Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.
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PMID:Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy. 985 22

A 37-year old woman, presenting with severe hypercalcaemia-associated pancreatitis with pseudocyst formation, was admitted to intensive care because she developed ARDS with respiratory failure. Skeletal metastasis from non-small cell bronchial carcinoma were subsequently diagnosed. After she developed arterial occlusion in the lower limb, supportive treatment was withdrawn. Severe pancreatitis is an exceedingly unusual presentation of non-small cell bronchial carcinoma. Concepts of diagnostic and therapeutic strategies in the context of suspected unusual pathology, and the concept of futility are briefly discussed.
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PMID:Lessons from an unusual case: malignancy associated hypercalcemia, pancreatitis and respiratory failure due to ARDS. 1004 93

The balance between the concentrations of free ionized Ca2+ and bicarbonate in pancreatic juice is of critical importance in preventing the formation of calcium carbonate stones. How the pancreas regulates the ionic composition and the level of Ca2+ saturation in an alkaline environment such as the pancreatic juice is not known. Because of the tight cause-effect relationship between Ca2+ concentration and lithogenicity, and because hypercalcemia is proposed as an etiologic factor for several pancreatic diseases, we have investigated whether pancreatic tissues express a Ca2+-sensing receptor (CaR) similar to that recently identified in parathyroid tissue. Using reverse transcriptase-polymerase chain reaction and immunofluorescence microscopy, we demonstrate the presence of a CaR-like molecule in rat pancreatic acinar cells, pancreatic ducts, and islets of Langerhans. Functional studies, in which intracellular free Ca2+ concentration was measured in isolated acinar cells and interlobular ducts, show that both cell types are responsive to the CaR agonist gadolinium (Gd3+) and to changes in extracellular Ca2+ concentration. We also assessed the effects of CaR stimulation on physiological HCO3- secretion from ducts by making measurements of intracellular pH. Luminal Gd3+ is a potent stimulus for HCO3- secretion, being equally as effective as raising intracellular cAMP with forskolin. These results suggest that the CaR in the exocrine pancreas monitors the Ca2+ concentration in the pancreatic juice, and might therefore be involved in regulating the level of Ca2+ in the lumen, both under basal conditions and during hormonal stimulation. The failure of this mechanism might lead to pancreatic stone formation and even to pancreatitis.
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PMID:Molecular and functional identification of a Ca2+ (polyvalent cation)-sensing receptor in rat pancreas. 1040 Jun 86

Alcohol consumption is the most important etiological factor of chronic pancreatitis (around 70%). Smoking, ethnic-racial predispositions, diets high and low in fat and high in protein may also contribute to the development of chronic pancreatitis. Non-alcoholic chronic pancreatitis of unknown cause makes up 10% to 30% of patients with chronic pancreatitis. Two subgroups have been reported: juvenile (about 25 years) and senile (up 65 years). Tropical pancreatitis has been observed in children and young men in many African and Asian countries. This disease develops because of fat and protein deficiency or nutritional deficiency in general, also due to cyanogenes present in cassava. Hereditary chronic pancreatitis is a rare disease connected with autosomal transmissions. Dr Whitcomb reported, that hereditary chronic pancreatitis developed because of trypsines mutation. Mutant "hypertrypsin" is not inactivated by enzymes; this way it leads to pancreas autodigestion. Obstructive chronic pancreatitis is caused by longterm pancreatic ducts obstruction. In many rare causes leading to chronic pancreatitis among other are: hypercalcaemia, hyperlipoproteinemia, some drugs and pancreatitis associated with autoimmune disorders. Newest information about etiology and pathogenesis of chronic pancreatitis is yielded by recent immunohistochemical research. This research shows increasing irregular improper antigens expression of class I and/or class II MHC in pancreas as well as the role of Transforming Growth Factor Alpha in chronic pancreatitis development. This illness is still a puzzling problem.
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PMID:[Contemporary opinions on the etiology of chronic pancreatitis]. 1050 45

In healthy subjects, the 3 known pancreatic trypsinogens, which are endopeptidases belonging to the chymotrypsin superfamily, are activated by enterokinase and partial autoactivation in the duodenum. The premature activation of trypsinogen in the pancreatic interstitium, with the subsequent activation of other pancreatic zymogens, is believed to lead to the autodigestion of the gland, this being the first event in acute pancreatitis. The mechanisms that lead to trypsinogen, activation in acute pancreatitis are largely unknown. However, ischemia, hypercalcemia and the activation of cathepsin B (by cholecystokinin) are thought to be of importance. The easiest and most reliable way to assess trypsinogen activation is the measurement of the activation peptide, TAP, in urine, plasma, pancreatic tissue or ascitic fluid. In the animal model of acute pancreatitis, TAP in ascites and pancreatic tissue has been shown to correlate with the presence and extent of necroses. It has proven to be a good marker for the severity of pancreatitis and is a useful marker in examining the pathophysiology and possible treatment modalities in the animal model of acute pancreatitis. Studies on TAP in human acute pancreatitis were most commonly focused on urinary TAP. Within a 48-hour time frame after the onset of the disease, TAP was a good predictor of the severity of acute pancreatitis. The main advantage over other markers, such as CRP, is that TAP is the earliest marker of necrosis to be increased. Also, increased levels of TAP in ascitic fluid were shown to correlate well with pancreatic necroses. In our experience, plasma TAP was found to have a "diagnostic window" within the first 3 days predicting pancreatic necroses. Positive TAP gave a very good positive prediction and a high specificity towards the development of pancreatic necroses, but did not differ between necrotizing pancreatitis with systemic complications or uncomplicated necrotizing pancreatitis. We therefore think that plasma TAP is a very good marker for local complication in acute pancreatitis and its routine measurements may help to identify patients at a high risk within the first days of the disease.
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PMID:Mechanism and role of trypsinogen activation in acute pancreatitis. 1057 41

