Most of us know the main symptoms of diabetes - usually thirst and excessive urination. Less well known are excess weight gain, fatigue, dry skin and frequent pustular rashes on the skin. Often these signs are an indication for laboratory examination.
But is the diagnosis of diabetes mellitus always so obvious: differential diagnosis of the disease is of great interest to the scientific world.
It should be noted that in medicine there are two forms of “sugar” pathology: DM-1 (type 1, insulin-dependent) and DM-2 (type 2, non-insulin-dependent).
- characterized by an almost complete absence of insulin in the body due to a violation of its synthesis in the beta cells of the pancreas, which have undergone autoimmune destruction.
- the problem is a violation of the sensitivity of cellular receptors: the hormone is there, but the body perceives it incorrectly.
How to distinguish between types of pathology? The differential diagnosis of type 1 and type 2 diabetes mellitus is given in the table below.
Table 1: Differential diagnosis of diabetes mellitus:
Important! All basic symptoms of the disease (polyuria, polydipsia, itching) are similar for IDDM and NIDDM.
Syndromes and diseases
Differential diagnosis of type 2 diabetes mellitus, like IDDM, is carried out according to the main syndromes.
In addition to diabetes, polyuria and polydipsia may be characteristic of:
- chronic kidney diseases and chronic renal failure;
- primary hyperaldosteronism;
- hyperparathyroidism;
- neurogenic polydepsia.
According to the hyperglycemia syndrome, differential diagnosis of type 1 and type 2 diabetes mellitus is carried out with:
- Itsenko-Cushing's disease/syndrome;
- steroid diabetes;
- acromegaly;
- hemochromatosis;
- pheochromocytoma;
- some diseases of the liver and pancreas;
- nutritional hyperglycemia.
With the development of glycosuria syndrome, the differential diagnosis of type 2 diabetes mellitus and IDDM is carried out with the following diseases:
- nutritional glucosuria;
- glucosuria in pregnant women;
- toxic lesions;
- renal diabetes.
This is interesting. False-positive results when testing urine for glucose can be observed when taking large doses of vitamin C, Acetylsalicylic acid, and cephalosporins.
Differential diagnosis
Diabetes insipidus
Differential diagnosis of diabetes mellitus and diabetes insipidus is of great interest to endocrinologists. Despite the fact that the symptoms of these pathologies are similar, their mechanism of development and pathogenesis are strikingly different.
Diabetes insipidus is associated with an acute lack of the hypothalamic hormone vasopressin, which is responsible for maintaining normal water balance.
Secreted in the hypothalamus, vasopressin is transported to the pituitary gland, and then distributed through the bloodstream throughout the body, including the kidneys. At this level, it promotes the reabsorption of fluid in the nephron and its retention in the body.
Depending on the cause, diabetes insipidus can be central or nephrogenic (renal). The first often develops against the background of traumatic brain injury, neoplasms of the hypothalamus or pituitary gland. The second is the result of various tubulopathies and impaired hormone sensitivity of the renal tissues.
Are both diabetes and the pathology in question clinically manifested by thirst and excessive urination? But what are the differences between them?
Table 2: Diabetes insipidus and diabetes mellitus - differential diagnosis:
| Sign | Diabetes | |
| Sugar | Non-sugar | |
| Thirst | Moderately expressed | Intolerable |
| Daily urine volume | Less than 3 l | Up to 15 l |
| Onset of the disease | Gradual | Sudden, very acute |
| Enuresis | Absent | Available |
| Hyperglycemia | + | — |
| Glucosuria | + | — |
| Relative density of urine | Increased | Very low |
| Test with dry eating | The patient's condition does not change | The patient's condition noticeably worsens, signs of dehydration appear |
Chronic kidney disease
In chronic renal failure at the stage of polyuria, patients often complain of frequent, excessive urination, which may indicate the development of hyperglycemia. However, in this case, a differential diagnosis will help: type 2 diabetes mellitus and IDDM are also characterized by elevated blood sugar levels and glucosuria, and with chronic renal failure, signs of fluid retention in the body (edema), a decrease in rel. urine density.
Adrenal and other endocrine disorders
Primary hyperaldosteronism (Conn's syndrome) is a clinical syndrome characterized by excessive production of the hormone aldosterone by the adrenal glands.
Its symptoms are quite typical and are manifested by three syndromes:
- defeat of the cardiovascular system;
- neuromuscular disorders;
- kidney dysfunction.
