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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.
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PMID:[Interaction between gastrointestinal hormones and endocrine regulation]. 0 83

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

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.
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PMID:Pancreatitis and renal disease. 31 21

Serum calcitonin (Ct) levels, serum calcium, and urine amylast were analyzed in 29 patients with an acute pancreatitis collected at random. In two of the patients the acute pancreatitis complicated a primary hyperparathyroidism. It was found that the calcitonin levels in serum were usually elevated during the acute phase of the pancreatitis. During this phase of the disease 22 of 27 examined patients had Ct-values above the upper normal limit of 1 mug/ml. The patients with normal Ct-values also had moderately elevated amylast values and a less pronounced pancreatitis. Normal Ct-values were usually found in patients more than 10 days after the onset of symptoms. Serum calcium was mostly within normal limits. However, a slight fall in serum calcium or low values was recorded in six patients with a pronounced disese. One patient with hyperparathyroidism normalized a previously elevated serum calcium during the calcitonin release.
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PMID:Serum calcitonin in acute pancreatitis in man. 83 66

A female with premary hyperparathyroidism and secondary renal lesions, as well as lesions of the stomach and pancreas is described. The initial illness was manifested by repeated renal crises. Later, gastroenterological complaints appeared--epigastralgia, vomiting, frequent hematemesis with melena. That was the cause for a gastric resection, diffuse erosive gastritis being found. After the operation, the pains and the vomiting of hematin matter repeatedly recidivated. Clinically and at the laboratory, data were formed for a chronic recidivating pancreatitis with the presence of primary hyperparathyroidism. The postoperative treatment of the parathyroid adenoma led to an improvement of the gastroenterological complaints.
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PMID:[Chronic recurrent pancreatitis with erosive gastritis in a patient with primary hyperparathyroidism]. 101 31

The major symptoms presented by the elderly patient with primary hyperparathyroidism (HPT) were studied in 30 patients, all of whom were over 70 years of age (70-89). Neuromuscular symptoms, fatigue or mental symptoms were the main complaint in 14 patients. Nephrolithiasis, pancreatitis, skeletal changes or thyroid diseases were associated with HPT in 13 patients. Three patients were considered to be asymptomatic. Seven out of the eight patients with neuromuscular symptoms, and two of the three patients with extreme fatigue as the dominant symptom, improved postoperatively. This study indicates that for elderly patients with HPT especially when associated with neuromuscular symptoms or fatigue, surgical therapy is the treatment of choice.
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PMID:Indications for surgery in the elderly patient with primary hyperparathyroidism. 102 May 88

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.
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PMID:Pancreatitis after renal transplantation. 109 48

The only causal treatment of primary hyperparathyroidism (PHPT) is parathyroidectomy. There are indications in the literature that despite operation expectation of life is shortened because of an increased frequency of cardiovascular and malignant diseases leading to the recommendation for early surgery even in uncomplicated PHPT. It is easier to convince an asymptomatic patient of an operation when he is informed about complications and consequences of an expectative attitude. Therefore, we reviewed our 71 patients operated upon during a 4-year-interval, 58 of whom were followed-up. During 82 operations 115 pathologically altered parathyroid glands were removed. Two persistent paralyses of the recurrent nerve occurred, however, without alteration of the voice. Follow-up of 82% of patients revealed 2 cases of recurrent nephrolithiasis (1 hypercalcaemia, 1 normocalcaemia). Three (5%) true recurrences were found, but neither a pancreatitis nor a peptic ulcer was noted during long-term follow-up. None of the 137 patients operated for a bleeding or perforated peptic ulcer during the last 10 years and 1 of 55 patients with acute pancreatitis during the past 8 years suffered from a PH-PT. However, morbidity and mortality of these two conditions was high. Although correlation to PHPT was low we recommend early operation of PHPT because of the low morbidity rate, zero lethality and reduced expectation of life.
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PMID:[Preventive or therapeutic parathyroidectomy in primary hyperparathyroidism]. 140 51

In pregnant women with symptomatic hyperparathyroidism, parathyroidectomy should be undertaken during the second trimester. We feel that the woman who is initially diagnosed well into the third trimester should be treated medically unless the hypercalcemia worsens or other complications occur. Since the treatment of asymptomatic hyperparathyroidism itself is controversial, it is even more difficult to define the treatment plan for an asymptomatic pregnant patient who has primary hyperparathyroidism. However, a recent consensus panel recommended that young patients with asymptomatic hyperparathyroidism be treated surgically. Accordingly, we believe that the asymptomatic pregnant patient should also be treated surgically, preferably in the second trimester. Whether a patient is treated medically or surgically in these situations, the pregnancy should be considered high-risk. The neonate should be monitored carefully for signs of hypocalcemia or impending tetany. If the mother is treated medically to term (or if spontaneous or elective abortion occurs), the mother should be monitored for hyperparathyroid crisis postpartum. Sudden worsening of hypercalcemia can result from the loss of the placenta (active placental calcium transport may be somewhat protective) and dehydration. Finally, every effort should be made to make the definitive diagnosis early in pregnancy in order to initiate optimal management. The diagnosis should be suspected during pregnancy if the following conditions exist: appropriate clinical signs or symptoms (especially nephrolithiasis or pancreatitis), hyperemesis beyond the first trimester, history of recurrent spontaneous abortions/stillbirths or neonatal deaths, neonatal hypocalcemia or tetany, or a total serum calcium concentration greater than 10.1 mg/dL (2.52 mmol/L) or 8.8 mg/dL (2.2 mmol/L) during the second or third trimester, respectively.
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PMID:Hyperparathyroidism and pregnancy: case report and review. 150 54

In 1957, Cope and his associates first noted 2 cases of pancreatitis associated with primary hyperparathyroidism. They emphasized the association of hyperparathyroidism and pancreatitis. Since then pancreatitis has become a diagnostic clue to primary hyperparathyroidism. We report herein a 39-year-old woman who had suffered from acute relapsing pancreatitis 3 times in the past 2 years. Hypercalcemia persisted throughout the course. A movable mass 3 x 3 cm in diameter was noted over the right thyroid area on physical examination. A hypoechogenic mass 3.5 x 2.7 x 1.4 cm was found between the right lobe of the thyroid and the carotid artery. Because of a persistently high serum level of Ca2+, normal saline and furosemide were infused; the serum Ca2+ decreased gradually. After aspiration of the suspected mass, the serum level of Ca2+ increased from 8.7 mg/dL to 18 mg/dL. Because of the impression of parathyroid adenoma, surgery was performed and a 3 x 2.5 x 1.5 cm well-encapsulated mass was excised without difficulty. Pathologic examination revealed a well-encapsulated parathyroid adenoma. This case reveals that primary hyperparathyroidism maybe one of the causes of pancreatitis, and aspiration cytology, although it may be helpful for the diagnosis, can aggravate the hypercalcemia.
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PMID:Acute relapsing pancreatitis in primary hyperparathyroidism with hypercalcemia aggravated after aspiration cytology: report of a case. 168 89


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