Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients having high-level quadriplegia developed elevated serum calcium concentrations (11 to 15.8 mg/100 ml) within three months of injury. All were young males (ages 15 to 19 years) and quadriplegic (C4-C7). Presenting symptoms were nausea, vomiting, polydipsia, polyuria and lethargy. In two patients severe muscle wasting and cachexia with clinical symptoms developed and persisted for several months. Laboratory studies in all patients showed negative calcium balance with hypercalciuria. Reduced renal function was seen in all patients but returned to normal with return of normal serum calcium. Alkaline phosphatase level was normal in three and elevated in one. Serum parathormone levels were normal. Roentgenograms revealed diffuse demineralization. Nephrocalcinosis and soft tissue calcifications developed in one patient. Primary treatment included reduced calcium intake, correction of dehydration, sodium infusion and remobilization. Corticosteroids, oral phosphates, furosemide and mithramycin were used with varying success to control prologned symptoms and severe hypercalcemia.
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PMID:Immobilization hypercalcemia in spinal cord injury. 83 59

The case history of a 65 year old female patient has been reported here by the authors. The patient was admitted to the Intensive Therapy Unit owing to her repeated heart pain. Later she was transferred to the Department of Medicine to establish the exact diagnosis. Prepyloric ulcer and hypertension were occurred in her history. The symptoms of her preceding as well as her recent illness were: pain in epigastric field, nausea, adynamia, weakness, polyuria, significant loss of weight, somnolence and the shortened Q--T time in electrocardiogram related to hypercalcemia syndrome. The calcium value in blood proved to be at critically high level from time to time. The possibility of the secondary hypercalcemic state was excluded by sonographic examination and the elevated level of parathormone in blood established the diagnosis of the hyperparathyroidism. The surgical resection of parathyroidic adenoma yielded a complete recovery of the patient. The authors call the attention to the significance of the clinical signs in the diagnosis of the disease.
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PMID:[Hyperparathyroidism simulating severe hypercalcemia syndrome]. 186 40

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.
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PMID:Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. 763 71

Primary hyperparathyroidism is a rather frequent pathology characterised by hypersecretion of parathormone (PTH) which is caused by adenomas in 85% of all cases. At clinical onset, the most common symptoms are hypercalcemia-related (pain due to kidney stones, polyuria, gastrointestinal and neurological disorders) while rarer symptoms are due to brown tumors, expansive lesions often found in fibro-cystic osteitis. A case in which the patient showed recurrent mandibular brown tumors as initial clinical symptoms of primary hyperparathyroidism is described. This patient was examined for hypercalcemia, and a tumor mass at the left inferior mandibular branch was found. The patient had undergone surgical removal of a tumor in the left mandibular some years before, which was diagnosed as osteoclastoma. Primary hyperparathyroidism was diagnosed during recovery, and surgical removal of the parathyroid adenoma and mandibular tumor was performed. A histological diagnosis of large cell brown tumor was made. A microscopic observation of brown tumors which are made up of large multinuclear osteoclastic cells can often be confused with other large cell tumors during diagnosis. It is therefore necessary to exclude the presence of hyperparathyroidism with ionised calcium and, in cases of high values, intact PTH (iPTH), before performing a histological diagnosis of a large cell bone tumor. Throughout the course of primary hyperparathyroidism, brown tumors might appear in the absence of other specific symptoms and localize at the level of a single bone segment.
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PMID:[Recurrent brown tumors as initial manifestation of primary hyperparathyroidism. An unusual presentation]. 1108 46

A case of 35-year-old woman with parathyroid cancer is presented. Five years ago she underwent surgery for follicular thyroid cancer. Parathyroid cancer was evidenced by palpable, solid, irregularly shaped cervical tumor 5 cm in diameter. The patient had severe hyperparathyroidism confirmed by biochemical findings of hypercalcemia reaching 16 mg%, hypophosphatemia and hyperphosphatasemia. Serum parathormone level was 23-fold higher than the norm. These findings were accompanied by polyuria, polidypsia, symptoms of bone damage and renal calcification. After the surgery the patient's condition improved significantly despite persistent hyperparathyroidism. The level of parathormone decreased, but was still 11 times higher than the norm. Two months after the surgery she noticed a single node on her neck. The patient was re-operated for recurrence of parathyroid cancer. Serum parathormone level was then 6-8 times above the norm. Medical treatment with furosemide, calcitonin and biphosphonate resulted in normalization of calcemia and phosphatemia. Further management will aim at localization of foci of hyperactive parathyroid tissue in order to enable radical reoperation. The case is reported because of rare occurrence of parathyroid carcinoma as well as because the carcinoma occurred in a patient who previously had follicular thyroid cancer. There are no reports of coexistence of these two neoplasms in available literature.
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PMID:Coexistence of parathyroid carcinoma and non-medullary carcinoma of the thyroid. 1138 24

Congenital mesoblastic nephroma (CMN) can present with atypical clinical and imaging findings. A premature male neonate was born to an 18-year-old woman after 33 weeks' gestation, which was complicated by polyhydramnios and placenta abruptio. A right abdominal mass was diagnosed antenatally. From the 1st day of life, the newborn had hypercalcemia with initially normal parathormone levels and polyuria for the first hours of life and normal urine output afterwards. Ultrasonographic study and magnetic resonance imaging of the abdomen showed at the upper pole of the right kidney a heterogeneous, solid, poorly defined mass, partially surrounded by a subcapsular fluid collection mimicking malignant rhabdoid tumor of the kidney. Surgical resection revealed a CMN of mixed, classic, and in areas, cellular type. One year after the resection, the patient is asymptomatic and normocalcemic. In conclusion, CMN may present with atypical clinical and imaging findings, necessitating an extensive work-up in order to exclude highly malignant renal tumors of the neonatal period.
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PMID:Congenital mesoblastic nephroma associated with polyhydramnios and hypercalcemia. 1195 58