Damage to the cardiovascular system is primarily represented by arterial hypertension. Neuromuscular syndrome is associated with hypokalemia and is manifested by attacks of muscle weakness, cramps and short-term paralysis.
Nephrogenic syndrome is represented by:
- decreased contracting abilities of the kidneys;
- nocturia
- polyuria.
Unlike both forms of diabetes, the disease is not accompanied by disturbances in carbohydrate metabolism.
Cushing's disease/syndrome is another neuroendocrine disease affecting the adrenal glands that is included in the differential diagnosis. It is accompanied by excessive secretion of glucocorticosteroids.
Clinically manifested by the following symptoms:
- obesity of a special type (excess weight is deposited mainly in the upper half of the body, the face becomes moon-shaped, and the cheeks are covered with a bright red blush);
- the appearance of pink or purple stretch marks;
- excess hair growth on the face and body (including in women);
- muscle hypotension;
- arterial hypertension;
- impaired insulin sensitivity, hyperglycemia;
- weakening of the immune system.
Gradually developing insulin resistance and signs of hyperglycemia may prompt the doctor to diagnose type 2 diabetes mellitus: the differential diagnosis in this case is carried out by assessing the additional symptoms described above.
In addition, the appearance of signs of hyperglycemia is possible with some other endocrine diseases (primary hyperthyroidism, pheochromocytoma), etc. Diff. Diagnosis of these diseases is carried out on the basis of advanced laboratory tests.
Pancreatitis and other gastrointestinal diseases
Chronic inflammatory damage to pancreatic tissue causes gradual death of functionally active cells with their sclerosis. Sooner or later this leads to organ failure and the development of hyperglycemia.
The secondary nature of the syndrome can be suspected based on the patient’s complaints (girdling pain in the epigastrium, radiating to the back, nausea, vomiting after eating fatty fried foods, various stool disorders), as well as laboratory and instrumental tests (increased levels of the enzyme alpha-amylase in the blood, ECHO - signs of inflammation on ultrasound, etc.).
Note! Separately, we should highlight such conditions as nutritional hyperglycemia and glycosuria. They develop in response to the intake of excess carbohydrates into the body and, as a rule, persist for a short time.
Thus, differential diagnosis of the main syndromes of diabetes is carried out with many diseases. A diagnosis based only on clinical data can be considered only preliminary: it must necessarily be based on data from a complete laboratory and instrumental examination.
Questions for the doctor
Asymptomatic diabetes
Hello! I am 45 years old, female, and have no particular complaints. I recently measured my sugar – 8.3. I didn’t donate blood on an empty stomach, maybe that’s the reason.
A little later, I decided to take the test again. On an empty stomach, the result from the vein was also elevated - 7.4 mmol/l. Is this really diabetes? But I have absolutely no symptoms.
Hello! Hyperglycemia in laboratory tests most often indicates the development of diabetes mellitus. Be sure to consult with an endocrinologist in person to decide whether to undergo additional examination (first of all, I would advise you to donate blood for HbAc1, ultrasound of the pancreas).
Self-diagnosis
Good evening! Tell me if there are any reliable signs that will help determine whether you have diabetes. I recently noticed that I started eating a lot of sweets. This may not be a symptom of a health problem.
Hello! Cravings for sweets are not considered a manifestation of diabetes. From a physiological point of view, such a need may indicate a lack of energy, overwork, stress, and hypoglycemia.
Diabetes mellitus, in turn, may be indicated by:
- dry mouth;
- strong thirst;
- frequent and copious urination;
- weakness, decreased performance;
- sometimes - skin manifestations (severe dryness, pustular diseases).
Signs of diabetes in a child
With adults everything is more or less clear. How to suspect diabetes in a child? I heard that in children the disease is very severe, even to the point of coma and death.
Hello! Indeed, children are a special category of patients that require close attention from both medical professionals and parents.
The first thing that attracts attention when someone gets sick in childhood is thirst: the child begins to drink noticeably more, sometimes he can even wake up at night, asking for water.
The second frequently encountered “childhood” symptom of diabetes is frequent urination and enuresis. You may notice sticky urine stains on the potty or near the toilet if your baby is wearing a diaper; due to the high sugar content in the urine, it can stick to the skin.
Then weight loss becomes noticeable: the baby quickly loses kilograms even despite a good appetite. In addition, signs of asthenia appear: the baby becomes lethargic, drowsy, and rarely participates in games.
All this should alert attentive parents. Such symptoms require immediate examination and medical consultation.
RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013
Diabetes insipidus (E23.2)
Endocrinology
general information
Short description
Approved
minutes of the meeting of the Expert Commission
on health development issues of the Ministry of Health of the Republic of Kazakhstan
Diabetes insipidus(ND) (lat. diabetes insipidus) is a disease caused by a violation of the synthesis, secretion or action of vasopressin, manifested by the excretion of large amounts of urine with low relative density (hypotonic polyuria), dehydration and thirst.
Epidemiology .
The prevalence of ND in different populations varies from 0.004% to 0.01%. There is a worldwide trend toward an increase in the prevalence of ND, in particular, due to its central form, which is associated with an increase in the number of surgical interventions performed on the brain, as well as the number of traumatic brain injuries, in which cases of ND development account for about 30%. It is believed that ND affects both women and men equally often. The peak incidence occurs at the age of 20-30 years.
Protocol name:Diabetes insipidus
ICD-10 code(s):
E23.2 - Diabetes insipidus
Date of development of the protocol: April 2013.
Abbreviations used in the protocol:
ND - diabetes insipidus
PP - primary polydipsia
MRI - magnetic resonance imaging
BP - blood pressure
DM - diabetes mellitus
Ultrasound - ultrasound examination
Gastrointestinal tract - gastrointestinal tract
NSAIDs - non-steroidal anti-inflammatory drugs
CMV - cytomegalovirus
Patient category: men and women aged 20 to 30 years, a history of trauma, neurosurgical interventions, tumors (craniopharynoma, germinoma, glioma, etc.), infections (congenital CMV infection, toxoplasmosis, encephalitis, meningitis).
Protocol users: local therapist, endocrinologist at a clinic or hospital, neurosurgeon at a hospital, traumatologist at a hospital, local pediatrician.
Classification
Clinical classification:
The most common are:
1. Central (hypothalamic, pituitary), caused by a violation of the synthesis and secretion of vasopressin.
2. Nephrogenic (renal, vasopressin-resistant), characterized by kidney resistance to the action of vasopressin.
3. Primary polydipsia: a disorder in which pathological thirst (dipsogenic polydipsia) or compulsive desire to drink (psychogenic polydipsia) and associated excess water consumption suppress the physiological secretion of vasopressin, ultimately leading to the characteristic symptoms of diabetes insipidus, while the synthesis of vasopressin occurs when the body is dehydrated is being restored.
There are also other rare types of diabetes insipidus:
1. Progestational, associated with increased activity of the placental enzyme - arginine aminopeptidase, which destroys vasopressin. After childbirth the situation returns to normal.
2. Functional: occurs in children of the first year of life and is caused by the immaturity of the renal concentration mechanism and increased activity of phosphodiesterase type 5, which leads to rapid deactivation of the vasopressin receptor and a short duration of action of vasopressin.
3. Iatrogenic: use of diuretics.
Classification of ND by severity:
1. mild form - urine output up to 6-8 l/day without treatment;
2. average - urine output up to 8-14 l/day without treatment;
3. severe - urine output more than 14 l/day without treatment.
Classification of ND by degree of compensation:
1. compensation - during treatment, thirst and polyuria do not bother;
2. subcompensation - during treatment there are episodes of thirst and polyuria during the day;
3. decompensation - thirst and polyuria persist.
Diagnostics
List of basic and additional diagnostic measures:
Diagnostic measures before planned hospitalization:
- general urine analysis;
- biochemical blood test (potassium, sodium, total calcium, ionized calcium, glucose, total protein, urea, creatinine, blood osmolality);
- assessment of diuresis (>40 ml/kg/day, >2l/m2/day, urine osmolality, relative density).
Basic diagnostic measures:
- Test with dry food (dehydration test);
- Test with desmopressin;
- MRI of the hypothalamic-pituitary zone
Additional diagnostic measures:
- Ultrasound of the kidneys;
- Dynamic tests of kidney function status
Diagnostic criteria:
Complaints and anamnesis:
The main manifestations of ND are severe polyuria (urine output more than 2 l/m2 per day or 40 ml/kg per day in older children and adults), polydipsia (3-18 l/day) and associated sleep disorders. A preference for plain cold/ice water is typical. There may be dry skin and mucous membranes, decreased salivation and sweating. Appetite is usually reduced. The severity of symptoms depends on the degree of neurosecretory insufficiency. With partial vasopressin deficiency, clinical symptoms may not be so clear and may manifest themselves in conditions of drinking deprivation or excessive fluid loss. When collecting anamnesis, it is necessary to clarify the duration and persistence of symptoms in patients, the presence of symptoms of polydipsia, polyuria, diabetes in relatives, a history of trauma, neurosurgical interventions, tumors (craniopharyngioma, germinoma, glioma, etc.), infections (congenital CMV infection , toxoplasmosis, encephalitis, meningitis).
