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)

Here we report a patient diagnosed with small cell lung cancer after first presenting with parathyroid hormone-related peptide-induced hypercalcemic pancreatitis and developed walled-off necrosis that resulted in disruption of the main pancreatic duct. Disconnected duct syndrome (DDS) is a rare syndrome that occurs when the main pancreatic duct exocrine flow is disrupted resulting in leakage of pancreatic enzymes and further inflammatory sequela. To date, no prior reports have described DDS occurring with paraneoplastic reactions. Diagnostic imaging techniques and therapeutic interventions are reviewed to provide insight into current approaches to DDS.
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PMID:First report of small cell lung cancer with PTHrP-induced hypercalcemic pancreatitis causing disconnected duct syndrome. 2906 79

Vitamin D deficiency state is endemic in the Kashmir valley of the Indian subcontinent. Clinicians frequently treat patients with Vitamin D for diverse clinical symptoms to improve the general health and to reduce the frailty of elderly and these doses may at times be inappropriately high. Vitamin D toxicity-induced acute kidney injury (AKI), often considered rare, can be life-threatening and associated with substantial morbidity if not identified promptly. We aimed to describe clinical and biochemical features, risk factors, and management of AKI patients with Vitamin D toxicity seen at a single tertiary care centre in Sher-i-Kashmir Institute of Medical Sciences, Srinagar, India, between January 2014 and January 2016. Evaluation included detailed clinical history and biochemical tests including serum calcium, phosphorus, creatinine, intact parathyroid hormone, and 25-hydroxyvitamin D [25(OH)D]. Nineteen patients with Vitamin D toxicity-induced AKI could be identified. Clinical manifestations included nausea, vomiting, altered sensorium, constipation, pancreatitis, AKI, acute on chronic kidney disease, and weight loss. Median (range) age was 64 (45-89) years. Median (range) serum 25(OH)D level and median (range) total serum calcium level were 99 (190-988) ng/mL and 139 (119-152) mg/dL, respectively. Overdose of Vitamin D caused by prescription of megadoses of Vitamin D was the cause of AKI in all cases. Median (range) cumulative Vitamin D dose was 6,000,000 (3,600,000-9,000,000) IU. On three- and six-month follow-up, the creatinine and estimated glomerular filtration rate normalized and returned to baseline in all patients except three cases who had underlying chronic kidney disease. Three patients needed rehospitalization for another episode of AKI. Our data demonstrate an emergence of Vitamin D toxicity as a cause of AKI in this part of the world. Irrational use of Vitamin D in megadoses resulted in AKI in all cases. Persistence of Vitamin D in the body for longer time resulted in rehospitalization of patients with AKI. Awareness among health-care providers regarding the toxic potential of high doses of Vitamin D and cautious use of Vitamin D supplements can have immense value to prevent this AKI.
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PMID:Acute kidney injury due to overcorrection of hypovitaminosis D: A tertiary center experience in the Kashmir Valley of India. 2926 43

Traditionally, classical complications of primary hyperparathyroidism are mainly represented by skeletal, kidney and gastrointestinal involvement. The old picture of osteitis fibrosa cystica is no longer commonly seen, at least in the western world. However, new imagining techniques have highlighted deterioration of skeletal tissue in patients with primary hyperparathyroidism not captured by traditional DXA measurement. Concerning the kidney, the most common consequences of excessive parathyroid hormone secretion are hypercalciuria and kidney stones; however, the exact pathogenesis of urinary stone formation is still unknown. The 2013 International Congress on the management of Asymptomatic Primary Hyperparathyroidism, emphasized the role of imaging techniques for early discovery of both skeletal and renal complications in asymptomatic patients. Gastrointestinal manifestations include acid-peptic disease, constipation, pancreatitis and gall stone disease. More studies are needed in this area to find the exact pathophysiological mechanism underlying these manifestations and the effect of parathyroid surgery.
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PMID:Classical complications of primary hyperparathyroidism. 3066 47

