Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium homeostasis was studied serially in six patients admitted to the surgical intensive care unit because of acute pancreatitis. All developed ionized hypocalcemia. Serial assays of serum parathyroid hormone (PTH) revealed a prompt response to this hypocalcemia (1143 +/- 239 versus 574 +/- 24 pg/ml, P less than 0.05). Serum 1,25-dihydroxyvitamin D (1,25(OH)2D) levels rose from 26 +/- 8 to 104 +/- 17 pg/ml (P less than 0.01) in the expected time frame subsequent to the PTH peak, confirming the biologic significance of the PTH increases observed. Despite these significant elevations of PTH and 1,25(OH)2D, the expected prompt return of ionized calcium concentrations to normal levels was not seen. Also, urinary cyclic adenosine monophosphate production was not stimulated. These results suggest an acute functional resistance of bone to physiologic levels of PTH stimulation during the acute phase of pancreatitis. Fluid sequestration and hypovolemia are marked at this time. We suggest that pancreatitic hypocalcemia may occur when oligemic bone cannot respond normally to PTH and 1,25(OH)2D stimulation. As such, it may represent an end organ failure syndrome associated with shock and poor tissue perfusion.
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PMID:Calcium homeostasis in patients with acute pancreatitis. 619 46

Six patients receiving total parenteral nutrition (TPN) developed hypercalcemia and acute pancreatitis. Four were long-term home TPN patients, and two were short-term hospital TPN patients. Causes of pancreatitis other than hypercalcemia were not found. The etiology of the hypercalcemia remained unclear and in particular was not due to calcium infusion or hyperparathyroidism. In 4 patients in whom it was measured, the plasma parathyroid hormone was normal (in 2) or nondetectable (in 2). Hypercalcemia and pancreatitis subsided with discontinuation of TPN. Thus, some patients receiving TPN develop hypercalcemia, and in some of these pancreatitis ensues.
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PMID:Pancreatitis in association with hypercalcemia in patients receiving total parenteral nutrition. 677 4

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.
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PMID:Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction. 701 27

To assess the coexistence of pancreatic alterations and elevation of parathyroid hormone (PTH) as contributors to morbidity, a study correlating evidence of histological pancreatitis with elevated PTH has been undertaken. A retrospective autopsy study of pancreatic histology in 21 patients who died during maintenance hemodialysis (MD) (group I) compared their level of serum PTH with a group of patients who died without historical or clinical evidence of renal insufficiency (group II). Each patient in this group had creatinine clearance of less than 5 ml/min and had been treated with hemodialysis from 4 to 120 months preceding death. There was a difference in the incidence of histological and PTH levels between groups I and II. A total of 15 out of 21 (71.4%) of group I patients had severe pancreatic disease. By contrast, none of the group II control patients had marked pancreatic disease (p less than 0.01). Also a statistically different demarcation was present between groups I and II on the basis of PTH levels. Group I patients with pancreatic disease (n = 5) had a higher PTH level (567 +/- 76 pg/ml) than those (n = 6) without diseased pancreata (218 +/- 6.5 pg/ml). These data infer that a possible correlation between measured iPTH excess and histological alterations in pancreas may exist.
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PMID:Pancreatic disease in uremia and parathyroid hormone excess. 717 79

A 32-year-old man with insulin-dependent diabetes secondary to chronic calcifying pancreatitis of alcoholic origin in whom hypocalciuria (22 to 88 mg/24 hours) was discovered by chance, renal function being normal. Plasma phosphate levels were between 25 and 35 mg/l and the level of parathyroid hormone was at the upper limit of normal. Cervicotomy led to the discovery of three parathyroid glands which were removed. Their weight was increased and their histological appearance normal. The fourth parathyroid was not seen. Hypercalcaemia and hypocalciuria were found during the operation and persis 3 years after, with none of the usual causes being found. This patient has a certain number of characteristics reminiscent of familial hypercalcaemia-hypocalciuria syndrome: high plasma calcium levels associated with low calciuria despite normal renal function and a plasma parathyroid level normal in most cases. The physiopathology of this syndrome remains unknown. Its course is benign, without renal complications. Partial parathyroidectomy is ineffective.
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PMID:[An unrecognised cause of hypercalcaemia: hypercalcaemia-hyocalcluria syndrome]. 736 69