In newborns and infants, the clinical picture of the disease differs significantly from that in adults, since they cannot express their desire for increased fluid intake, which makes timely diagnosis difficult and can lead to the development of irreversible brain damage. Such patients may experience weight loss, dry and pale skin, lack of tears and sweating, and increased body temperature. They may prefer water to breast milk, and sometimes the disease becomes symptomatic only after the baby is weaned. Urine osmolality is low and rarely exceeds 150-200 mOsmol/kg, but polyuria appears only if the child’s fluid intake is increased. In children of such an early age, hypernatremia and hyperosmolality of the blood with convulsions and coma very often and quickly develop.
In older children, thirst and polyuria may come to the fore in clinical symptoms; with inadequate fluid intake, episodes of hypernatremia occur, which can progress to coma and convulsions. Children grow poorly and gain weight; they often vomit when eating, lack appetite, experience hypotension, constipation, and delayed mental development. Overt hypertensive dehydration occurs only in cases of lack of access to fluid.
Physical examination:
Upon examination, symptoms of dehydration may be detected: dry skin and mucous membranes. Systolic blood pressure is normal or slightly decreased, diastolic blood pressure is increased.
Laboratory research:
According to a general urine analysis, it is discolored, does not contain any pathological elements, and has a low relative density (1.000-1.005).
To determine the concentration ability of the kidneys, a Zimnitsky test is performed. If in any portion the specific gravity of urine is higher than 1.010, then the diagnosis of ND can be excluded, but it should be remembered that the presence of sugar and protein in the urine increases the specific gravity of urine.
Plasma hyperosmolality is more than 300 mOsmol/kg. Normal plasma osmolality is 280-290 mOsmol/kg.
Urine hypoosmolality (less than 300 mOsmol/kg).
Hypernatremia (more than 155 mEq/L).
In the central form of ND there is a decrease in the level of vasopressin in the blood serum, and in the nephrogenic form it is normal or slightly increased.
Dehydration test(test with dry food). G.I. Dehydration Test Protocol Robertson (2001).
Dehydration phase:
- take blood for osmolality and sodium (1)
- collect urine to determine volume and osmolality (2)
- measure the patient’s weight (3)
- blood pressure and pulse control (4)
In the future, at regular intervals, depending on the patient’s condition, repeat steps 1-4 after 1 or 2 hours.
The patient is not allowed to drink, it is also advisable to limit food, at least during the first 8 hours of the test; When feeding, food should not contain a lot of water and easily digestible carbohydrates; boiled eggs, grain bread, lean meats and fish are preferred.
The test stops when:
- loss of more than 5% of body weight
- unbearable thirst
- objectively serious condition of the patient
- an increase in sodium and blood osmolality above normal limits.
Desmopressin test. The test is carried out immediately after the end of the dehydration test, when the maximum possibility of secretion/action of endogenous vasopressin has been reached. The patient is given 0.1 mg of tableted desmopressin under the tongue until completely absorbed or 10 mcg intranasally as a spray. Urine osmolality is measured before taking desmopressin and 2 and 4 hours after. During the test, the patient is allowed to drink, but not more than 1.5 times the volume of urine excreted during the dehydration test.
Interpretation of the results of the test with desmopressin: Normally or with primary polydipsia, urine concentration occurs above 600-700 mOsmol/kg, blood osmolality and sodium remain within normal values, well-being does not change significantly. Desmopressin practically does not increase urine osmolality, since the maximum level of its concentration has already been reached.
With central ND, urine osmolality during dehydration does not exceed blood osmolality and remains at a level of less than 300 mOsmol/kg, blood osmolality and sodium increase, severe thirst, dry mucous membranes, increased or decreased blood pressure, and tachycardia are noted. When desmopressin is administered, urine osmolality increases by more than 50%. With nephrogenic ND, blood osmolality and sodium increase, urine osmolality is less than 300 mOsmol/kg, as with central ND, but after using desmopressin, urine osmolality practically does not increase (up to 50% increase).
The interpretation of the sample results is summarized in Table. .
