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

A 39-year-old white man with a history of right renal pelvic stones treated 1 year before by extracorporeal shock wave lithotripsy, but with no history of major surgery, alcoholism, pancreatitis, hyperparathyroidism or trauma, was admitted, suffering from an abdominal mass. Abdominal and pelvic computed tomography revealed an enlarged pancreatic head (9 cm in transverse diameter) with, inside it, a heterogeneous, cyst-like structure, measuring 7 cm in diameter. It was suspected that this lesion was a cystic neoplasm and the patient underwent a proximal pancreaticoduodenectomy and a cholecystectomy. After the operation, the microscopic findings ruled out the presence of a neoplasm and we were obliged to reconsider the case. Speculating as to the possible role of past extracorporeal shock wave lithotripsy in determining the pancreatic pseudocyst, it was found that damage to the intra-abdominal organs during extracorporeal shock wave lithotripsy has been mentioned in published series, but it was also noted that this case seemed to differ from the other published cases, where cirrhosis and thrombocytopenia, gallbladder stones, or adhesions between the pancreas and surrounding tissue caused by laparotomy were considered the causes of the lithotripsy complications. We suggest a direct traumatic disruption of the pancreas as a result of the extracorporeal shock wave lithotripsy and conclude that the post-lithotripsy follow-up should include periodic ultrasonographic investigation of the pancreas and serum amylase level determinations in order to diagnose pancreatic complications, if any, and plan the correct treatment.
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PMID:Pancreatic pseudocyst caused by extracorporeal shock wave lithotripsy for right renal pelvic calculi. 1274 7

Records of patients undergoing parathyroidectomy at our institute in the period 1991-2003 were retrospectively analyzed. Pancreatitis was associated in six of 87 patients (6.8%) with primary hyperparathyroidism (PHPT). Pancreatitis was the presenting symptom in five patients, while it developed postoperatively in one case. All patients with a past history of pancreatitis had suffered two or more attacks. All patients had a history of renal stone disease. Four patients also had overt bone disease with multiple fractures. Parathyroid adenoma (4) or carcinoma (1) was the cause in all patients. All five patients who underwent successful parathyroidectomy had resolution of pancreatitis on conservative management and no further attacks during a mean follow up of 28 months (3-84 months). Surgical exploration for parathyroid adenoma failed in one patient; this patient has had further attacks of pancreatitis. Repeat surgical exploration for parathyroidectomy has been advised. Hyperparathyroidism is a rare but treatable cause of pancreatitis. Parathyroidectomy has a salutary effect on the course of pancreatitis.
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PMID:Pancreatitis in patients with primary hyperparathyroidism. 1503 35

Treatment of giant cell lesions of the jaws is currently a subject of acute interest in the maxillofacial community. Based on their presumptive histological and biological similarities to both the "brown tumors" of hyperparathyroidism as well as proliferative vascular lesions, both calcitonin and interferon alpha administration have been attempted in patients suffering from these lesions. We present a case report of one young female in which both of these treatment modalities were instituted. We also discuss a rarely reported complication consisting of drug-induced lupus erythematosis and pancreatitis secondary to interferon alpha use.
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PMID:Complications of alpha-interferon therapy for aggressive central giant cell lesion of the maxilla. 1612 54

There is a high prevalence of protein-energy malnutrition (PEM) in chronic dialysis patients. Causes of PEM include the catabolic effects of hemodialysis treatments, acidemia associated with end-stage renal disease, common comorbid conditions, and uremia-induced anorexia. Morbidity and mortality increase with PEM. Before considering parenteral nutrition (PN) as a nutrition intervention in a maintenance dialysis patient, all other efforts to promote optimal nutrition need to be exhausted. The first step is careful evaluation of protein-energy status, followed by intensive nutrition counseling. If necessary, this is followed by oral nutrition supplementation, appetite stimulation, enteral tube feedings, and finally PN. Short-term parenteral nutrition (PN) became a crucial component of the management of a 38-year-old hemodialysis (HD) patient who endured serious complications after kidney transplant rejection. A profound and prolonged malnourished state followed her treatment for necrotizing pancreatitis. She had developed persistent hypercalcemia believed secondary to tertiary hyperparathyroidism (HPT) and immobilization. Later, she developed hungry bone syndrome (HBS) after parathyroidectomy (PTX). She also developed refeeding syndrome after initiation of PN. The patient's persistent, poorly understood hypercalcemia did not resolve even after PTX and removal of all other sources of vitamin D and calcium from her feedings, medications, and dialysis bath. The close communication of the inpatient and outpatient dialysis multidisciplinary teams became a key component to the successful outcome in this complex patient.
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PMID:The use of parenteral nutrition in a severely malnourished hemodialysis patient with hypercalcemia. 1620 98

Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As alcoholic pancreatitis is manifested at first as a rule by a potent attack, it is classified in this stage as acute pancreatitis. The most frequent etiological factors in our civilization are thus cholelithiasis and alcoholism (both account for 20-50% in different studies). The assumed pathogenetic principles in acute biliary pancreatitis are the common canal of both efferent ducts above the obturated papilla, duodenopancreatic reflux and intrapancreatic hypertension. A detailed interpretation is however lacking. The pathogenesis of alcoholic pancreatitis is more complicated. Among others some part is played by changes in the calcium concentration and fusion of cellular membranes. Idiopathic pancreatitis occurs in up to 10%, part of the are due to undiagnosed alcoholism and cholelithiasis. Other etiologies are exceptional. Similarly as in cholelithiasis pancreatitis develops also during other pathological processes in the area of the papilla of Vater such as dysfunction of the sphincter of Oddi, ampulloma and juxtapapillary diverticulum, it is however usually mild. The incidence of postoperative pancreatitis is declining. Its lethality is 30% and the diagnosis is difficult. In the pathogenesis changes of the ion concentration are involved, hypoxia and mechanical disorders of the integrity of the gland. Pancreatitis develops in association with other infections--frequently in mumps, rarely in hepatitis, tuberculosis, typhoid and mycoses. Viral pancreatitis is usually mild. In parasitoses pancreatitis develops due to a block of the papilla Vateri. In hyperparathyroidism chronic pancreatitis is more likely to develop, recent data are lacking. As to dyslipoproteinaemias, pancreatitis develops in the Ist, IVth and Vth type of Frederikson's classification, in rare recessive disorders and other conditions such as hypothyroidism, renal insufficiency, oestrogen substitution and others. In pancreas divisum chronic pancreatitis is more likely to develop. In exotic countries tropical pancreatitis is most frequent. It is however similarly as alcoholic pancreatitis primarily chronic. A very serious course is usual in traumatic pancreatitis. Risk factors of pancreatitis after ERCP are in particular undilated biliary pathways, dysfunction of the sphincter of Oddi and the use of a needle knife (bistoury). Medicamentous prevention is not substantiated. Drug induced pancreatic damage is much rarer than hepatotoxicity. Pancreatitis is caused most frequently by immunosuppressives, methyldopa, corticoids and oestrogens. The question remains to what extent the course of pancreatitis is influenced by its etiology. Biliary, alcoholic, traumatic and postoperative pancreatitis is usually severe, pancreatitis associated with viroses and induced by drugs is usually mild.
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PMID:[Etiological factors of acute pancreatitis]. 1673 20

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 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.
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PMID:Acute pancreatitis associated with hypercalcemia. A report of two cases. 1933 36

Hyperparathyroidism is a rare cause of pancreatic inflammatory disease, however their causal relationship has been widely accepted. The appropriate therapy is less clear when patients with hyperparathyroidism-associated pancreatitis develop complications such as pseudocysts. We describe a 51-year-old woman with primary hyperparathyroidism who developed pancreatic pseudocysts extending into the mediastinum. After the correction of hyperparathyroidism by removal of a parathyroid adenoma, the pseudocysts were resolved and no additional treatment was necessary. In patients with primary hyperparathyroidism who develop uncomplicated pancreatic pseudocysts, surgical correction of primary hyperparathyroidism may precede the interventional treatment on the pancreas when possible.
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PMID:Mediastinal pancreatic pseudocysts that were resolved following parathyroidectomy for primary hyperparathyroidism. 1975 72

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

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.
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PMID:The parathyroids and the gut. 2048 90


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