1/53. Adipsic hypernatremia in two patients with AIDS and cytomegalovirus encephalitis.In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. survival after onset of hypernatremia was 6 and 4 weeks, respectively. autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with hiv or CMV most likely caused the dysfunction of the central osmostat.- - - - - - - - - - ranking = 1keywords = antidiuretic hormone, antidiuretic, hormone (Clic here for more details about this article) |
2/53. 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.- - - - - - - - - - ranking = 1.9702629511593keywords = vasopressin, hormone (Clic here for more details about this article) |
3/53. Idiopathic hypothalamic dysfunction with precocious puberty and adipsic hypernatremia first presenting in adolescence.BACKGROUND: Idiopathic hypothalamic dysfunction is a rare syndrome that has been described in young children. This syndrome is characterized by a disturbance of thirst regulation with hypernatremia, hyperosmolarity, and altered hypothalamic function. PATIENT REPORT: At age 6 years the reported patients presented with precocious puberty, by age 12 years she had hypernatremia presumed secondary to central diabetes insipidus and was treated with DDAVP, and at age 14 was identified to have hyperprolactinemia. At age 19 she presented with serum sodium of 185 mg/dl during an episode of illness associated with dehydration. After hydration, her sodium remained elevated. arginine vasopressin was measurable but inappropriate to serum sodium, while urinary cyclic amp response to vasopressin was appropriate. CONCLUSIONS: This is the first case of precocious puberty identified in association with the more classic features of idiopathic hypothalamic dysfunction, including later-onset hypernatremia, poor thermoregulatory function, obesity, and hyperprolactinemia.- - - - - - - - - - ranking = 3.9344209001741keywords = vasopressin (Clic here for more details about this article) |
4/53. Hypodipsic hypernatremia with intact AVP response to non-osmotic stimuli induced by hypothalamic tumor: a case report.Anatomical lesions of hypothalamic area associated with hypodipsic hypernatremia have been reported only rarely. We report here a case of hypodipsic hypernatremia induced by a hypothalamic lesion. A 25-yr-old man, who had been treated with radiation for hypothalamic tumor 5-yr before, was admitted for evaluation of hypernatremia and hypokalemia. He never felt thirst despite the elevated plasma osmolality and usually refused to drink intentionally. plasma arginine vasopressin (AVP) level was normal despite the severe hypernatremic hyperosmolar state and urine was not properly concentrated, while AVP secretion was rapidly induced by water deprivation and urine osmolality also progressively increased to the near maximum concentration range. All of these findings were consistent with an isolated defect in osmoregulation of thirst, which was considered as the cause of chronic hypernatremia in the patient without an absolute deficiency in AVP secretion. hypokalemia could be induced by activation of the renin-angiotensin-aldosterone system as a result of volume depletion. However, inappropriately low values of plasma aldosterone levels despite high plasma renin activity could not induce symptomatic hypokalemia and metabolic alkalosis. The relatively low serum aldosterone levels compared with high plasma renin activity might result from hypernatremia. hypernatremia and hypokalemia were gradually corrected by intentional water intake only.- - - - - - - - - - ranking = 2.0859947598015keywords = vasopressin, secretion (Clic here for more details about this article) |
5/53. Severe hypernatremic dehydration in an infant with netherton syndrome.Netherthon syndrome is a rare autosomal recessive disease characterized by ichthyosis, the characteristic hair abnormality trichorrhexis invaginata and atopic manifestations. We report a female child with the severe hypernatremic dehydration form of the netherton syndrome born as the first child of consanguineous parents. ichthyosis was present at birth. She was admitted to the intensive care unit at the age of 4 days with important loss of weight and dehydration. Severe hypernatremia and convulsions occurred. Despite intensive care the baby died at the age of 11 days. The diagnosis of netherton syndrome was confirmed by the finding of the pathognomonic hair shaft anomaly trichorrhexis invaginata (bamboo hair) and premature lamellar body secretion and foci of electron-dense material in the intercellular spaces of stratum corneum as relatively specific markers for netherton syndrome. netherton syndrome is characterized by a large variability in phenotypic expression. The major neonatal complication is the hypernatremic dehydration, which can be fatal as in this patient or complicated by neurologic signs (intracranial hemorrhage) and secondary sequellae. Molecular studies revealed a mutation in SPINK 5, encoding a serine protease inhibitor. prenatal diagnosis was performed in the second pregnancy and showed that the fetus was equally affected.- - - - - - - - - - ranking = 0.059392154857235keywords = secretion (Clic here for more details about this article) |