Instrumental studies:
Central ND is considered a marker of pathology of the hypothalamic-pituitary region. MRI of the brain is the method of choice for diagnosing diseases of the hypothalamic-pituitary region. For central ND, this method has several advantages over CT and other imaging modalities.
MRI of the brain is prescribed to identify the causes of central ND (tumors, infiltrative diseases, granulomatous diseases of the hypothalamus and pituitary gland, etc. For nephrogenic diabetes insipidus: dynamic tests of renal function and renal ultrasound. In the absence of pathological changes according to MRI, this study is recommended in dynamics, since there are often cases when central ND appears several years before the detection of a tumor
Indications for consultation with specialists:
If pathological changes in the hypothalamic-pituitary region are suspected, consultations with a neurosurgeon and ophthalmologist are indicated. If a pathology of the urinary system is detected, see a urologist, and if the psychogenic variant of polydipsia is confirmed, a referral for consultation to a psychiatrist or neuropsychiatrist is necessary.
Differential diagnosis
It is carried out between three main conditions accompanied by hypotonic polyuria: central ND, nephrogenic ND and primary polydipsia. Differential diagnosis is based on 3 main stages. 
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Treatment
Treatment goals:
Reducing the severity of thirst and polyuria to such an extent that would allow the patient to lead a normal lifestyle.
Treatment tactics:
Central ND.
Desmopressin remains the drug of choice. Most patients can be treated with desmopressin tablets (0.1 and 0.2 mg), although many patients continue to be treated successfully with desmopressin intranasal spray. Due to individual pharmacokinetic characteristics, it is extremely important to determine the duration of action of a single dose of the drug individually for each patient.
Therapy with desmopressin in tablet form is prescribed at an initial dose of 0.1 mg 2-3 times a day orally 30-40 minutes before meals or 2 hours after meals. Average doses of the drug vary from 0.1 mg to 1.6 mg per day. Concomitant food intake can reduce the degree of absorption from the gastrointestinal tract by 40%. For intranasal use, the initial dose is 10 mcg. When injected, the spray is distributed over the anterior surface of the nasal mucosa, which ensures a longer concentration of the drug in the blood. The need for the drug varies from 10 to 40 mcg per day.
The main goal of treatment with desmopressin is to select the minimum effective dose of the drug to relieve thirst and polyuria. A mandatory increase in the relative density of urine should not be considered as a goal of therapy, especially in each of the Zimnitsky urine test samples, since not all patients with central ND against the background of clinical compensation of the disease achieve normal indicators of concentrated renal function in these tests (physiological variability of urine concentration during the day, concomitant kidney pathology, etc.).
Diabetes insipidus with inadequate thirst.
When the functional state of the thirst center changes towards a decrease in the sensitivity threshold, hyperdipsia, patients are predisposed to the development of such a complication of desmopressin therapy as water intoxication, which is a potentially life-threatening condition. Such patients are advised to periodically skip doses of the drug to release retained excess fluid or a fixed fluid intake.
The state of adipsia in central ND can manifest itself as alternating episodes of hypo- and hypernatremia. Management of such patients is carried out with a fixed daily volume of fluid intake or with recommendations for fluid intake according to the volume of urine excreted + 200-300 ml of additional fluid. Patients with impaired thirst sensation require special dynamic monitoring of their condition with monthly, and in some cases more often, determination of blood osmolality and sodium.
Central ND after surgery on the hypothalamus or pituitary gland and after head trauma.
The disease in 75% of cases has a transient course, and in 3-5% - a three-phase course (phase I (5-7 days) - central ND, phase II (7-10 days) - syndrome of inadequate secretion of vasopresiin, phase III - permanent central ND ). Desmopresiin is prescribed in the presence of symptoms of diabetes insipidus (polydipsia, polyuria, hypernatremia, blood hyperosmolality) at a dose of 0.05-0.1 mg 2-3 times a day. Every 1-3 days, the need to take the drug is assessed: the next dose is skipped, and the resumption of symptoms of diabetes insipidus is monitored.
Nephrogenic ND.
Thiazide diuretics and a low-sodium diet are prescribed to reduce symptomatic polyuria. The antidiuretic effect in this case is due to a reduction in the volume of extracellular fluid, a decrease in the glomerular filtration rate, increased reabsorption of water and sodium from primary urine in the proximal tubules of the nephrons and a decrease in the amount of fluid entering the collecting ducts. However, studies demonstrate that thiazide diuretics can increase the number of aquaporin-2 molecules on the membranes of nephron tubular epithelial cells independently of vasopressin. While taking thiazide diuretics, it is advisable to compensate for potassium losses by increasing its intake or prescribing potassium-sparing diuretics.
