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Query: UMLS:C0020437 (hypercalcemia)
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A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.
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PMID:Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992-2002). 1623 10

Primary hyperparathyroidism is a clinical condition related to an excessive and abnormally regulated secretion of parathyroid hormone (PTH) from the parathyroid glands which is responsible for an alteration of the calcium and phosphorus metabolism. Parathyroid adenomas are the most important cause of primary hyperparathyroidism (80-85%). A case of parathyroid adenoma observed in a patient aged 47, admitted to the Emergency Medicine Department of our Hospital with a diagnosis of hypertensive crisis, cephalea, vomiting, and a clinical history of recurrent episodes of severe abdominal and renal pain, is presented. Lab data showed severe hypercalcemia and a progressive worsening of the renal function. A severe neurological involvement with stupor, derangement of mind, the arising of acute respiratory depression, lethargy compelled the colleagues to transfer him to the Intensive Care Unit; a neck ultrasonography showed a poor-echogenous area under the right thyroid inferior pole, with signs of vascularization. The suspect of a primary hyperparathyroidism related to a single adenoma of the parathyroid gland suggested a surgical treatment. A ''concise parathyroidectomy'' was performed. Our surgical approach was confirmed by the comparison of the preintervention and the post-intervention iPTH values: 2080 pg/mL (normal range: 12-65 pg/mL) before excision vs 101 pg/mL after the removal. The histologycal exam reported a parathyroid adenoma with large areas with haemorrage. Three days after surgery the patient was in good general conditions. Patients affected by primary hyperparathyroidism are often misdiagnosed because their clinical conditions can create differential diagnosis problems with other diseases. However the surgical option remains the gold standard treatment.
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PMID:Primary hyperparathyroidism related to a parathyroid adenoma: the dramatic clinical evolution of a misdiagnosed patient and its surgical solution. 1656 23

We report a case of bone pain associated with primary hyperparathyroidism in a patient with sickle cell disease. A 17-year-old girl with sickle cell disease (SS phenotype) was seen for bilateral knee and back pain. She had had recurrent severe vaso-occlusive crises and acute chest syndrome in the course of her disease. In the last 2 years, she had frequent visits to the emergency department for severe bone pain. She complained of long-standing fatigue and lethargy. Her physical examination was normal. Hydroxyurea treatment, as well as and long- and short-acting narcotics were given, with little improvement in symptoms. Poor compliance with medication, family dysfunction, and potential narcotic addiction were felt to be significant contributors to the patient's symptoms. She was incidentally found to have an extremely elevated total calcium level of 3.19 mmol/L (range: 2.25-2.76) with an ionized calcium level of 1.9 mmol/L (range: 1.15-1.35). Phosphorus level was 0.82 mmol/L (range: 0.90-1.50), alkaline phosphatase level was elevated at 519 U/L (range: 10-170), and parathyroid hormone level was extremely high at 1645 pg/mL (range: 10-60). Her renal function was normal. Ultrasonography of the neck and a Sestamibi scan revealed a single left inferior parathyroid adenoma adjacent to the thyroid lobe. There was no evidence of an underlying multiple endocrine neoplasia. The patient was diagnosed with primary hyperparathyroidism. Fluid hydration, hydrocortisone, calcitonin, and bisphosphonates were initiated for acute hypercalcemia management before surgical excision of the left parathyroid adenoma. On review of previous blood work, a borderline calcium level of 2.72 was present 18 months before this admission. Two years postsurgery, she has normal renal function, calcium, and parathyroid hormone levels. The weekly visits to the emergency department for pain episodes decreased to 1 every 2 months within the first few months after her surgery. The decrease in pain episodes, even if it coincided with the treatment of primary hyperparathyroidism, may still reflect the natural evolution of sickle cell disease in this patient. However, the high morbidity associated with primary hyperparathyroidism was successfully prevented in this patient. Primary hyperparathyroidism is rare in childhood. In a recent study, it occurred more commonly in female adolescents and was because of a single adenoma, as in our patient. Significant morbidity, mainly secondary to renal dysfunction, was because of the delay in diagnosis after the onset of symptoms (2.0-4.2 years), emphasizing the need for a rapid diagnosis. Sickle cell disease affects approximately 1 of every 600 blacks in North America. Acute episodes of severe vaso-occlusive crisis account for > 90% of sickle cell-related hospitalizations and are a significant cause of morbidity in patients. There is no known association between sickle cell disease and primary hyperparathyroidism, and this case is most probably a random occurrence. However, as emphasized by this case report, pain may also be a harbinger of other disease processes in sickle cell disease. Because management may vary, we suggest that care providers consider the diagnosis of vaso-occlusive crisis as the diagnosis of exclusion and that other etiologies for pain be envisaged in this patient population, especially in the presence of prolonged pain or unusual clinical, radiologic, or biological findings.
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PMID:Primary hyperparathyroidism mimicking vaso-occlusive crises in sickle cell disease. 1688 90

