. Alcohol and gallstone disease remain the commonest causes of AP but metabolic abnormalities, obesity and genetic susceptibility are thought be increasingly important aetiological factors. The prompt diagnosis of AP and stratification of disease severity is essential in directing rapid delivery of appropriate therapeutic measures. In this review, the range of diagnostic and prognostic assays, severity scoring systems and radiological investigations used in current clinical practice are described, highlighting their strengths and weaknesses. Increased understanding of the complex pathophysiology of AP has generated an array of new potential diagnostic assays and these are discussed. The multidisciplinary approach to management of severe pancreatitis is outlined, including areas of controversy and novel treatments.
 ...
PMID:Acute pancreatitis. 2092 69

A 34-year-old man with obesity who was an avid consumer of soft drinks was found in a coma after complaining of a poor physical condition for a few days. On arrival, he had hyperglycemia of 2700 mg/dL, coma, shock, sepsis, aspiration pneumonia, acute renal failure, acute pancreatitis, liver dysfunction, and systemic mycosis. The rapid infusion of a large volume of isotonic saline, insulin, antibiotics, and ulinastatin was performed, and mechanical ventilation was applied. The treatment was complicated by transient hypernatremia resulting from osmostasis, which gradually decreased. He demonstrated transient decerebrate posturing upon stimulation; however, he became conscious within a week of admission, and his associated diseases also improved. After correcting his hyperglycemia, the patient was discharged on foot. We report our case of a patient with hyperglycemia of 2700 mg/dL, which was the highest value reported in the English literature. During the correction of the hyperglycemia, transient hypernatremia occurred to prevent abrupt decrease in osmolality, which thus resulted in cell swelling.
 ...
PMID:A case of successful treatment of a patient with hyperglycemia of 2700 mg/dL. 2108 69

More research is now focused on pancreatic steatosis. Multiple definitions, clinical associations and synonyms for pancreatic steatosis are described in the literature and can be confusing. The integration and comparison of several studies concerning this topic is therefore challenging. In the past, pancreatic steatosis was considered an innocuous condition, a bystander of many underlying diseases (such as congenital syndromes, hemochromatosis and viral infection). However, evidence that pancreatic steatosis (strongly associated with obesity and the metabolic syndrome) has a role in type 2 diabetes mellitus, pancreatic exocrine dysfunction, acute pancreatitis, pancreatic cancer and the formation of pancreatic fistula after pancreatic surgery is emerging. This Review focuses on the different etiological factors and the clinical consequences of pancreatic steatosis.
 ...
PMID:The clinical significance of pancreatic steatosis. 2130 75

Obesity increases the risk of adverse outcomes during acute critical illnesses such as burns, severe trauma, and acute pancreatitis. Although individuals with more body fat and higher serum cytokines and lipase are more likely to experience problems, the roles that these characteristics play are not clear. We used severe acute pancreatitis as a representative disease to investigate the effects of obesity on local organ function and systemic processes. In obese humans, we found that an increase in the volume of intrapancreatic adipocytes was associated with more extensive pancreatic necrosis during acute pancreatitis and that acute pancreatitis was associated with multisystem organ failure in obese individuals. In vitro studies of pancreatic acinar cells showed that unsaturated fatty acids were proinflammatory, releasing intracellular calcium, inhibiting mitochondrial complexes I and V, and causing necrosis. Saturated fatty acids had no such effects. Inhibition of lipolysis in obese (ob/ob) mice with induced pancreatitis prevented a rise in serum unsaturated fatty acids and prevented renal injury, lung injury, systemic inflammation, hypocalcemia, reduced pancreatic necrosis, and mortality. Thus, therapeutic approaches that target unsaturated fatty acid-mediated lipotoxicity may reduce adverse outcomes in obese patients with critical illnesses such as severe acute pancreatitis.
 ...
PMID:Lipotoxicity causes multisystem organ failure and exacerbates acute pancreatitis in obesity. 2214 68


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>