Whether elderly patients with asymptomatic or minimally symptomatic primary hyperparathyroidism (PHPT) should be treated or not is still under debate. Several literature reports have shown improvements in terms of bone density and physical and mental well-being after surgical resolution of PHPT. Here, we present the case of a 93-year-old hypertensive woman, who had suffered for one year from cognitive impairment, accompanied during the last month by behavioral alterations (and polyuria and polydipsia), which resulted in sopor leading to hospitalization. A CT brain scan evidenced cortical atrophy and cerebrovascular disease, and biochemical analyses were remarkable for hypercalcemia (11.4-12.6 mg/dL, corrected for albumin levels) associated with increased parathormone levels (95.4-100.6 pg/mL). A diagnosis of PHPT was established. Densitometry evaluation of radius showed osteopenia. Withdrawal of psycho-therapy drugs and thiazidic, together with i.v. saline hydration and loop diuretics, significantly improved the patient's mental state and resolved behavioral alterations. As the patient and her relatives refused the surgical option, and the clinical situation improved after medical normalization of calcium levels, PHPT was managed conservatively, and calcium levels were maintained within the normal range through i.v. administration of zoledronate at 8-week intervals. Our case highlights the importance of considering hypercalcemia as the cause of onset of behavioral alterations and worsening of mental condition in elderly patients with cognitive decline. Therapy with bisphosphonates in patients with PHPT who are unfit for or refuse surgery seems advisable, but needs further study.
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PMID:Primary hyperparathyroidism and neuropsychiatric alterations in a nonagenarian woman. 1584 25

A 48-year-old women admitted with polyuria and polydipsia. She was found to be hypercalcemic despite suppressed parathormone (iPTH) levels. Subsequently checked parathormone related-protein (PTHrP) level was 2.5 pmol/L (expected normal level <1.3 pmol/L). An extensive workup for a malignancy revealed no abnormality, except for an uterine leiomyoma, 7.1 cm in size. Total abdominal hysterectomy and salpingo-oophorectomy were performed. After the surgical removal of uterine leiomyoma, serum calcium (9.3 mg/dL), iPTH (29.4 pg/mL), and PTHrP (<1.3 pmol/L) levels were normalized. The diagnosis of humoral hypercalcemia of benignancy secondary to PTHrP was confirmed. One month later, her calcium and iPTH levels were normal and 1 year later still remain within the normal ranges. Our case indicates that PTHrP associated hypercalcemia does not solely result from a malignant tumor. Benign tumors like uterine leiomyoma might also cause humoral hypercalcemia.
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PMID:Humoral hypercalcemia of benignancy secondary to parathyroid hormone-related protein secreting uterine leiomyoma. 1848 Jun 62

A 4-year-old, neutered male Golden Retriever was presented with a 1-week history of weight loss, polyuria, and polydipsia. The diagnostic workup showed an increased ionized calcium concentration, mild increase in serum creatinine and urea concentration, and severe hyperlipasemia. A complete abdominal ultrasound revealed multiple hepatic nodules. A cytological diagnosis of malignant epithelial neoplasia, highly suggestive of bile duct adenocarcinoma was made. In order to confirm the presumptive diagnosis of hypercalcemia of malignancy due to the presence of a hepatic neoplasia, serum parathormone-related peptide concentration was measured, and the result revealed an increased concentration. The dog was hospitalized and received supportive treatments consisting of intravenous furosemide and fluid therapy. After ruling out lymphoma and hypoadrenocorticism, oral prednisone was initiated and ionized calcium concentration decreased gradually down to normal concentration after 7 days of hospitalization. Chemotherapy with intravenous epirubicin was initiated based on the cytological diagnosis. One month after diagnosis and due to the worsening of its clinical condition, the dog was humanely euthanized. Postmortem examination confirmed a cholangiocellular carcinoma. To our knowledge, this is the first report of malignant hypercalcemia associated with cholangiocellular carcinoma in a dog.
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PMID:Hypercalcemia of Malignancy in a Dog Diagnosed With Cholangiocellular Carcinoma. 3112 81

A finely balanced control system keeps the extracellular calcium concentration within narrow limits. Disorders of calcium metabolism are often based on altered parathormone levels. Symptoms are not always clear, sometimes they are even missing: the more it is important to know possible associated diseases. The author presents basics, current diagnostics and concrete therapy options. Central hormone for the regulation of the calcium balance is the parathyroid hormone. With decreasing calcium, PTH leads to an increase in extracellular free calcium concentration in three ways. The classic symptoms of pHPT (polyuria, polydipsia, "stone, leg, and stomach pain") are rare now, as the condition is diagnosed much earlier. Treatment of choice in all symptomatic patients with pHPT is surgery. FHH and pHPT are both characterized by hypercalcaemia and increased parathyroid hormone. The differential diagnosis of urinary calcium excretion, which is usually lower in FHH but normal or elevated in pHPT, is crucial. In primary hypoparathyroidism, parathyroid failure interferes with calcium homeostasis at a central location. Consequences are hypocalcaemia, hyperphosphatemia and lack of active vitamin D. Due to increased urinary calcium excretion, patients with ADH are at high risk for kidney stones, nephrocalcinosis and the development of renal insufficiency. Recently, rhPTH 1-84 has been available for the treatment of hypoparathyroidism. However, long-term data is still lacking to provide a safe indication, considering potential effects and side effects.
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PMID:[Update - Calcium Metabolism]. 3141 4


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