Primary hyperparathyroidism is rarely produced by parathyroid carcinoma. We present the case of a 63-yr-old man who was admitted due to recent onset of constipation, weakness and progressive lethargy. At physical examination, a left cervical mass was palpated. Marked hypercalcemia (serum calcium 25 mg/dl) (6.22 mmol/l) complicated by renal insuficiency (serum creatinine 4.4 mg/dl) (388 micromol/l) was found, but both were unresponsive to conventional therapy and hemofiltration. Autopsy examination showed a carcinoma of the upper left parathyroid gland, multiple foci of metastatic calficications in the vessel walls and parenchyma of both lungs and kidneys, and the myocardium, which contributed to multi-organ failure and death. In addition to describing the clinical presentation, we review the mechanism of metastatic calcifications as well as the role of renal function and hyperphosphatemia, and the basis for therapy of hypercalcemic crisis.
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PMID:Metastatic calcifications and severe hypercalcemia in a patient with parathyroid carcinoma. 1695 13

Multiple mycloma causes a disproportionate amount of the malignancy-related renal insufficiency. Acute renal insufficiency in myeloma patients can occur due to dehydration, hypercalcemia, side effects of medications (NSAIDs) or tumor lysis syndrome in addition to cast nephropathy, amyloidosis and light chain deposition disease. Patients on hemodialysis have traditionally been excluded from antineoplastic therapy due to fear of side effects and lack of studies addressing benefit. Melphalan is the most effective chemotherapeutic agent in myeloma and its PK (pharmacokinetics) are not adversely affected by impaired renal function. Because of more pronounced toxicity of Melphalan 200 mg/m2 conditioning regimen, Melphalan 140 mg/m2 has become the standard of care. 24% of patients become dialysis-independent at a median of 4 months after autotransplantation. Favorable factors for becoming dialysis independent were duration of dialysis <or=6 months and pretransplant creatinine clearance >10 ml/min. While no good data are available on the use of thalidomide in the presence of renal failure, it is our experience that severe neuropathy, constipation, lethargy and bradycardia are more frequent in patients with creatinine >or=3 mg/dl. It has become apparent that bisphosphanates-zoledronic acid more than pamidronate-cause renal dysfunction. If patients remain dialysis-dependent after autotransplantation, we recommend to delay considering a renal transplant until at least 3 years after the first transplant.
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PMID:High-dose therapy in patients with plasma cell dyscrasias and renal dysfunction. 1707 30

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.
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PMID:Vitamin D toxicity redefined: vitamin K and the molecular mechanism. 1714 39

Primary hyperparathyroidism (PHPT) is classically thought of as the somatic manifestation of hypercalcemia in which patients suffer from a variety of complaints including abdominal pain, nephrolithiasis, osteopenia, and mental status changes. Contemporary PHPT patients are generally free of somatic manifestations and are most often diagnosed when routine biochemical testing shows an elevated serum calcium level. The modern day patient may present with much more subtle neurocognitive symptoms including fatigue, lethargy, muscle weakness, depression, and cognitive impairment. Advances in imaging technology, intraoperative parathyroid hormone measurement, and surgical technique now allow parathyroidectomy to be performed using a focused approach without the absolute need of a four-gland exploration. Minimally invasive techniques allow the procedure to be accomplished under local anesthesia on an outpatient basis. This brief review summarizes the presentation, biochemical evaluation, operative intervention, and follow-up care of the modern day PHPT patient.
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PMID:Primary hyperparathyroidism. 1760 56

