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)

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89

Indirect evidence suggests a causative role for intraperitoneal free fatty acids (FFA) in hypocalcemia associated with pancreatitis. We examined the effects of intraperitoneal injection of four naturally occurring FFAs on serum calcium in rats. Two saturated FFAs, stearate and palmitate, induced little or no hypocalcemia. Two unsaturated FFAs, oleate and linoleate, caused dramatic hypocalcemia in treated versus control rats (6.3 +/- 1.4 and 5.3 +/- 0.7 mg/dl, respectively, versus 10.1 +/- 0.6). Dose-response studies demonstrated that minute quantities of oleate (100 microliters per 250 g rat) caused marked hypocalcemia (7.2 +/- 0.3 mg/dl). Treated versus control rats also revealed a decrease in ionized calcium (3.15 +/- 0.2 versus 5.6 +/- 0.05 mg/dl) and magnesium (1.4 +/- 0.15 versus 2.0 +/- 0.10), an appropriate increase in PTH levels (1670 +/- 451 versus 396 +/- 235 pg/ml), and a fall in calcitonin levels (70.4 +/- 21.3 versus 47.5 +/- 16.4 pg/ml) but no change in albumin or phosphate levels. In vitro, the Ksp of calcium dioleate was shown to be 5.3 x 10(-8) m3/liter3; thus under physiologic conditions 100 microliters oleate binds 7.2 mg calcium, or approximately twice the total ECF ionized calcium in the rat. The amounts of intraperitoneal FFA that can easily be achieved in pancreatitis complex pathophysiologically significant amounts of calcium and may lead to severe hypocalcemia.
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PMID:Intraperitoneal free fatty acids induce severe hypocalcemia in rats: a model for the hypocalcemia of pancreatitis. 207 38

Over an 18 month interval at the University of Louisville Affiliated Hospitals, 40 patients were evaluated in a nonrandomized prospective study to determine the value of methylthionine chloride / tetramethylthionine chloride (methylene blue--MB) as an aid for the rapid intraoperative identification of parathyroid hyperplasia of end-stage renal disease (ESRD). Patients assigned to the MB infusion subgroup had infusion of 1 per cent MB (5.5 milligrams per kilogram) over a time interval of 25 to 60 minutes (mean of 43.9) prior to anesthetic induction. A total of 159 glands were identified in both the control and MB infusion groups (3.98 glands per patient) of which the predominant histopathologic diagnosis on frozen section was chief cell hyperplasia (78.3 per cent). Of 91 hyperplastic glands submitted for analysis after subtotal parathyroidectomy in those in the MB infusion group, 82 glands (90.1 per cent) were observed to have positive staining with identifiable differentiation from surrounding tissues. Analyses of the correlation of the serum calcium value and probability of MB staining or its relation to serum intact parathyroid hormone (intact-PTH) values were not statistically significant (p greater than 0.05, correlation coefficient equals 0.149). Furthermore, no relationship existed between the glandular size (millimeter to the third power) and probability of MB staining (chi-square equals 1.750, p greater than 0.05) or between hyperplastic size and serum intact-PTH value (correlation coefficient equals 0.068). Conversely, analysis of MB gland staining with regard to intact PTH concentration disclosed 59 of 59 glands stained intensely with MB when intact-PTH concentration was not less than 700 picograms per milliliter (p less than 0.01). Non-staining of hyperplastic parathyroid tissue was observed in 28.1 per cent of glands submitted for histopathologic analysis in which preoperative intact PTH values were more than 699 picograms per milliliter. Time of operation was reduced from 119.0 +/- 47.53 minutes (mean +/- S.E.M.) in control patients to 92.1 +/- 20.12 minutes (mean +/- S.E.M.) for the MB infusion group (V per cent equals 21.85, p less than 0.01). Furthermore, this technique appears to have value in the detection of ectopically located parathyroid tissue as demonstrated by the in vivo staining of seven ectopic glands in six patients of the infused group. Complications were restricted to the patients in the MB infusion group (21.7 per cent) and included: pseudo-cyanosis in three; pain in the infusion site in two, wound hematoma in one patient, pancreatitis in one and angina in one.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intraoperative localization of parathyroid glands using methylthionine chloride / tetramethylthionine chloride in secondary hyperparathyroidism. 257 72

Familial benign hypercalcemia, or hypocalciuric hypercalcemia, may be defined as a dominantly inherited disorder of calcium and magnesium metabolism, characterized by lifelong hypercalcemia and hypermagnesemia (both of variable degree), that usually is not associated with any symptoms, physical signs, reduced vitality, or ill health. Chondrocalcinosis, pancreatitis, gallstones, and neonatal primary hyperparathyroidism are possible rare associations, but findings differ among various studies. The biochemical findings are bland, with "normal" values for serum PTH by many techniques, modest hypophosphatemia, and other findings usually normal. A low calcium:creatinine clearance ratio is suggestive of, but not diagnostic for, FBH; urinary calcium excretion less than 100 mg per day may be just as helpful. The diagnosis should not be made casually or without family screening, because the findings in a given patient may be identical to those in mild primary hyperparathyroidism. The major rationale for careful evaluation is to diagnose the syndrome of FBH and to help affected family members avoid needless expense and the risk of further evaluation and treatment.
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PMID:Familial benign (hypocalciuric) hypercalcemia. A troublesome mimic of mild primary hyperparathyroidism. 267 70

