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

Hypercalcemia is an important etiology to consider in the evaluation of acute pancreatitis. Not only is it a treatable cause, but understanding the basis for this etiology may provide new insight into the common biochemical mechanisms involved in the pathogenesis of pancreatitis. We report a case of an 11-year-old girl with hypercalcemia due to primary hyperparathyroidism who developed recurrent pancreatitis. We review clinical and experimental data that implicate hypercalcemia as the cause and discuss mechanisms for the association.
 ...
PMID:Recurrent acute pancreatitis in a child with primary hyperparathyroidism. 1918 94

Solid pseudopapillary tumor (SPT) of the pancreas is a rare pancreatic tumor mostly seen in young women. We here report a twelve-year-old girl presenting with recurrent attacks of pancreatitis. No history of a systemic disease, trauma, drug usage or infection was present. All other etiologic factors like familial, hypertriglyceridemia, hypercalcemia, cystic fibrosis, medications were excluded. On abdominal ultrasound a heterogeneous mass was noticed at the tail of pancreas. Computerized tomography and magnetic resonance imaging proved that the mass was cystic. The mass was surgically removed. The diagnosis was pancreatic solid cystic papillary epithelial neoplasm. Although acute pancreatitis due to SPT was exceptionally reported, this is the first description of SPT leading to recurrent pancreatitis especially in children.
 ...
PMID:Solid pseudopapillary tumor of the pancreas as a cause of recurrent pancreatitis. 1931 80

Hypercalcemia due to hyperparathyroidism is a rare etiology for acute pancreatitis, oscillating between 1.5 and 7% in the different series. Although the cause-effect relationship and the pathophysiology of the condition are not clear, it seems that the association among them is not incidental, and serum calcium could be a major risk factor, so that pancreatitis would come to occur during severe hypercalcemia attacks. Mutations in different genes have been proposed as well to justify why only some patients with primary hyperparathyroidism and hypercalcemia develop acute pancreatitis. References to cases like these ones are rare in the literature. We report two patients with acute pancreatitis associated with hyperparathyroidism and hypercalcemia, one of them with a fatal outcome.
 ...
PMID:Acute pancreatitis associated with hypercalcemia. A report of two cases. 1933 36

Acute pancreatitis and chronic pancreatitis are complex inflammatory disorders of the pancreas with unpredictable severity, complications, and clinical courses. Growing evidence for genetic risk and modifying factors, plus strong evidence that only a minority of patients with these disorders are heavy alcohol drinkers, has revolutionized our concept of these diseases. Once considered a self-inflicted injury, pancreatitis is now recognized as a complex inflammatory condition like inflammatory bowel disease. Genetic linkage and candidate gene studies have identified six pancreas-targeting factors that are associated with changes in susceptibility to acute and/or chronic pancreatitis, including cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), serine protease inhibitor Kazal 1 (SPINK1), cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsinogen C (CTRC) and calcium-sensing receptor (CASR). Patients with mutations in these genes are at increased risk of pancreatitis caused by a variety of stresses including hyperlipidemia and hypercalcemia. Multiple studies are reporting new polymorphisms, as well as complex gene x gene and gene x environmental interactions.
 ...
PMID:Genetic aspects of pancreatitis. 2005 46

Hypercalcemia is a relatively common finding after kidney transplant, and when correctly evaluated has been reported to be present in around 5-15% of patients. The peak of its incidence can be found after the third month from transplantation and it usually maintains relatively constant levels, even though a moderate attenuation of the phenomenon can be expected in the long term. Many factors have been claimed to cause hypercalcemia after kidney transplant. However, the main recognized factor is the degree of persistent hyperparathyroidism deriving from a long previous history of uremia. It has been suggested that hypercalcemia can be damaging to both graft (induction of nephrocalcinosis, reduction of graft survival) and other organ or system functions (vascular calcification, erythrocytosis, pancreatitis, etc.). However, there is no definitive demonstration of a cause-effect relationship between hypercalcemia and the above-mentioned clinical events. Furthermore, it is not possible to establish to what extent these effects are due to hypercalcemia per se or also to increased PTH levels, which are often associated with hypercalcemia. In addition, there is no definitive evidence that correction of hypercalcemia might solve the above-mentioned clinical events. The best way to reduce the incidence of hypercalcemia is considered to be the optimization of therapy for secondary hyperparathyroidism during the pretransplant period. It has long been thought that parathyroidectomy was the only way to solve the problem of stabilized hypercalcemia associated with moderate-severe persistent hyperparathyroidism after kidney transplant. The introduction of calcimimetics, which have substantially changed the therapeutic approach to secondary hyperparathyroidism in dialysis patients, seems to be promising also in this field. However, many issues need to be clarified before its definitive inclusion into the therapeutic armamentarium of the transplant patient who is already burdened by so many medications.
 ...
PMID:[Clinical impact of hypercalcemia after kidney transplant]. 2019 60

A 54-year-old man was transferred to our ICU because of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). He died after 38 days of intensive care. During treatment, his serum calcium (Ca) levels continued to increase and reached 3.95 mmol/L, while the ionized Ca levels reached 2.30 mmol/L before his death. He presented with severe kidney injury, pancreatitis, and hemorrhagic gastric erosion that worsened his prognosis; these were possibly associated with the hypercalcemia. His circulating 1alpha,25-dihydroxyvitamin D [1,25(OH)(2)D] level was elevated (75.7 to 204 pg/mL), whereas the levels of 25-hydroxyvitamin D, parathyroid hormone, and parathyroid hormone-related peptide were not. Liver histology revealed immunoreactivity for 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1) in some of the hepatocytes, in which the localization pattern was similar to that of lysozyme-positive hepatocytes. Our ICU has previously encountered 22 similar MODS patients who presented with hypercalcemia over the last 8 years. SIRS with severe kidney and liver injuries are common clinical findings in hypercalcemic patients with MODS. Of the 23 hypercalcemic MODS patients, including the present patient, 17 had circulating 1,25(OH)(2)D levels exceeding 70 pg/mL despite severe kidney injury. Extrarenal activation of CYP27B1 seems to play a role in the development of hypercalcemia in this disease condition. Clinicians need to be aware that severe hypercalcemia may occur in MODS patients.
 ...
PMID:A patient with severe hypercalcemia in multiple organ dysfunction syndrome: role of elevated circulating 1alpha,25(OH)2 vitamin D levels. 2020 Sep 33