A 10-year-old female Dachshund was presented with a history of mammary masses, slight lethargy, polyuria, and polydipsia. Physical examination findings included masses involving the first, second, and fourth mammary glands of the left side. The mandibular, axillary, and right popliteal lymph nodes were mildly enlarged. Serum chemistry results included hypercalcemia (13.9 mg/dL, reference interval 8.0-11.5 mg/dL). Although intact parathyroid hormone (PTH) concentration (1.05 pmol/L) was below the reference interval (2-13 pmol/L), PTH-related protein (PTHrP) concentration was markedly increased (9.40 pmol/L, reference value < 2 pmol/L). The masses were surgically removed, and the histopathologic diagnosis was complex mammary carcinoma. Three weeks after surgery, serum total calcium concentration had decreased to 10.5 mg/dL. Resolution of the hypercalcemia and clinical signs supported a diagnosis of humoral hypercalcemia of malignancy associated with mammary gland carcinoma.
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PMID:Hypercalcemia and high parathyroid hormone-related peptide concentration in a dog with a complex mammary carcinoma. 1804 7

An 11-year-old male castrated Australian Shepherd was presented with a history of lethargy, panting, and weight loss for 1 month. Physical examination revealed a moderately enlarged spleen. Laboratory abnormalities included thrombocytopenia and marked hypercalcemia, with hyperglobulinemia, hypoalbuminemia, and a monoclonal spike in the beta-globulin region on serum protein electrophoresis. Serum total calcium concentration was markedly increased (16.5 mg/dL, reference interval 8.9-11.4 mg/dL) but ionized calcium concentration (1.39 mmol/L) was within the reference interval (1.25-1.45 mmol/L). Isosthenuria was noted, but the dog was not polyuric or polydipsic. Serum parathyroid hormone concentration was within reference limits and parathyroid hormone-related peptide concentration was 0 pmol/L. Radiographic findings were largely unremarkable. Results of cytologic evaluation of a fine-needle aspirate specimen from the spleen indicated plasma cell neoplasia. Based on the results of the electrophoresis, splenic aspirates, radiographs, and hypercalcemia, a diagnosis of splenic multiple myeloma was made. The marked hypercalcemia, normal ionized calcium and parathyroid hormone concentrations, and lack of osteolytic lesions indicated a presumptive increase in protein-bound serum calcium, likely due to binding to molecules of the paraprotein (M protein). Protein binding of calcium in dogs with multiple myeloma should be considered as a potential mechanism of elevated total serum calcium concentration.
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PMID:Presumptive increase in protein-bound serum calcium in a dog with multiple myeloma. 1917 Oct 18

We retrospectively studied seven children (six girls, one boy) aged from 7.5 to 25 months who presented to our institution after taking large doses of vitamin D (900 000-4 000 000 U) prescribed by medical practitioners for wrong indications like failure to thrive, etc. The clinical manifestations were constipation, decreased appetite, lethargy, polyuria, dehydration and failure to thrive. All patients had hypercalcemia (serum calcium ranging from 12 to 16.8 mg/dl), high 25[OH]D levels (ranging from 96 to >150 ng/ml), suppressed intact parathyroid hormone (ranging from <3 to 8.1 pg/ml). Hypercalciuria (urinary calcium/creatinine ranging from 1 to 2.45) was found in all patients, while nephrocalcinosis was present in five patients. All were treated with intravenous fluids, oral prednisolone, restriction of calcium in diet, while four patients received pamidronate infusion for reducing hypercalcemia.
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PMID:Hypercalcemia due to hypervitaminosis D: report of seven patients. 1933 14


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