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Query: UMLS:C0032617 (polyuria)
 3,056 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.
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PMID:Myelodysplastic syndrome with central diabetes insipidus manifesting hypodipsic hypernatremia and dehydration. 1505 12

The skeleton is the most common organ to be affected by metastatic cancer. Hypercalcemia of malignancy (HM) affects 10 to 20% of patients with advanced cancer. HM causes a series of symptoms, constipation, nausea and vomiting, confusion and/or stupor, polyuria and polydipsia, bone pains, which decrease quality of life. The normalization of calcemia significantly improves all these symptoms. Despite that, HM remains largely underdiagnosed and undertreated. HM is an emergency. Treatment of HM includes rapid rehydration of isotonic saline and i.v. bisphosphonates. Complications from metastatic bone disease include pathological fracture, HM, spinal cord compression, bone marrow infiltration, pain, and reduced mobility. Treatment with bisphosphonates are effective to reduce these complications. They should be started when bone metastases are diagnosed and continue until it is no longer clinically relevant. The most currently used bisphosphonates were clodronate and pamidronate. The increase convenience of a 15 minutes infusion, the greater efficacy and longer duration of response makes zoledronate the standard of care for HM and metastatic bone disease.
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PMID:[Bisphosphonates in malignant hypercalcemia and bone pain]. 1509 27

Metastatic brain tumors from gastric cancer are extremely rare. A 61-year-old Korean woman, initially presenting with polydipsia and polyuria, was found to have metastatic lesions in the brain by MRI. We performed several diagnostic procedures to determine the origin of the brain metastases. She was revealed to have a soft tissue mass of the right adrenal gland and fungating ulcers in the stomach. Histologic studies of both the adrenal gland mass and gastric tissues revealed malignant tumors composed of anaplastic cells. Based on the electron microscopy study, the malignant tumor of the right adrenal gland was a metastatic lesion from the anaplastic carcinoma of stomach. Therefore, the malignant tumors of the brain were assumed to have originated from the gastric cancer. This case report is presented to make clinicians aware of the possibility that diabetes insipidus (polydipsia) may present as an initial manifestation of brain metastases.
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PMID:A case of gastric cancer initially presenting with polydipsia. 1568 17

Hypercalcemia associated with malignancies is reported in up to 20 to 30% of patients with cancer during the course of the disease, and points to a poor prognosis. Symptoms related to the central nervous system, as progressive mental impairment, stupor and coma, predominate. Alterations in kidney function (water-concentrating defect leading to polyuria) and gastrointestinal tract (anorexia, nausea, vomiting) corroborate to dehydration and a further increase in serum calcium. Cancer-induced hypercalcemia may be classified as: 1) local osteolytic hypercalcemia (LOH), due to marked increase in osteoclastic bone resorption in areas surrounding the malignant cells within the marrow space; 2) humoral hypercalcemia of malignancy, caused by the secretion of parathyroid hormone-related protein (PTHrP) by the malignant tumor; 3) ectopic hyperparathyroidism; 4) 1,25(OH)2 D-secreting tumors. Adequate control of hypercalcemia is necessary to give the patient time to respond to anti-cancer therapy. Volume expansion with saline will correct dehydration, improve glomerular filtration and increase urinary calcium excretion, which may be further stimulated by loop diuretics. Intravenous bisphosphonates are the most effective agents to control hypercalcemia, as they block osteoclastic osteolysis and also have antitumoral effects, decreasing bone metastases. New approaches to control the skeletal manifestations of malignancies are anti-PTHrP and anti-RANKL antibodies, osteoprotegerin, and also proteasome inhibitors in the case of multiple myeloma.
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PMID:[Hypercalcemia of malignancy: clinical features, diagnosis and treatment]. 1644 66

Pituitary metastasis and sarcoidosis are two causes of pituitary stalk thickening. Their association has been described ago three decades. In this setting, we report a case of panhypopituitarism revealing pituitary metastasis from a small-cell lung carcinoma associated with sarcoidosis. A 49 year-old smoking patient with type 2 diabetes was admitted for acute adrenal failure with polyuria polydipsia syndrome and a pituitary tumor syndrome. Hormone explorations confirmed anterior pituitary insufficiency. Water restriction revealed central diabetes insipidus. The hypothalamic-pituitary MRI revealed a 1-cm sellar mass with nodular thickening of the stalk. The chest radiograph showed a heterogeneous opacity in the left lung. The thoraco-abdominal scan demonstrated a mass in the left lung highly suggestive of malignancy and many enlarged mediastinal nodes, hepatic nodules, and hypertrophy of the left adrenal. Bronchoscopy was performed three times and showed infiltration of the left bronchial tree but histological examination of the bronchial biopsies was negative for all samples. Ultrasound-guided biopsy of the liver was achieved and histology demonstrated sarcoidosis. The diagnosis of sarcoidosis was incompatible with the deterioration of the patient's general status. Subsequent radiographic explorations showed an increase in the size of the tumor mass and histological evaluation of a scan-guided trans-thoracic biopsy demonstrated small-cell carcinoma. Small-cell lung carcinoma is the most common cancer with pituitary metastasis. The proposed link between sarcoidosis and malignancy has remained controversial but has not been proven false.
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PMID:[Panhypopituitarism revealing metastasis of small-cell lung carcinoma associated with sarcoidosis]. 1684 Sep 19