6/53. Hypodipsia-hypernatremia syndrome associated with holoprosencephaly in a child: a case report.We report a child with diabetes insipidus and hypodipsia associated with holoprosencephaly. A two-year-old girl with the history of several admittances to hospital during and after the newborn period with hypernatremic dehydration, acute renal failure and convulsions is presented. The patient had hypodipsia, hypernatremia, microcephaly, failure to thrive, and unilateral cleft lip and palate. magnetic resonance imaging revealed lobar type holoprosencephaly. Increased plasma osmolality and decreased urinary osmolality were detected. Her urine ADH level was 10 ng/day. plasma osmolality levels returned to normal after hydration and administration of a vasopressin analogue. These findings suggest that in children with hypernatremia-hypodipsia syndrome, the possibility of cerebral malformations should always be kept in mind.- - - - - - - - - - ranking = 1.967210450087keywords = vasopressin (Clic here for more details about this article) |
7/53. Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.- - - - - - - - - - ranking = 1.967210450087keywords = vasopressin (Clic here for more details about this article) |
8/53. Studies of acquired sustained hypernatraemia occurring in a diabetic patient.We describe studies undertaken in a diabetic patient with acquired sustained severe hypernatraemia. arginine vasopressin levels and thirst scores were grossly subnormal in the presence of marked hypernatraemia but arginine vasopressin increased normally under the influence of negative pressure-induced hypovolaemia. Despite very low levels of arginine vasopressin, polyuria was not a feature suggesting acquired renal hyper-responsiveness. This patient is an additional case of acquired osmoregulatory dysfunction, whose features do not fall neatly into previously described categories.- - - - - - - - - - ranking = 5.9016313502611keywords = vasopressin (Clic here for more details about this article) |
9/53. A new quantitative approach to the treatment of the dysnatremias.Rapid correction of the dysnatremias can result in significant patient morbidity and mortality. To avoid overly rapid correction of the dysnatremias, the sodium deficit equation, water deficit equation, and Adrogue-Madias equation are frequently utilized to predict the change in plasma sodium concentration (Delta[Na ]p) following a therapeutic maneuver. However, there are significant limitations inherent in these equations. Specifically, the sodium deficit equation assumes that total body water (TBW) remains unchanged. Similarly, when using the Adrogue-Madias equation, the volume of infusate required to induce a given Delta[Na ]p is determined by dividing the target Delta[Na ]p by the result of this formula. This calculation also assumes that TBW remains constant. In addition, neither of these equations are applicable in the management of symptomatic syndrome of inappropriate antidiuretic hormone secretion (SIADH) because they fail to consider the subsequent increase in sodium excretion following the administration of infusate. Furthermore, in the treatment of hypernatremia, the water deficit equation is only applicable if the hypernatremia is caused by pure water loss. In hypernatremia caused by hypotonic fluid losses, the water deficit equation does not provide any information on the differential effect of infusates of variable [Na ] and [K ] on the [Na ]p. Finally, all these equations fail to consider any ongoing Na , K , or H2O losses. Taking all these limitations into consideration, we have derived two new equations which determine the volume of a given infusate required to induce a target Delta[Na ]p. These equations consider the mass balance of Na , K , and H2O, as well as therapy-induced changes in TBW. The first equation is applicable to both hypernatremia and hyponatremia. The second equation is applicable to the management of severe symptomatic SIADH requiring intravenous therapy.- - - - - - - - - - ranking = 1.0593921548572keywords = antidiuretic hormone, antidiuretic, secretion, hormone (Clic here for more details about this article) |
10/53. Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy.BACKGROUND: Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin. CASE: While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. CONCLUSION: Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.- - - - - - - - - - ranking = 5.9016313502611keywords = vasopressin (Clic here for more details about this article) |
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