Hypercalcemia rarely causes acute pancreatitis due to secretory block in the pancreas and damage by accumulated proteases. Hypercalcemia, though described in granulomatous disorders, is uncommon in tuberculosis. Acute kidney injury is known to occur with acute pancreatitis, secondary to sepsis and septic shock; however, acute pancreatitis resulting in acute cortical necrosis is very rare. We report a 22-year-old woman, who presented with pain abdomen and vomiting. She was found to have features of acute pancreatitis, both biochemically and radiologically. She had hypercalcemia on presentation and this was attributed to be the cause for pancreatitis as other causes were ruled out. 1, 25-dihydroxyvitamin D level was high with normal parathyroid hormone level. Whole-body positron emission tomography-computed tomography showed increased fluorodeoxyglucose uptake in the terminal ileum and histology from that area showed noncaseating granuloma with acid-fast bacilli in the tissue. She was treated with antituberculosis therapy; hypercalcemia improved over a period of time and pancreatitis resolved. She developed anuric renal failure, and kidney biopsy showed patchy acute cortical necrosis. She is dialysis dependent at the end of 6 months. To the best of our knowledge, this is the first case report of a patient with ileal tuberculosis presenting with hypercalcemia and acute pancreatitis. This case is reported due to the rarity of extrapulmonary tuberculosis presenting with symptomatic hypercalcemia, acute pancreatitis, and acute renal cortical necrosis.
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PMID:Ileal Tuberculosis Causing Hypercalcemia and Renal Failure. 3081 95

Primary hyperparathyroidism (PHPT) is characterised by the overproduction of parathyroid hormone (PTH) due to parathyroid hyperplasia, adenoma or carcinoma and results in hypercalcaemia and a raised or inappropriately normal PTH. Symptoms of hypercalcaemia occur in 20% of patients and include fatigue, nausea, constipation, depression, renal impairment and cardiac arrythmias. In the most severe cases, uraemia, coma or cardiac arrest can result. Primary hyperparathyroidism in pregnancy is rare, with a reported incidence of 1%. Maternal and fetal/neonatal complications are estimated to occur in 67 and 80% of untreated cases respectively. Maternal complications include nephrolithiasis, pancreatitis, hyperemesis gravidarum, pre-eclampsia and hypercalcemic crises. Fetal complications include intrauterine growth restriction; preterm delivery and a three to five-fold increased risk of miscarriage. There is a direct relationship between the degree of severity of hypercalcaemia and miscarriage risk, with miscarriage being more common in those patients with a serum calcium greater than 2.85 mmol/L. Neonatal complications include hypocalcemia. Herein, we present a case series of three women who were diagnosed with primary hyperparathyroidism in pregnancy. Case 1 was diagnosed with multiple endocrine neoplasia type 1 (MEN1) in pregnancy and required a bilateral neck exploration and subtotal parathyroidectomy in the second trimester of her pregnancy due to symptomatic severe hypercalcaemia. Both case 2 and case 3 were diagnosed with primary hyperparathyroidism due to a parathyroid adenoma and required a unilateral parathyroidectomy in the second trimester. This case series highlights the work-up and the tailored management approach to patients with primary hyperparathyroidism in pregnancy. Learning points: Primary hyperparathyroidism in pregnancy is associated with a high incidence of associated maternal fetal and neonatal complications directly proportionate to degree of maternal serum calcium levels. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism in pregnancy and was used in the management of all three cases in this series. It is recommended when serum calcium is persistently greater than 2.75 mmol/L and or for the management of maternal or fetal complications of hypercalcaemia. Surgical management, when necessary is ideally performed in the second trimester. Primary hyperparathyroidism is genetically determined in ~10% of cases, where the likelihood is increased in those under 40 years, where there is relevant family history and those with other related endocrinopathies. Genetic testing is a useful diagnostic adjunct and can guide treatment and management options for patients diagnosed with primary hyperparathyroidism in pregnancy, as described in case 1 in this series, who was diagnosed with MEN1 syndrome. Women of reproductive age with primary hyperparathyroidism need to be informed of the risks and complications associated with primary hyperparathyroidism in pregnancy and pregnancy should be deferred and or avoided until curative surgery has been performed and calcium levels have normalised.
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PMID:Management of primary hyperparathyroidism in pregnancy: a case series. 3109 81


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