This review discusses gastrointestinal manifestations of parathyroid diseases. Parathyroid hormone is the primary regulator of calcium physiology. Hypoparathyroidism can be idiopathic, hereditary, or secondary to surgery in the neck. Hyperparathyroidism is usually from adenomas or hyperplasia. Hypoparathyroidism is associated with steatorrhea that may improve with medium-chain triglycerides, correction of the hypoparathyroidism, or administration of vitamin D. Hyperparathyroidism results in constipation because of reduction in neuromuscular excitability by high calcium levels. According to old literature, the incidence of peptic ulcer disease (PUD) in patients with hyperparathyroidism is 9% compared with autopsy rates of 4% to 5%. Any association is difficult to prove today, as hyperparathyroidism is usually mild due to early detection of cases through routine automated measurements of calcium. In addition, PUD is less prevalent now than before the advent of proton pump inhibitors. The presence of ulcers or ulcer symptoms may correct in some patients after parathyroidectomy, suggesting an association. The incidence of pancreatitis in patients with primary hyperparathyroidism ranges from 1.5% to 12% and may be because of the hypercalcemia. Complicating the issue is secondary hyperparathyroidism in response to hypocalcemia from pancreatitis. Pancreatitis may improve in some individuals after parathyroidectomy. Pancreatitis may follow parathyroid surgery because of an acute rise in calcium levels with manipulation of the parathyroid glands or to a blunted response of calcitonin-producing cells from fatigue. Parathyroid diseases have a few distinct effects on the gut: steatorrhea in hypoparathyroidism, and constipation, PUD, and pancreatitis in hyperparathyroidism.
 ...
PMID:The parathyroids and the gut. 2048 90

Hypercalcemia, which results from the rate of calcium influx into the extracellular fluid exceeding the rate of calcium efflux from the extracellular fluid, has been reported as occurring in approximately 1% to 4% of the adult population in general, and anywhere from 0.5% to 3% of hospitalized adult populations. Hypercalcemia associated with primary hyperparathyroidism has frequently resulted in the development of pancreatitis and peptic ulcer disease; however, the pathophysiologic mechanism of this association remains uncertain. This article examines the etiology and differential diagnosis of hypercalcemia, in particular regarding its association with primary hyperparathyroidism.
 ...
PMID:Evaluation of hypercalcemia in relation to hyperparathyroidism. 2051 Jul 22

We report the case of a female patient with severe acute necrotizing pancreatitis associated with hypercalcemia as first manifestation of primary hyperparathyroidism caused by a benign parathyroid adenoma. Initially the acute pancreatitis was treated conservatively. The patient subsequently underwent surgical resection of the parathyroid adenoma and surgical clearance of a large infected pancreatic pseudocyst. Although the association of parathyroid adenoma-induced hypercalcemia and acute pancreatitis is a known medical entity, it is very uncommon. The pathophysiology of hypercalcemia-induced acute pancreatitis is therefore not well known, although some mechanisms have been proposed. It is important to treat the provoking factor. Therefore, the cause of hypercalcemia should be identified early. Surgical resection of the parathyroid adenoma is the ultimate therapy.
 ...
PMID:Acute necrotizing pancreatitis as first manifestation of primary hyperparathyroidism. 2055 45

Calcium sensing receptor (CaSR) mutations implicated in familial hypocalciuric hypercalcemia, pancreatitis and idiopathic epilepsy syndrome map to an extended arginine-rich region in the proximal carboxyl terminus. Arginine-rich motifs mediate endoplasmic reticulum retention and/or retrieval of multisubunit proteins so we asked whether these mutations, R886P, R896H or R898Q, altered CaSR targeting to the plasma membrane. Targeting was enhanced by all three mutations, and Ca(2+)-stimulated ERK1/2 phosphorylation was increased for R896H and R898Q. To define the role of the extended arginine-rich region in CaSR trafficking, we independently determined the contributions of R890/R891 and/or R896/K897/R898 motifs by mutation to alanine. Disruption of the motif(s) significantly increased surface expression and function relative to wt CaSR. The arginine-rich region is flanked by phosphorylation sites at S892 (protein kinase C) and S899 (protein kinase A). The phosphorylation state of S899 regulated recognition of the arginine-rich region; S899D showed increased surface localization. CaSR assembles in the endoplasmic reticulum as a covalent disulfide-linked dimer and we determined whether retention requires the presence of arginine-rich regions in both subunits. A single arginine-rich region within the dimer was sufficient to confer intracellular retention comparable to wt CaSR. We have identified an extended arginine-rich region in the proximal carboxyl terminus of CaSR (residues R890 - R898) which fosters intracellular retention of CaSR and is regulated by phosphorylation. Mutation(s) identified in chronic pancreatitis and idiopathic epilepsy syndrome therefore increase plasma membrane targeting of CaSR, likely contributing to the altered Ca(2+) signaling characteristic of these diseases.
 ...
PMID:Calcium sensing receptor mutations implicated in pancreatitis and idiopathic epilepsy syndrome disrupt an arginine-rich retention motif. 2079 21


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