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A case of successful pregnancy in a patient with the complete DIDMOAD syndrome is described. Attention is drawn to the need to monitor fluid balance carefully during and after pregnancy in this condition. The current literature in the area is reviewed.
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Diabetes insipidus, characterized by the excretion of copious volumes of unconcentrated urine, results from a deficiency in the action of the antidiuretic hormone arginine vasopressin and can be caused by any of four fundamentally different defects, including impaired secretion (neurohypophyseal diabetes insipidus), impaired renal response (nephrogenic diabetes insipidus), excessive fluid intake (primary polydipsia), or increased metabolism of the hormone (gestational diabetes insipidus). Differentiation between their causes, pathophysiology, and treatment methods is essential for effective management and is best achieved by a combination of hormonal, clinical, and neuroradiologic observations. Understanding of the genetic forms has advanced greatly and may soon lead to improved methods of prevention, diagnosis, and treatment.
Diabetes insipidus is an uncommon condition characterized by polyuria and polydipsia. The symptoms and biochemical changes of this condition result from either a lack of antidiuretic hormone or renal insensitivity to its effect. Failure to produce or release antidiuretic hormone may result from cranial pathology, including trauma and surgery. The renal insensitivity to antidiuretic hormone that occurs in patients with nephrogenic diabetes insipidus may be caused by genetic factors, drugs (especially lithium) or specific disease processes. Patients may compensate for polyuria and nocturia by excessive water intake but show marked decreases in urine specific gravity and osmolality. Patients with severe and uncompensated symptoms develop marked dehydration, neurologic symptoms and encephalopathy. The water deprivation test is useful in diagnosing diabetes insipidus and in differentiating neurogenic from nephrogenic cases. Neurogenic diabetes insipidus may respond to nasal administration of desmopressin. Nephrogenic diabetes insipidus requires good hydration and monitoring of body chemistry. Thiazides and amiloride may relieve symptoms.
Diabetes insipidus is a clinical syndrome characterized by the excretion of copious volumes of dilute urine combined with persistent intake of abnormally large quantities of fluid. There are two general forms of the disease, central (vasopressin deficient) and nephrogenic (vasopressin resistant). Diabetes insipidus of central origin most often results from lesions in the hypothalamic-neurohypophyseal axis. Twenty-six cases of central diabetes insipidus were evaluated with the use of high-field-strength MR imaging. A wide variety of precipitating conditions were found, including Langerhans cell histiocytosis, neoplasia, trauma, and infection. A thickened pituitary infundibulum was seen in most patients, and an absence of high intensity signal in the posterior pituitary lobe on T1-weighted images was seen in every case. Analysis of stalk morphology; associated brain findings; and correlation with the patient's age, sex, history, and radiographs of other body parts improved diagnostic specificity. When combined with clinical information, MR imaging is able to provide a specific diagnosis in almost all cases of central diabetes insipidus.
Diabetes insipidus is a heterogeneous condition characterised by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. The clinical and laboratory diagnosis is confirmed by standard tests, but recent advances in molecular biology and imaging techniques have shed new light on the pathophysiology of this disease. In many patients, central diabetes insipidus is caused by a germinoma or craniopharyngioma; Langerhans' cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma from surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Tumour-associated central diabetes insipidus is uncommon in children younger than 5 years old. Biopsy of enlarged pituitary stalk should be reserved for patients with hypothalamic-pituitary mass and progressive thickening of the pituitary stalk since spontaneous recovery may occur. Molecular biology in selected patients may identify those with apparently idiopathic diabetes insipidus carrying the vasopressin-neurophysin II gene mutation.