We present a 5-years old boy with acquired Fanconi-de Toni-Debre syndrome being a effect of therapy for Ewing's sarcoma. At the age of 3 years, this boy was diagnosed as suffering from Ewing sarcoma of his right femur. The boy received a course of 8-month pre-surgery (6 VIDE--Vincristine, Ifosfamide, Doxorubicin, Etoposide cycles and 2 VAI--Vincristine, Actinomycin, Ifosfamide cycles) and 6-month post-surgery (6 VAI--Vincristine, Actinomycin, Ifosfamide cycles) cytostatic therapies according to EWING, EURO 99 protocol. In forth month of post-surgery cytostatic therapy, progressive malaise, polyuria, polydypsia, and recurrent vomiting occurred. The association between those symptoms and malignancy was excluded. Laboratory studies revealed hypokaliemia, hypophosphatemia, proximal tubular acidosis, proteinuria, glucosuria, aminoaciduria, hyperkaliuria and hyperphosphaturia. Acquired Fanconi-de Toni-Debre syndrome due to toxic effect of cytostatic therapy on renal proximal tubules was diagnosed. At present, two years after the time the diagnosis was made, despite constant substitution of potassium, phosphates and bicarbonates, deficit of body mass and height, and bone mineral density abnormalities are observed.
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PMID:[Acquired Fanconi-de Toni-Debre syndrome due to therapy for Ewing's sarcoma in 5-years old boy]. 1689 36

The pituitary gland can be involved in a variety of medical conditions, including metastatic tumors. Metastases to the pituitary gland, although absolutely rare, more commonly affect the posterior pituitary lobe and so frequently present with diabetes insipidus. We report on a 48-year-old male heavy smoker patient suffering from sudden onset of polyuria and persistent thirst. Laboratory results revealed central diabetes insipidus. Computed tomography (CT) scan of the brain showed a mass located in the sella turcica and in the suprasellar region. CT scan of the chest showed a mass in the right superior lobe with mediastinal lymphadenopathy, with bronchoscopy and biopsy features of pulmonary adenocarcinoma. The patient received radiotherapy on the pituitary gland and adjuvant chemotherapy, and as intrasellar and suprasellar mass decreased in size, urinary output was accordingly reduced. Therefore, is that in patients with risk factors for cancer and sudden onset of diabetes insipidus pituitary metastasis should be taken into account in differential diagnosis.
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PMID:Smoking, polyuria and impaired vision. 1726

A 54-year-old woman had been given a diagnosis with scleroderma and interstitial pneumonia due to scleroderma when she was 45 years old. Thirst, with resulting polydipsia and polyuria (about 7 liters/day) were present since May, 2004, and bloody sputum appeared in June of 2004. The patient was admitted to our hospital. Chest CT examination showed multiple nodules in the bilateral lower lung field and multiple movable subcutaneous nodules on the abdomen. Small-cell lung cancer (metastases in the pituitary, subcutaneous tissue, and lungs) was diagnosed by transbronchial lung biopsy and subcutaneous nodule biopsy of the abdomen. The final diagnosis was diabetes insipidus and Cushing syndrome. Chemotherapy was done with CDDP and VP-16, which resulted in reduction of the tumor and improvement in endocrinological findings. Nevertheless, chemotherapy could not be continued because of infected bullae. The patient died of deteriorating illness after 91 sickness days. We concluded that this case was Cushing syndrome caused by ectopic adrenocorticotropic hormone-producing small cell lung cancer, and that it presented with diabetes insipidus because of pituitary metastasis. Therefore, when drastic endocrinological changes are found, it is important to examine for cancer, including lung cancer, as soon as possible.
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PMID:[Case of small cell lung cancer complicated with diabetes insipidus and Cushing syndrome due to ectopic adrenocorticotropic hormone secretion]. 1801 29

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

This article is a shortened version of the clinical guideline for lower urinary tract symptoms (LUTS), which has been developed in Japan for symptomatic men aged 50 years and over irrespective of presumed diagnoses. The guideline was formed on the PubMed database between 1995 and 2007 and other relevant sources. The causes of male LUTS are diverse and attributable to diseases/dysfunctions of the lower urinary tract, prostate, nervous system, and other organ systems, with benign prostatic hyperplasia, bladder dysfunction, polyuria, and their combination being most common. The mandatory assessment should comprise medical history, physical examination, urinalysis, and measurement of serum prostate-specific antigen. Symptom and quality of life questionnaires, bladder diary, residual urine measurement, urine cytology, urine culture, measurement of serum creatinine, and urinary tract ultrasonography would be optional tests. The Core Lower Urinary Tract Symptom Score Questionnaire may be useful in quickly capturing important symptoms. Severe symptoms, pain symptoms, and other clinical problems would indicate urological referral. One should be careful not to overlook underlying diseases such as infection or malignancy. The treatment should be initiated with conservative therapy and/or medicine such as alpha(1)-blockers. Treatment with anticholinergic agents should be reserved only for urologists, considering the risk of urinary retention. The present guideline should help urologists and especially non-urologists treat men with LUTS.
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PMID:Clinical guideline for male lower urinary tract symptoms. 1981 47


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