Surgery of primary hyperparathyroidism. Primary hyperparathyroidism is usually caused by a single parathyroid adenoma, rarely by multiple adenomas or hyperplasia and in 1-2% of cases by carcinoma. The definitive cure of the disease can be achieved only by surgical means. Unfortunately, only 10% of expected cases based on the number of population are diagnosed in Hungary. The main reason is that the disease has no specific symptoms and it causes only a few cases present with clinical entities such as nephrolithiasis, osteoporosis-osteopenia, pancreatitis, hypertension, peptic ulcer disease, depression, etc. The clue to the diagnosis of primary hyperparathyroidism is usually the laboratory result of hypercalcemia and in order to this aim the measurement of serum Ca would be an obligatory part of routine laboratory investigation in Hungary. The diagnosis of primary hyperparathyroidism rests on the laboratory confirmation of increased serum calcium and inappropriately elevated intact parathyroid hormone concentrations. If surgical intervention is planned, cervical ultrasonography and parathyroid-scintigraphy are indicated for the exact localization of hyperfunctioning parathyroid gland(s). CT and/or MRI are usually not necessary, except in cases of previous neck operation. The operation must be performed by surgeon skilled in parathyroid surgery. The surgical success can be assessed intraoperatively by the use of a gamma probe or by intraoperative measurement of parathyroid hormone concentrations in the serum or in the removed tissue(s). Support of these procedures is recommended. Although many recent publications deal with the minimal invasive methods of parathyroidectomy, the cost-effectiveness of these newer techniques are controversial.
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PMID:[Surgery of primary hyperparathyroidism]. 1722 13

A 38-year-old male was admitted to our hospital with epigastric pain, and he was confirmed to have acute exudative pancreatitis. After the episode of acute pancreatitis subsided, laboratory investigation revealed increased serum calcium (12.0 mg/dl), decreased serum phosphorus (2.7 mg/dl), and increased serum parathyroid hormone (intact) levels (131 pg/ml). A computed tomography (CT) scan of the neck did not reveal any mass lesions in the parathyroid gland. However, (99m)Tc sestamibi scintigraphy revealed that there was one functioning parathyroid gland in the upper mediastinum. Combined (99m)Tc sestamibi scintigraphy and CT scan confirmed the diagnosis of primary hyperparathyroidism in the mediastinum. Microscopic examination revealed the presence of a parathyroid adenoma (1.3 x 0.4 cm(2)) adjacent to the atrophic parathyroid gland in right thymus gland. We report the case of a patient diagnosed with primary hyperparathyroidism due to an ectopic mediastinal parathyroid adenoma. An ectopic mediastinal parathyroid adenoma may manifest as an episode of acute pancreatitis. Preoperative investigation to determine the exact location of an adenoma should include two types of imaging studies, preferably (99m)Tc sestamibi scintigraphy and CT of the neck and chest.
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PMID:Ectopic mediastinal parathyroid adenoma: a cause of acute pancreatitis. 1959 3

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.
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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

Hypercalcemia and hypophosphatemia are frequently observed in recipients of a kidney transplant (KTx). Hypercalcemia has been reported in up to 66% of KTx patients. Many factors have been suggested as the putative causal factors; however, the persistence of moderate-severe secondary hyperparathyroidism, associated with a change in the set-point of the Ca-controlled parathyroid hormone (PTH) secretion, is considered to play a prominent role. Hypercalcemia can negatively impact on both the graft and patient outcome, increasing the incidence of nephrocalcinosis, which can induce a worse graft outcome, inducing vascular calcifications, and increasing the incidence of pancreatitis. In addition, severe hypercalcemia after KTx often requires parathyroidectomy, which is not universally considered a safe medical solution in this clinical setting. After KTx, phosphate levels often fall below the normal range, with hypophosphatemia being observed in up to 40% of patients. The putative causal factors for this metabolic alteration are persistent hyperparathyroidism, increased levels of FGF-23, tubular damage secondary to the immunological effects, and toxic and vascular effectors. Hypophosphatemia can negatively impact on either skeletal or muscular systems, contributing to the increased incidence of bone fractures in KTx patients. The current therapeutic options should take into account an accurate pretransplant treatment and screening of the waiting-list patient and should also evaluate the efficacy and safety profile of the new pharmacological tools (calcimimetics) in comparison with the classical surgical approach (parathyroidectomy).
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PMID:Calcium and phosphate changes after renal transplantation. 2117 Aug 77

Coexistence of primary hyperparathyroidism and acute pancreatitis has widely been reported in literature, but a causal relationship remains controversial. A case of acute pancreatitis as a first symptom of primary hyperparathyroidism with severe hypercalcemia is reported. In this patient a reduction of serum calcium level was obtained with medical therapy and resulted in the resolution of acute pancreatitis symptoms within 10 days. At the same time a parathyroid adenoma was clinically identified and elective parathyroidectomy was performed with complete normalization of intact parathyroid hormone and serum calcium level. At three-year follow-up, no recurrence or complications of pancreatitis were documented. The presented case suggests a cause and effect relationship between acute pancreatitis and severe hypercalcemia which should be kept in mind in the differential diagnosis of non-biliary, non-alcoholic acute pancreatitis. Reduction of hypercalcemia with medical treatment can represent a good chance for elective surgical neck exploration.
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PMID:Acute pancreatitis associated with primary hyperparathyroidism. 2128 93


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