Hypocalcemia frequently occurs in acute pancreatitis (AP), but its pathogenesis remains unknown. Since AP is often accompanied by acute alteration in the structure and function of cellular membranes, we investigated whether hypocalcemia associated with AP can be explained by acute translocation of Ca from extracellular to intracellular compartments. AP was induced in dogs by injection of autologous bile into the pancreatic duct, and in rats by controlled infusion of artificial bile containing Na-taurochlorate, Keflin, and trypsin into the cannulated bile duct. Plasma Ca, Mg, amylase, and PTH concentrations were determined in the serial samples. Tissue [Ca] and [Mg] were determined in pancreas, liver, kidney, and abdominal wall muscle biopsies obtained immediately before and 24 h after induction of AP in dogs or 2 h following induction of AP in rats to evaluate the temporal correlation between hypocalcemia and excessive intracellular Ca accumulation in soft tissues. Hypocalcemia (p less than 0.001) and hyperamylasemia (p less than 0.01) occurred within 6 h of AP in dogs, and persisted throughout. Plasma [Mg] was lowered and PTH activity was elevated at 6 and 18 h, and returned to a near normal level by 24 h. Concomitant with persisting hypocalcemia and lower ultrafilterable plasma [Ca2+], tissue [Ca] was significantly elevated in pancreas (71%), liver (24%), and abdominal muscle (112%), but was depleted in kidney by 25%. Pancreas biopsy following AP revealed histological signs of fulminant pancreatitis. [Mg] was depleted only in the pancreas (18%) and remained unaltered in other tissues. No significant changes were noted in the sham-operated animals. The observed temporal correlation between profound hypocalcemia and acute excessive intracellular Ca accumulation in soft tissues strongly suggests that hypocalcemia in AP may be precipitated by leaky-plasma-membrane-mediated excessive intracellular Ca accumulation. Similar data together with significantly reduced cellular energy charge (p less than 0.01) obtained from AP rats provided additional support to our hypothesis.
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PMID:Mechanism of calcium and magnesium translocation in acute pancreatitis: a temporal correlation between hypocalcemia and membrane-mediated excessive intracellular calcium accumulation in soft tissues. 339 93

A 44 year old Japanese woman with adult T-cell leukaemia (ATL) was admitted to Kyushu University hospital to receive a course of alpha-interferon treatment. She experienced a sudden onset of hypercalcaemia and epigastric pain associated with an increase in the level of pancreatic enzymes. Her serum parathyroid hormone related protein level was above normal although her high sensitive PTH level was within the normal range. Ultrasonography and computed tomography (CT) of the abdomen showed enlargement of the pancreas with indistinct margins and massive accumulation of extrapancreatic fluid. Cullen's sign was observed. A few days after the onset of acute pancreatitis, the serum amylase level increased to 3400 IU/L, and the serum calcium level fell to 4.2 mg/dL from 13.3 mg/dl. Her fasting blood glucose level increased to 242 mg/dL. Although the first episode of pancreatitis appeared to respond to treatment, she experienced a second episode of pancreatitis accompanied by an elevation of the serum calcium level. These findings suggest that acute pancreatitis was caused by hypercalcaemia associated with ATL.
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PMID:Acute pancreatitis induced by hypercalcaemia associated with adult T-cell leukaemia: a case report. 867 68

We present case report of primary hyperparathyroidism treated surgically as well as a review of literature concerning this subject. The disease of not well known etiology presents with elevated parathormon levels and hypercalcemia. Primary hyperparathyroidism which states 85% percent of all kinds of hyperparathyroidism is usually parathyroid adenoma, in 11-15% glandular hyperplasia and in 1-4% parathyroid cancer. Clinical symptoms are muscle weakness and fatigue, nephrolithiasis, occasionally peptic ulcers, pancreatitis, hypertension. Laboratory test reveal increased level of PTH, hypercalcemia, elevated alkaline phosphatase levels and decreased phosphorus levels. Diagnostic imaging techniques such as ultrasonography, MRI or CT have sensitivity about 52-75%. Highest sensitivity in localization of ectopic parathyroid adenoma has sestamibi scintigraphy with technetium-99. Skeleton x-rays show typical changes in distal parts of bones and osteopenia. Treatment of choice is surgical excision of adenoma. Normalization of PTH and calcium levels after surgery and improvement of renal, musculoskeletal and circulatory system function could be achieved in 95%. Most common complications are recurrent laryngeal nerve injury, hypo- or hyperparathyroidism, bleeding or stridor.
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PMID:[Primary hyperparathyroidism--case report and review of the literature]. 1682 51

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.
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PMID:[Clinical impact of hypercalcemia after kidney transplant]. 2019 60

Acute pancreatitis due to hypercalcemia secondary to primary hyperparathyroidism is a rare aetiology. We present a female patient with pancreatitis; with prior cholecystectomy, no alcohol usage or dyslipidemia. Laboratory studies showed, serum calcium 17.93 mg/dL and iPTH 441 pg/ml. Neck CT showed multinodular goiter and a parathyroid nodule. The patient underwent surgery after which serum Ca and PTH decreased. Biopsy showed follicular variant papillary thyroid carcinoma. This report discusses possible theories of association between parathyroid adenoma and hypercalcemic pancreatitis and describes the association with follicular variant papillary thyroid carcinoma, not previously described.
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PMID:[Hypercalcemia-induced pancreatitis in a patient with parathyroid adenoma and thyroid papillary carcinoma]. 2622 86


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