Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of calcitonin (CT) are highest in patients with medullary thyroid carcinoma (MTC). Plasma CT is also raised in some patients with carcinoma such as that of the breast, the lung or the pancreas, and in pheochromocytoma. It must be kept in mind, however, that plasma CT can be similarly raised in patients with renal failure, non-tumoral pulmonary disease or acute pancreatitis. In hypercalcemia patients with primary hyperparathyroidism the plasma CT is normal or only marginally elevated. It is speculated that the raised levels in pregnant and lactating women and in new-born infants prevent excessive bone destruction at times of greater physiological need for calcium. Larger molecular weight forms than monomeric CT (1--32) are circulating at least in plasma of patients with calcitonin-producing tumors and in renal insufficiency. The biological function of these larger molecular weight forms is not yet known. The discrepancies among the results of different laboratories can in part be explained by the immunoheterogeneity of the hormone and the different antigenic recognition sites of the antisera used. The measurement of plasma CT levels is nevertheless important for the diagnosis of MTC and may prove useful in some patients with malignant tumors unrelated to the C-cells of the thyroid gland. CT-radioimmunoassay may be improved by using antibodies specific to the different forms of circulating calcitonin.
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PMID:[The differential diagnosis of hypercalcitoninism]. 733 Jun 42

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

The management of acute pancreatitis (AP) is symptomatic and is adjusted to the clinical course of the disease, which is assessed by different clinical variables, laboratory findings as well as by contrast-medium-enhanced computed tomography. The therapy of AP consists of a general basic treatment (fluid substitution, antibiotics, etc.) and additional measures according to intensive-care principles. Antisecretory substances such as glucagon, calcitonin and somatostatin are ineffective; the value of peritoneal lavage and early ERCP with EPT as standard treatment is still under debate. Surgical treatment is only indicated if the clinical course worsens various of the supportive measures.
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PMID:[Therapy of acute pancreatitis]. 805 74

The mortality rate in acute pancreatitis (AP) is significantly lower in patients hospitalized directly at the intensive care unit than in patients admitted to hospital in 2 weeks after the assessment of diagnosis, prophylactic administration of low-molecular protease inhibitor reduces the occurrence of post ERCP pancreatitis a well a coincident complications. Despite rational considerations concerning the significance of pryphylactic administration of antibodies (ATB) in severe AP, there still not enough convincing data which could be recommended a standard therapy. One of the concepts of causal therapy of AP. Suggest that inhibition of exocrine pancreatic enzymatic secretion reduces autodigestion of the gland (setting the gland at rest). The reports on success of secretin-inhibiting substances a glucagon, calcitonin, atropine and somatostatin require confirmation in randomized or accurately defined comparable groups. The initial studies on the therapeutic significance of lexipanphate-antagonist of platelet activating factor (PAF) in acute pancreatitis is promising. A long-term lavage had reduced the mortality.
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PMID:[Therapy of acute pancreatitis]. 972 66

Stimulation of capsaicin sensitive nerves or administration of calcitonin gene-related peptide (CGRP) before induction of acute pancreatitis (AP) attenuates pancreatic damage, whereas CGRP administration after development of AP aggravates lesion of pancreatic tissue. The aim of this study was to determine the effect of prolonged activity of sensory nerves or CGRP administration on the pancreatic repair after repeated episodes of AP. Five episodes of acute caerulein-induced pancreatitis (10 microg/kg/h for 5 h s.c.) were performed at weekly intervals in rats receiving either vehicle or capsaicin at the sensory nerve stimulatory dose (0.5 mg/kg, 3 times daily), or CGRP (10 microg/kg, 3 times daily). Two weeks after the last induction of AP morphological signs of pancreatic damage, pancreatic blood flow (PBF), serum and pancreatic amylase activity, fecal chymotrypsin activity, pancreatic weight, pancreatic RNA and DNA content, as well as, serum interleukin-1beta (Il-1beta ) were assessed. Pancreata of animals receiving vehicle alone showed almost full recovery within two weeks after last episode of pancreatitis induction. In capsaicin-treated group of rats, we observed the increase in PBF by 44% and in serum Il-1beta concentration by 91%. The pancreatic amylase activity, fecal activity of chymotrypsin, pancreatic nucleic acids content and DNA synthesis were decreased. In rats treated with CGRP the alterations in PBF, serum Il-1beta concentration, as well as, in pancreatic and fecal activity of enzymes were similar to capsaicin treated group but less pronounced. We conclude that prolonged activity of capsaicin-sensitive sensory nerves and the presence of their main mediator-CGRP during pancreatic regeneration after AP leads to pancreatic functional insufficiency typical for chronic pancreatitis.
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PMID:The influence of sensory nerves and CGRP on the pancreatic regeneration after repeated episodes of acute pancreatitis in rats. 1101 64

