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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol consumption is the most important etiological factor of chronic pancreatitis (around 70%). Smoking, ethnic-racial predispositions, diets high and low in fat and high in protein may also contribute to the development of chronic pancreatitis. Non-alcoholic chronic pancreatitis of unknown cause makes up 10% to 30% of patients with chronic pancreatitis. Two subgroups have been reported: juvenile (about 25 years) and senile (up 65 years). Tropical pancreatitis has been observed in children and young men in many African and Asian countries. This disease develops because of fat and protein deficiency or nutritional deficiency in general, also due to cyanogenes present in cassava. Hereditary chronic pancreatitis is a rare disease connected with autosomal transmissions. Dr Whitcomb reported, that hereditary chronic pancreatitis developed because of trypsines mutation. Mutant "hypertrypsin" is not inactivated by enzymes; this way it leads to pancreas autodigestion. Obstructive chronic pancreatitis is caused by longterm pancreatic ducts obstruction. In many rare causes leading to chronic pancreatitis among other are: hypercalcaemia, hyperlipoproteinemia, some drugs and pancreatitis associated with autoimmune disorders. Newest information about etiology and pathogenesis of chronic pancreatitis is yielded by recent immunohistochemical research. This research shows increasing irregular improper antigens expression of class I and/or class II MHC in pancreas as well as the role of Transforming Growth Factor Alpha in chronic pancreatitis development. This illness is still a puzzling problem.
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PMID:[Contemporary opinions on the etiology of chronic pancreatitis]. 1050 45

The uremic milieu generates chronic stimulatory input to the parathyroid glands, which is mediated principally by low calcium, high phosphate and low calcitriol, and results in increased parathyroid hormone (PTH) synthesis and release and an increase in parathyroid mitotic activity with the development of monoclonal areas of nodular hyperplasia. Such glands do not fully express the machinery required to mediate the suppressive inputs to the parathyroids; the extracellular calcium receptor (CaR) and the vitamin D receptor (VDR) are both downregulated. In most of these patients ablation, by parathyroidectomy or ethanol injection, provides the only means of correcting the hyperparathyroidism; apoptosis in parathyroid cells is negligible and clinically irrelevant. In practice, surgery is often delayed by a doomed and ultimately futile attempt to effect control by medical means. Better predictors of the likely success or failure of optimal non surgical management are needed. Gland size exceeding 1 cm3 and elevated PTH despite hypercalcemia (implying loss of suppressibility by calcium), in the presence of good phosphate control and adequate calcitriol provision point strongly to eventual failure of medical treatment and the need for parathyroid ablation. Parathyroidectomy, usually subtotal, remains the standard management, with ultrasound guided injection of ethanol or calcitriol showing promise in some centers. The above scenario is unlikely to be changed greatly by the new emerging vitamin D metabolites, but calcimimetic agents may well increase the scope of non surgical management.
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PMID:Are parathyroidectomies still appropriate in chronic dialysis patients? 1101 87

A 15-year-old boy with chronic renal failure secondary to Alport's syndrome underwent living-related renal transplantation from his 48-year-old father. His primary immunosuppressive regimen was composed of tacrolimus, mizolibine, and methylprednisolone. The postoperative course was satisfactory with one episode of mild acute rejection, treated successfully with methylprednisolone pulse therapy. Two months later, hypercalcemia (11.8-13.2 mg/dl) and hypophosphatemia (2.5-3.0 mg/dl) were noted without any bone symptoms. The serum intact-parathyroid hormone (PTH) and serum alkaline phosphatase levels were 240 pg/ml and 2483 IU/l, respectively. Ultrasound studies revealed enlargement of the two parathyroid glands. Under the diagnosis of tertiary hyperparathyroidism, he underwent percutaneous ethanol injection (PEIT) into the left parathyroid gland. Although levels of serum calcium and phosphorus returned to normal ranges and the intact PTH level decreased to 95 pg/ml with the three injections, another injection was needed to normalize recurrent hypercalcemia 2 months later. The patient experienced only transient mild dysphonia and local pain after PEIT. Although PEIT is believed less effective than parathyroidectomy, it has some advantages such as applicability to high-risk patients, repeatability of treatment, low incidence and severity of side effects.
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PMID:A case of post-transplant hyperparathyroidism treated with ethanol injection. 1195 72

