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Diagnosis is often based on urine tests, blood tests and the fluid deprivation test. [1] Despite the name, diabetes insipidus is unrelated to diabetes mellitus and the conditions have a distinct mechanism, though both can result in the production of large amounts of urine. [1] Treatment involves drinking sufficient fluids to prevent dehydration ...
Wolfram syndrome, also called DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness), is a rare autosomal-recessive genetic disorder that causes childhood-onset diabetes mellitus, optic atrophy, and deafness as well as various other possible disorders including neurodegeneration.
Differential diagnosis includes nephrogenic diabetes insipidus, neurogenic/central diabetes insipidus and psychogenic polydipsia. They may be differentiated by using the water deprivation test. Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis.
Diagnosis is based on clinical and laboratory findings of low serum osmolality and low serum sodium. [13] Urinalysis reveals a highly concentrated urine with a high fractional excretion of sodium (high sodium urine content compared to the serum sodium). [14] A suspected diagnosis is based on a serum sodium under 138.
As a diagnosis of exclusion, a diagnosis of primary polydipsia may be the result of elimination of the possibility of diseases causing similar signs and symptoms, such as diabetes insipidus. [12] Diagnosis may be complicated by the fact that chronic and extreme compulsive drinking may impair the response of the kidneys to vasopressin, thus ...
As discussed in the entry on diabetes insipidus, "Habit drinking (in its severest form termed psychogenic polydipsia) is the most common imitator of diabetes insipidus at all ages. While many adult cases in the medical literature are associated with mental disorders, most patients with habit polydipsia have no other detectable disease.
Untreated central diabetes insipidus patients usually exhibit polyuria, nocturia, and polydipsia as a result of the initial rise of serum sodium and osmolality. [5] Patients may also experience neurologic symptoms associated with the underlying illness, such as headaches and diplopia, depending on the exact origin of the central diabetes insipidus.
A fasting blood sugar level of ≥ 7.0 mmol / L (126 mg/dL) is used in the general diagnosis of diabetes. [17] There are no clear guidelines for the diagnosis of LADA, but the criteria often used are that the patient should develop the disease in adulthood, not need insulin treatment for the first 6 months after diagnosis and have autoantibodies in the blood.
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