The function of primary sensory neurons is to receive and transmit information from external environment and these neurons are able to release neuromediators from the activated peripheral endings. The aim of this study was to determine the influence of sensory nerves and administration of their mediator--calcitonin gene related peptide (CGRP) on the course of acute pancreatitis (AP). Ablation of sensory nerves was performed by neurotoxic dose of capsaicin (100 mg/kg). Single or repeated episodes of AP were induced by caerulein infusion (10 microg/kg/h for 5 h). Five repeated AP were performed once a week. Capsaicin at the dose which stimulates sensory nerves (0.5 mg/kg/dose) or CGRP (10 microg/kg/dose) was administrated before and during or after single induction of AP, as well as, after each induction of repeated AP. Rats were killed at the time 0, 3 or 9 h after single induction of AP or two weeks after last induction of repeated AP. Ablation of sensory nerves aggravated pancreatic damage in caerulein-induced AP. Treatment with stimulatory doses of capsaicin or CGRP before and during single induction of AP attenuated the pancreatic damage in morphological examination. This effect was also manifested by partial reversion of AP evoked drop in DNA synthesis and pancreatic blood flow (PBF). Administration of CGRP after single AP induction aggravated histologically manifested pancreatic damage. The further decrease in PBF and DNA synthesis was also observed. Animals with five episodes of AP showed almost full pancreatic recovery two weeks after last induction of AP concerning all parameters tested. In stimulatory doses of capsaicin treated rats, we observed the decrease in pancreatic amylase and fecal chymotrypsin activity, as well as, the drop in DNA synthesis. Similar but less pronounced effects were observed after treatment with CGRP. We conclude that effect of sensory nerves and CGRP on AP is two-phase and time dependent. Stimulation of sensory nerves or the administration of CGRP during development of AP exhibits protective effects against pancreatic damage induced by caerulein overstimulation. After induction of AP, persistent activity of sensory nerves and presence of CGRP aggravate pancreatic damage and lead to functional insufficiency typical for chronic pancreatitis.
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PMID:Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery. 1178 67

Central nervous system affects pancreatic secretion of enzymes however, the neural modulation of acute pancreatitis has not been investigated. Leptin and melatonin have been recently reported to affect the inflammatory response of various tissues. The identification of specific receptors for both peptides in the pancreas suggests that leptin and melatonin could contribute to the pancreatic protection against inflammation. The aim of this study was: 1/ to compare the effect of intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) administration of leptin or melatonin on the course of caerulein-induced pancreatitis (CIP) in the rat, 2/ to examine the involvement of sensory nerves (SN) and calcitonin gene-related peptide (CGRP) in pancreatic protection afforded by leptin or melatonin, 3/ to assess the effect of tested peptides on lipid peroxidation products (MDA + 4-HNE) in the pancreas of CIP rats, 4/ to investigate the influence of leptin or melatonin on nitric oxide (NO) release from isolated pancreatic acini and 5/ to determine the effects of caerulein and leptin on leptin receptor gene expression in these acini by RT-PCR. CIP was induced by subcutaneous (s.c.) infusion of caerulein (25 microg/kg) to the conscious rats, confirmed by the significant increases of pancreatic weight and plasma amylase and by histological examination. This was accompanied in marked reduction of pancreatic blood flow and significant rise of MDA + 4-HNE in the pancreas. Leptin or melatonin were administered i.p. or i.c.v. 30 min prior to the start of CIP. Deactivation of SN was produced by s.c. capsaicin (100 mg/kg). An antagonist of CGRP, CGRP 8-37 (100 microg/kg i.p.), was given together with leptin or melatonin to the CIP rats. MDA + 4-HNE was measured using LPO commercial kit. NO was determined using the Griess reaction. Pretreatment of CIP rats with i.p. leptin (2 or 10 microg/kg) or melatonin (10 or 50 mg/kg) significantly attenuated the severity of CIP. Similar protective effects were observed following i.c.v. application of leptin (0.4 or 2 microg/rat) but not melatonin (10 or 40 microg/rat) to the CIP rats. Capsaicin deactivation of SN oradministration of CGRP 8-37 abolished above beneficial effects of leptin on CIP, whereas melatonin-induced protection of pancreas was unaffected. Pretreatment with i.p. melatonin (10 or 50 mg/kg), but not leptin, significantly reduced MDA + 4-HNE in the pancreas of CIP rats. Leptin (10(-10) - 10(-6) M) but not melatonin (10(-8) - 10(-5) M) significantly stimulated NO release from isolated pancreatic acini. Leptin receptor gene expression in these acini was significantly increased by caerulein and leptin. We conclude that 1/ central or peripheral pretreatment with leptin protects the pancreas against its damage induced by CIP, whereas melatonin exerts its protective effect only when given i.p., but not following its i.c.v. adminstration, 2/ activation of leptin receptor in the pancreatic acini appears to be involved in the beneficial effects of leptin on acute pancreatitis, 3/ the protective effects of leptin involve sensory nerves, CGRP and increased generation of NO whereas melatonin-induced protection of the pancreas depends mainly on the antioxidant local effect of this indole, and scavenging of the radical oxygen species in the pancreatic tissue.
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PMID:Sensory nerves in central and peripheral control of pancreatic integrity by leptin and melatonin. 1193 19