An 84-year-old woman was admitted to our hospital for the examination and treatment of painful right thyroid swelling on August 2, 2002. Thyroid ultrasonography showed a mass of about 6 cm in diameter at the right thyroid lobe. Aspiration biopsy cytology (ABC) of her mass showed a thyroid carcinoma. Her neck mass was cold on (123)I scintigraphy and hot on both early- and delayed- phase (201)Tl scintigraphy. Whole body (67)Ga scintigraphy scan showed a strong hot accumulation in the area from the right thyroid lobe to the right lateral lobe. Multiple lung tumors were observed from chest computed tomography (CT) scans. She was diagnosed as having an anaplastic thyroid carcinoma with metastatic lung tumors. As her thyroid carcinoma was inoperable, percutaneous injection therapy of lipiodol and ethanol (lip-PEIT) against the primary thyroid carcinoma was performed twice a week. However, the thyroid carcinoma gradually enlarged and oppressed her trachea. Two months after the initiation of lip-PEIT, parathyroid hormone-related protein (PTHrP)-dependent hypercalcemia was diagnosed because serum levels of calcium, phosphate and intact-PTHrP were 2.72 mmol/l (10.9 mg/dl), 0.71 mmol/l (2.2 mg/dl), 3.2 pmol/l, respectively. The hypercalcemia was reduced by the use of pamidronate. After one week she died of an airway obstruction caused by the developing thyroid carcinoma. Carcinoma cells with a mixed papillary and squamoid pattern were positively stained immunohistochemically by anti-PTHrP(1-34) antisera. Herein, we report a rare autopsy case of a PTHrP-producing thyroid carcinoma.
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PMID:Anaplastic thyroid carcinoma with humoral hypercalcemia of malignancy (HHM): an autopsy case report. 1525 75

Parathyromatosis, consisting of hyperfunctioning parathyroid tissues scattered throughout the neck, is a rare cause of recurrent hyperparathyroidism after parathyroidectomy. Medical management of patients with parathyromatosis usually is ineffective. Repeated surgery often is necessary, but generally is unsuccessful. We describe a case of parathyromatosis as a cause for recurrent hyperparathyroidism. A 32-year-old woman with a history of end-stage renal disease on hemodialysis therapy for 13 years developed secondary hyperparathyroidism requiring subtotal parathyroidectomy. Three years later, hyperparathyroidism relapsed. A technetium Tc 99m-sestamibi scan showed remnant parathyroid tissue on the left inferior thyroid lobe. Percutaneous ethanol infusion therapy failed to suppress parathormone excess, and neck exploration was performed. Histological examination of pathological lesions confirmed the diagnosis of parathyromatosis. Despite extended resection of multiple parathyroid nodules, symptoms worsened, leading progressively to severe morbidity. Imaging studies at this point showed widespread hyperfunctioning parathyroid tissue within the neck. The patient refused a third operation; thus, we resorted to coadministration of paricalcitol, a less hypercalcemic vitamin D analogue, and ibandronate, a new-generation bisphosphonate. Parathormone secretion was suppressed partially with this regimen, even at the expense of hypercalcemia and hyperphosphatemia. Sustained normalization of hormone levels and normocalcemia were accomplished only after substitution of ibandronate for the calcimimetic agent cinacalcet. The question of whether calcimimetics may maximize the chance of complete cure of parathyromatosis, especially when surgical treatment fails or is not feasible, remains to be answered by future studies.
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PMID:Parathyromatosis and the challenge of treatment. 1693 Dec 26

The medical records of 110 dogs treated for primary hyperparathyroidism were reviewed. Dogs were treated via parathyroidectomy (n=47), percutaneous ultrasound-guided ethanol ablation (n=15), or percutaneous ultrasound-guided heat ablation (n=48). Forty-five of 48 (94%) parathyroidectomies resulted in control of hypercalcemia for a median of 561 days. Thirteen of 18 (72%) ethanol ablation procedures resulted in control of hypercalcemia for a median of 540 days. Forty-four of 49 (90%) heat-ablation treatments resulted in control of hypercalcemia for a median of 581 days.
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PMID:Retrospective evaluation of three treatment methods for primary hyperparathyroidism in dogs. 1733 83

