Cases reported "Diabetes Insipidus"

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11/632. Hypophyseal non-Hodgkin's lymphoma presenting with diabetes insipidus: a case report.

    We report the case of a 64 year old male patient with a history of ischemic heart disease who underwent surgery for an abdominal mass. The histological diagnosis was highly malignant non-Hodgkin's lymphoma. After surgery the patient was admitted to our Department and received 6 courses of chemotherapy according to the COP schedule, followed by radiotherapy to the left upper abdominal region and ipsilateral lung base. The patient achieved partial remission. One month later he began to complain of left axillary lymphadenomegaly, polydipsia and polyuria. A NMR brain scan showed a hypophyseal mass. The patient was treated with DDAVP and chemotherapy with the PRO-MACE protocol; the polyuria and lymphadenomegaly disappeared and the size of the hypophyseal mass reduced markedly. The clinical picture was, therefore, attributed to a hypophyseal localization of the non-Hodgkin's lymphoma, which is a very rare manifestation of lymphomatous spread to the central nervous system. Our case is also interesting because it shows that a favorable outcome can be obtained with chemotherapy, provided that the latter is sufficiently aggressive. This is not necessarily the case with radiotherapy which may also be followed by late and severe neurologic sequelae. ( info)

12/632. Langerhans cell histiocytosis of the vulva: an ultrastructural study.

    langerhans cells histiocytosis (LCH) is a proliferative disorder of langerhans cells. The lesions are normally characterized by infiltration of eosinophils, neutrophils, lymphocytes, plasma cells, and langerhans cells. The specific cells of LCH contain Birbeck granules, express the phenotype of langerhans cells but with markers fixed at an early stage of activation, and are functionally defective in antigen-presenting ability. The disease most often affects children; when it occurs in older patients, anal and groin involvement is quite common and vulvar lesions can be found in older females. The authors report a case of a 64-year-old woman with LCH of the vulva and diabetes insipidus. An immunohistochemical and ultrastructural study of the vulvar lesions showed an infiltrate in which antigenically and morphologically mature langerhans cells, monocytoid cells, and cells with an intermediate phenotype between monocytes and langerhans cells were concurrently observed. Although the clinical and histological aspects of LCH are well established, the pathogenetic mechanism of lesions is not yet known. The finding of an infiltrate composed by langerhans cells and many putative precursors of these cells suggests the hypothesis of an in situ differentiation of langerhans cells from immature monocytoid precursors. ( info)

13/632. Autosomal recessive familial neurohypophyseal diabetes insipidus with continued secretion of mutant weakly active vasopressin.

    Familial neurohypophyseal diabetes insipidus is an autosomal dominant disorder characterized by post-natal development of arginine vasopressin (AVP) deficiency due to mutations in the AVP gene. All published mutations affect the signal peptide or the neurophysin-II carrier protein and are presumed to interfere with processing of the preprohormone, leading to neuronal damage. We studied an unusual Palestinian family consisting of asymptomatic first cousin parents and three children affected with neurohypophyseal diabetes insipidus, suggesting autosomal recessive inheritance. All three affected children were homozygous and the parents heterozygous for a single novel mutation (C301->T) in exon 1, replacing Pro7 of mature AVP with Leu (Leu-AVP). Leu-AVP was a weak agonist with approximately 30-fold reduced binding to the human V2 receptor. Measured by radioimmunoassay with a synthetic Leu-AVP standard, serum Leu-AVP levels were elevated in all three children and further increased during water deprivation to as high as 30 times normal. The youngest child (2 years old) was only mildly affected but had Leu-AVP levels similar to her severely affected 8-year-old brother, suggesting that unknown mechanisms may partially compensate for a deficiency of active AVP in very young children. ( info)

14/632. diabetes insipidus in Langerhans' cell histiocytosis: report of a case.

    The incidence of diabetes insipidus secondary to Langerhans' cell histiocytosis (LCH) varies among different reports, ranging from 9.5 to 50%, but it has never been reported in literature in taiwan. Therefore, we presented a case suffering from polyuria, polydipsia, body weight loss for more than one year and seborreic dermatitis-like skin lesions over the scalp and trunk for more than two years. Her body weight and body length were both less than 3 percentile. Fluid restriction and vasopressin test were performed to differentiate nephrogenic from neurogenic diabetes insipidus. skin biopsy revealed picture of LCH and LCH with complete central diabetes insipidus was diagnosed. brain MRI and other laboratory examinations were all within normal limits. She received nasal DDAVP treatment and chemotherapy with TPOG-H 94 protocol. After 3 months treatment, her skin lesions disappeared and daily urine amount returned to normal range. ( info)

15/632. hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor.