Results of investigation of the calcitonin and calcium level in the blood serum in dynamics in 15 patients with various forms of an acute pancreatitis were analyzed. In oedematous form of an acute pancreatitis the calcitonin content had constituted 4.5 pg/ml at average, promoting the calcium level rising up to 2.97 mmol/l; in necrotic form of an acute pancreatitis the calcitonin concentration had constituted 164.4 pg/ml, calcium--1.74 mmol/l; in purulent--necrotic form--accordingly 288 pg/ml and 1.5 mmol/l.
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PMID:[The role of calcitonin in the diagnosis, treatment and prognosis of acute pancreatitis and its complications]. 1244 Feb 5

Stimulation of primary sensory neurons produces local vasodilation, plasma extravasation, and pain and is due largely to the release of the tachykinins substance P and calcitonin-gene-related peptide. Pathological activation of sensory neurons and the inflammatory sequelae are known as neurogenic inflammation and appear to be important in many organ systems, including the pancreas. Factors that stimulate primary sensory neurons include hydrogen ions, heat, leukotrienes, arachidonic acid metabolites, bradykinin, and proteases such as trypsin, all of which may participate in the generation of acute pancreatitis. The current review examines the cellular and molecular mechanisms involved in sensory nerve activation within the pancreas and the potential contribution of neurogenic inflammation to the pathogenesis of pancreatitis.
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PMID:Neurogenic inflammation and pancreatitis. 1555 Jul 64

Calcitonin is an endogenous regulator of calcium homeostasis, which acts principally on bone. At present, the principal indications for the therapeutic use of calcitonin are disorders involving hypercalcemia Paget's disease, acute pancreatitis, high-bone-turnover osteoporosis, pain associated with osteoporosis or bone metastases, and Sudeck's atrophy. The aim of this study was to compare the analgesic effects on postoperative pain of salmon calcitonin versus opioids administered epidurally. Our prospective study included 53 ASA I-II patients who were scheduled for total hip arthoplasty under epidural anaesthesia and who did not fulfill 1 or more of the exclusion criteria: a history of pituitary gland dysfunction; diabetes mellitus; obesity; contraindications to performing an epidural block and/or an allergy to calcitonin. These patients were randomly allocated into 3 groups (A, B, and C), each of which received postoperatively a different analgesic epidural mixture of 10 mL to control postoperative pain. Group A was given bupivacaine 0.5% (5 mL) + fentanyl 100 (2 mL) + NaCl 0.9% (3 mL). Group B was given bupivacaine 0.5% (5 mL) + salmon calcitonin 100IU (1 mL) + NaCl 0.9% (4 mL). Group C was given salmon calcitonin 100IU (1 mL) + NaCl 0.9% (9 mL). Perioperatively, 4 blood samples were taken from each patient at the following specific times: 1. Before the induction of anesthesia; 2. At the end of the operation and before the epidural administration of the analgesic mixture; 3. At the end of the first postoperative hour (1 hour after the administration of the analgesic mixture); and 4. At the end of the second postoperative hour (2 hours after the administration of the mixture). In each blood sample, glucose, cortisol, growth hormone, and prolactin plasma levels were determined in order to investigate the changes of these parameters as a result of the endocrine reaction to stress, and to pain relief. The analgesic solution was administered immediately after the second blood sample was taken. At the same time as the 4 blood samples were taken, haemodynamic parameters and pain scores were recorded. Epidural salmon calcitonin in combination with local anaesthetic produces an analgesic effect similar to fentanyl and with stable hemodynamic results. It also eliminates postoperative hyperglycaemia. The cortisol plasma level does not increase during the first postoperative hour, but increases significantly during the second postoperative hour. Growth hormone and prolactin plasma levels were stable in all patients in all 3 groups. This study shows that calcitonin is a suitable alternative for the treatment of acute postoperative pain.
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PMID:Epidural calcitonin: does it provide better postoperative analgesia? An analysis of the haemodynamic, endocrine, and nociceptive responses of salmon calcitonin and opioids in epidural anesthesia for hip arthroplasty surgery. 1715 40


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