Persistent hyperparathyroidism is frequent in postrenal transplant patients. Percutaneous ethanol injection therapy (PEIT) is an alternative for treatment of patients with secondary hyperparathyroidism but it was not described in postrenal transplant patients. We report our experience with PEIT to control hyperparathyroidism in the post-transplant period. We performed PEIT under ultrasonographic guidance and local anesthesia in eight patients because of persistent secondary hyperparathyroidism after renal transplantation. Indications for PEIT were: high intact parathyroid hormone (iPTH) levels with hypercalcemia, hypophosphatemia, osteopenia and/or bone pain. All patients had at least one visible parathyroid nodule by ultrasonography. Biochemical assays were performed immediately before PEIT, between 1 and 7 days after last PEIT, and a mean of 8.0 +/- 2.8 months after PEIT. Serum iPTH and calcium levels decreased significantly after treatment and remained unchanged until final control. Serum iPTH decreased from 286.9 +/- 107.2 to 154.6 +/- 42.2 pg/ml (P < 0.01) after PEIT (percentual reduction 36.5 +/- 9.5%). This response was significantly correlated to total ethanol volume used (r: 0.94, P < 0.0001). Hypercalcemia disappeared in six of eight patients treated. Only minor complications were registered. There were no changes in renal function related to the treatment. Our findings show that PEIT is a useful and safe alternative for patients with persistent post-transplant secondary hyperparathyroidism.
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PMID:Percutaneous ethanol injection therapy in post-transplant patients with secondary hyperparathyroidism. 1788 71

Management of acute pancreatitis in pregnancy is based on expert opinion only, due to geographic and ethic variations. Nonbiliary causes should be sought as they are associated with worse outcomes. Alcohol as a cause of acute pancreatitis is not rare. Hemoconcentration as a marker of fluid deficit and severity should be predicted with caution and fluid resuscitation should be done carefully by closely monitoring the central venous pressure, cardiac and respiratory system. Hypercalcemia of hyperparathyroidism may be falsely lowered due to hypoalbuminemia or suppressed by magnesium tocolysis.
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PMID:Acute pancreatitis in pregnancy: an unresolved issue. 1996 May 59

The case of a parathyroid carcinoma in a 61-year-old woman is described. The patient was referred to our hospital, with the diagnosis of medullary thyroid carcinoma, after a prior thyroidectomy performed at another hospital. On admission, serum calcium was 3.92 mmol/l (n.r. 2.2-2.5), PTH level was 320 ng/l (n.r. 10-65), urinary cAMP was 508.9 mmol/mmol creatinine (n.r. 330- 630) and serum calcitonin was 2.1 ng/l (n.r.<10). The patient was then submitted to a complete neck exploration and multiple nodules were removed. Histopathological diagnosis of parathyroid carcinoma was made by local recurrence and retrospectively upon closer examination of the original specimen. After surgery, normocalcemia was achieved and maintained for about four months. Serum PTH decreased to 28.8 ng/l after surgery but increased quickly to 75.6 ng/l ten days later. Three months later, there was both biochemical and clinical evidence of disease. In the following eight months, calcium levels ranged from 2.99 mmol/l to 4-24 mmol/l and PTH from 135 ng/l to 1431 ng/l. However no distant metastases were found. To Control hypercalcemia, the patient was treated with bisphosphonates but normocalcemia was never achieved. A slight and transient reduction in serum calcium as response to an acute administration of octreotide, made us not to consider this eventual modality of therapy. Sonographically guided percutaneous injection of ethanol was performed but the treatment was not found to be effective. Finally, the use of chemotherapy with 5-fluorouracil, cyclophosphamide and dacarbazine was also unsuccessful. The patient died two years after the initial diagnosis.
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PMID:Difficulties in the management of a parathyroid carcinoma - case-report. 2160 21

Acute pancreatitis is a medical emergency. Alcohol and gallstones are the most common etiologies accounting for 60%-75% cases. Other important causes include postendoscopic retrograde cholangiopancreatography procedure, abdominal trauma, drug toxicity, various infections, autoimmune, ischemia, and hereditary causes. In about 15% of cases the cause remains unknown (idiopathic pancreatitis). Metabolic conditions giving rise to pancreatitis are less common, accounting for 5%-10% cases. The causes include hypertriglyceridemia, hypercalcemia, diabetes mellitus, porphyria, and Wilson's disease. The episodes of pancreatitis tend to be more severe. In cases of metabolic pancreatitis, over and above the standard routine management of pancreatitis, careful management of the underlying metabolic abnormalities is of paramount importance. If not treated properly, it leads to recurrent life-threatening bouts of acute pancreatitis. We hereby review the pathogenesis and management of various causes of metabolic pancreatitis.
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PMID:Metabolic pancreatitis: Etiopathogenesis and management. 2408 60


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