    A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin d (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure. ( info)

16/632. Pregnant woman with transient diabetes insipidus resistant to 1-desamino-8-D-arginine vasopressin.

    We encountered a pregnant woman with transient diabetes insipidus which developed during the third trimester. A hypertonic saline infusion study did not concentrate the osmolality of urine. Her laboratory data showed hypokalemia, hyperreninemia, an increased concentration of plasma aldosterone and an increased urinary excretion rate of prostaglandin E2, which resembled hyperprostaglandin E-syndrome. T1-weighted magnetic resonance imaging of the posterior pituitary gland revealed decreased intensity. polyuria reached 4-6 L daily, and urine osmolality remained dilute despite a lapse of four days since treatment with intranasal 1-desamino-8-D-arginine vasopressin (dDAVP: 10-25 microg every 12 h). The patient was conservatively managed without medical treatment, then delivered in the 38th week of pregnancy without complication. The osmolality of the patient's urine was higher than that of the plasma when tested 3 days postpartum. The abnormality of magnetic resonance imaging of the posterior pituitary gland disappeared at 6 months after delivery. We consider that subclinical nephrogenic diabetes insipidus in our patient was exacerbated during pregnancy. ( info)

17/632. hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism.

    We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca. ( info)

18/632. Symptomatic Rathke's cleft cyst coexisting with central diabetes insipidus and hypophysitis: case report.

    We describe a 48-year-old female with acute onset of central diabetes insipidus followed by mild anterior pituitary dysfunction. magnetic resonance imaging (MRI) revealed enlargement of the hypophysis-infundibulum accompanied by a cystic component. She underwent a transsphenoidal exploration of the sella turcica. Histological examination showed foreign body type xanthogranulomatous inflammation in the neurohypophysis which might have been caused by rupture of a Rathke's cleft cyst. The MRI abnormalities and anterior pituitary dysfunction improved after a short course of corticosteroid administration, but the diabetes insipidus persisted. The histological findings in this case indicated the site of RCC rupture and the direction of the progression of RCC induced neurohypophysitis and adenohypophysitis. ( info)

19/632. Embolization of the meningohypophyseal trunk as a cause of diabetes insipidus.

    We present an unusual case of diabetes insipidus occurring after selective embolization of 50% dextrose and pure ethanol into an enlarged left meningohypophyseal trunk (MHT) supplying a dural carotid cavernous fistula. The inferior hypophyseal artery was not opacified during the selective preembolization MHT injection; however, diabetes insipidus developed abruptly a few hours after the procedure. The patient required intranasal 1-deamino-(8-D-arginine)-vasopressin for approximately 3 months, after which his symptoms resolved. The hazards of using liquid embolic agents, especially ethanol, in the cavernous branches of the internal carotid artery should always be borne in mind. ( info)

20/632. MRI detection of suprasellar germinoma causing central diabetes insipidus.

    This is a case report of an 18-year-old man with central diabetes incipidus (DI). An MRI done three months after the onset of the DI did not disclose a responsible lesion. Four months later, a second MRI showed the location of the tumor origin at the upper pituitary stalk and median eminence. Eight months later, the tumor occupied the hypothalamic area. The tumor became large and contrast-making enough to be visible on MRI between 3 and 4 months after the onst of DI. Besides the suprasellar tumor, another mass was noted in the pineal region. The growth pattern of the latter mass corresponded well to that of the former. Although the MRI is a sensitive diagnostic tool for the detection of intracranial tumors, no adequate rationale has been given as to how the MRI might be repeated for children and adolescents who have been diagnosed as having the central DI, when their initial MRIs may have been normal. In our patient, the superconductive thin slice MRI revealed the suprasellar germinoma 4 months after the onset. The suprasellar and pineal tumors in this report originated and developed simultaneously. This may indicate a multi-center origin of the tumor. Another possibility is a very early dissemination from the onset of the tumor development. ( info)
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