We present a rare case of acute pancreatitis associated with temporal lobectomy due to intractable seizure in a 23-year-old man. The patient underwent elective right temporal lobectomy and hippocampectomy. Severe upper abdominal pain occurred just 10 hours after surgery. The diagnosis of acute pancreatitis was based on the elevation of serum amylase and lipase levels, and the findings of abdominal computerized tomography. Other possible causative factors of acute pancreatitis including alcohol, biliary tract stone, hypertriglyceridemia, hypercalcemia, hyperparathyroidism, biliary dysmotility and autoimmune disease were excluded by a series of examinations. The possibility of drug-induced pancreatitis was very low in this patient. The patient was discharged after supportive treatment. No recurrence of seizure or abdominal pain was noted in the three months after discharge. Acute abdominal pain after brain surgery deserves clinical evaluation for acute pancreatitis.
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PMID:Acute pancreatitis associated with temporal lobectomy and intractable seizure. 1074 19

Induction of acute pancreatitis follows a uniform mechanism independent of the different etiologic factors such as gallstones, alcohol, ischemia, hyperlipidemia, hypercalcemia, hereditary and others. Each cause seems to affect primarily the acinar cell, resulting in premature intracellular activation of trypsinogen and other digestive enzymes. Activated enzymes and oxygen free radicals injure the acinar cell and cause a release of cytokines and vasoactive mediators, attract inflammatory cells and activate the vascular endothelium as well as the expression of adhesion molecules. The disturbance of the pancreatic microcirculation induces a progression from edematous to necrotizing pancreatitis independent of the early intracellular events, including protease activation. Specific therapy must be directed towards microperfusion failure as a secondary pathogenetic step, since the initial enzyme activation and cytokine release is irreversible by the time of clinical presentation. In experimental designs comparable to the clinical situation the following therapeutic principles have proven beneficial: increase of blood fluidity by dextran, inhibition of leukocyte-endothelium interaction by ICAM-1 antibodies, and blockade of local vasoconstriction by endothelin-receptor antagonists.
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PMID:[New pathophysiologic knowledge about acute pancreatitis]. 1078 41

Milk alkali syndrome is rare and although pancreatitis secondary to hypercalcaemia is well recognised, there has only been one other reported case of pancreatitis secondary to the milk alkali syndrome. Such a case, caused by self medication of over the counter medication, is reported.
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PMID:Milk alkali syndrome-an unusual syndrome causing an unusual complication. 1087 6

Some clinical cases published in literature show that angiotensin-converting enzyme (ACE)-inhibitor administration may cause acute pancreatitis. In this work, the authors report a case of a patient affected by hypertension. Upon admission, the authors started antihypertensive therapy using captopril, which caused an important amylase and lipase rise within 13 days. When the ACE-inhibitor therapy was stopped, a rapid decrease of the serum enzyme was observed within 3 days. The high levels of serum amylase and lipase were linked to neutrophilia but were not associated with relevant symptomatic findings or features of pancreatopathy. The absence of the usual conditions that may cause pancreatitis, such as biliary stasis, hypercalcemia, or alcohol abuse, and the rapid decrease of serum enzyme levels after drug suspension suggested an ACE-inhibitor-induced pancreatitis. This is the first clinical report of an ACE-inhibitor-induced pancreatitis in which captopril administration was found after hospitalization. The drug suspension probably prevented other complications. This case report suggests that, when ACE-inhibitor administration is started, serum amylase and lipase should be monitored in order to prevent acute pancreatitis without waiting for clinical evidence of a pancreatopathy.
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PMID:Angiotensin-converting-enzyme inhibitor administration must be monitored for serum amylase and lipase in order to prevent an acute pancreatitis: a case report. 1157 Jun 65

Acute pancreatitis is a well-recognized complication of endoscopic retrograde cholangiopancreatography but is not considered to be a complication associated with other endoscopic procedures. We present a case of acute pancreatitis that occurred after uneventful upper and lower gastrointestinal endoscopy. The temporal relationship of the endoscopic procedures and development of acute pancreatitis suggests a causal relation. Furthermore, the patient had none of the usual etiologic factors associated with pancreatitis, i.e., alcoholism, cholelithiasis, hypertriglyceridemia, hypercalcemia, or use of a drug associated with pancreatitis. The causal mechanism of acute pancreatitis is uncertain but might potentially involve local trauma to the pancreas during a procedure or release of as yet undefined inflammatory mediators. In summary, three previous reports of clinical pancreatitis associated with endoscopy, in addition to the current case, suggests that acute pancreatitis should be considered as a rare complication of routine upper endoscopy or colonoscopy.
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PMID:Acute pancreatitis after gastrointestinal endoscopy. 1174 55


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