Diabetes insipidus is an extremely rare condition complicating pregnancy. The deficiency in antidiuretic hormone production has led to the assumption that oxytocin synthesis may also be affected. For this reason spontaneous onset of labor in a number of previously reported cases has been considered as evidence against implicating oxytocin as a relevant factor in the evolution and maintenance of labor. For the first time, plasma oxytocin levels were determined in a patient with known idiopathic diabetes insipidus during pregnancy, labor, and postpartum, using radioimmunoassay. Oxytocin was not detectable in plasma before labor. There was however a surge of plasma oxytocin detected during labor and puerperium, a pattern somewhat similar to that seen in normal pregnancy. Our findings suggest that at least some patients with diabetes insipidus do secrete oxytocin and that the role of oxytocin, threfore, cannot be discounted in the labor process.
Diabetes insipidus may first present before, during, or immediately after pregnancy. The characteristics of two unusual cases of transient postpartum diabetes insipidus are described and discussed.
Diabetes insipidus as the presenting manifestation of acute myeloblastic leukemia in a nine-year-old female is reported. In patients with recent onset of diabetes insipidus an underlying leukemic process should be excluded as an etiologic factor.
Diabetes insipidus is a heterogeneous condition characterized by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. In many patients, it is caused by the destruction or degeneration of the neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus. Known causes of these lesions include: germinoma or craniopharyngioma; Langerhans cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma following surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Magnetic resonance imaging (MRI) allows identification of the posterior pituitary hyperintensity and of hypothalamic-pituitary abnormalities. Thickening of the pituitary stalk is the second most common finding on MRI scans in several local inflammatory pathologies and autoimmune diseases or germinoma, but it is not specific to any single subtype. A progressive increase in the size of the anterior pituitary gland should alert physicians to the possibility that a germinoma is present, whereas a decrease can suggest the presence of an inflammatory or autoimmune process. Most children with acquired central diabetes insipidus and a thickened pituitary stalk have anterior pituitary hormone deficiencies during follow-up. Biopsy of enlarged pituitary stalk should be reserved for patients with a hypothalamic-pituitary mass and progressive thickening of the pituitary stalk, since spontaneous recovery may occur.
INTRODUCTION: Langerhans' cell histiocytosis is a rare disorder of unknown etiology characterized by a wide clinical spectrum and varied behavior. Diabetes insipidus is a relatively common feature in Langerhans' cell histiocytosis. The presence of both diabetes insipidus and mellitus associated with histiocytosis in an adult is rare. To our knowledge, only three previous cases have been reported. EXEGESIS: We report the clinical presentation, pathologic findings and clinical progress in an adult female who had disseminated Langerhans' cell histiocytosis (hypothalamic infiltration, multifocal bone involvement) associated with both diabetes insipidus and mellitus. CONCLUSION: The pathogenesis of diabetes mellitus in such an association will be discussed.
Diabetes insipidus usually shows a Normo- or Hypernatraemia. In our case, a 21 months old boy, we could contrarily find a hyponatraemic crisis as the leading symptom to our diagnosis. As reason for this we discuss a chronical overhydration with hypotonic liquid and enteral loss of electrolytes.
Diabetes insipidus and thrombocytosis were presenting symptoms in a case of adult ANLL-M1. Cytogenetic investigations revealed a typical 3q rearrangement, i.e. inv(3)(q21q26). A subclone with monosomy 7 was also found and documented by FISH analysis. Correlations between clinical/hematological features and cytogenetic/FISH results are discussed.
Diabetes insipidus is seen most frequently in neurosurgical patients. The transient form is more common and usually subsides prior to discharge. Permanent DI is seen in patients with extensive damage in the hypothalamic area. Treatment of either form of DI is usually with a preparation of vasopressin. Nursing assessements and interventions are crucial to a successful outcome in patients with this disorder. Health teaching for patients with permanent DI is an integral part of the nursing responsibility.
Diabetes insipidus (DI), an acute or chronic condition, results from either of two situations: An inadequate secretion of antidiuretic hormone (ADH) from the posterior pituitary gland or an insufficient renal response to adequate levels of ADH. Characterized by massive urinary output despite progressive serum hyperosmolality, hypernatremia, and dehydration, DI can be life-threatening if not promptly diagnosed and appropriately managed. Individuals with renal disease, surgical patients, and persons with cerebral trauma are at risk to develop this condition.