When indomethacin is prescribed, additional very beneficial effects develop, but NSAIDs can provoke the development of duodenal ulcers and gastrointestinal bleeding.
Non-drug treatment:
In case of central ND with normal function of the thirst center - free drinking regime, normal diet. In the presence of dysfunction of the thirst center: - fixed fluid intake. For nephrogenic ND - limit salt, eat foods rich in potassium.
Drug treatment:
Minirin, tablets 100, 200 mcg
Minirin, oral lyophilisate 60, 120, 240 mcg
Presaynex, spray for nasal use dosed 10 mcg/dose
Triampur-compositum, tablets 25/12.5 mg
Indomethacin - enteric-coated tablets 25 mg
Other types of treatment: -
Surgical intervention: for neoplasms of the hypothalamic-pituitary region.
Preventive actions: unknown
Further management: outpatient observation
Indicators of treatment effectiveness and safety of diagnostic and treatment methods described in the protocol: reduction of thirst and polyuria.
- List of used literature: 1. Methodological recommendations, ed. Dedova I.I., Melnichenko G.A. “Central diabetes insipidus: differential diagnosis and treatment”, Moscow, 2010, 36 p. 2. Melnichenko G.A., V.S. Pronin, Romantsova T.I. and others - “Clinic and diagnosis of hypothalamic-pituitary diseases”, Moscow, 2005, 104 p. 3. Endocrinology: national guide, ed. Dedova I.I., Melnichenko G.A., Moscow, GEOTAR-Media, 2008, 1072 pp. 4. Pigarova E.A. - Diabetes insipidus: epidemiology, clinical symptoms, treatment approaches, - “Doctor.ru”, No. 6, part II, 2009. 5. Practical endocrinology / ed. Melnichenko G.A.-Moscow, “Practical Medicine”, 2009, 352 pp. 6. Neuroendocrinology / Henry M. Kronenberg, Shlomo Melmed, Kenneth S. Polonsky, P. Ried Larsen, translation from English. Ed. Dedova I.I., Melnichenko G.A., Moscow, ReadAlsiver, 2010, 472 pp.
Information
List of developers:
1. Danyarova L.B. - Candidate of Medical Sciences, Head of the Endocrinology Department of the Research Institute of Cardiology and Internal Medicine, endocrinologist of the highest category.
2. Shiman Zh.Zh. - Junior Researcher, Department of Endocrinology, Research Institute of Cardiology and Internal Medicine, endocrinologist.
Disclosure of no conflict of interest: absent.
Reviewers: Erdesova K.E. - Candidate of Medical Sciences, Professor, Internship Department of KazNMU.
Indication of the conditions for reviewing the protocol: The protocol is revised at least once every 5 years, or upon receipt of new data on the diagnosis and treatment of the corresponding disease, condition or syndrome.
Attached files
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Diabetes insipidus – a disease caused by an absolute or relative deficiency of the hypothalamic hormone vasopressin (ADH-antidiuretic hormone).
The frequency of the disease is unknown; it occurs in 0.5-0.7% of endocrine patients.
Regulation of vasopressin release and its effects
Vasopressin and oxytocin are synthesized in the supraoptic and paraventicular nuclei of the hypothalamus, packaged into granules with the corresponding neurophysins and transported along axons to the posterior lobe of the pituitary gland (neurohypophysis), where they are stored until released. The reserves of vasopressin in the neurohypophysis with chronic stimulation of its secretion, for example, with prolonged abstinence from drinking, are sharply reduced.
Vasopressin secretion is caused by many factors. The most important of them is blood osmotic pressure, i.e. osmolality (or otherwise osmolarity) of plasma. In the anterior hypothalamus, close to, but separate from the supraoptic and paraventicular nuclei, is located osmoreceptor . When plasma osmolality is at a certain normal minimum, or threshold value, the concentration of vasopressin in it is very low. If plasma osmolality exceeds this set threshold, the osmocenter perceives this, and the concentration of vasopressin rises sharply. The osmoregulation system reacts very sensitively and very accurately. Some increase osmoreceptor sensitivity is associated with age.
The osmoreceptor is unequally sensitive to different plasma substances. Sodium(Na +) and its anions are the most powerful stimulators of the osmoreceptor and vasopressin secretion. Na and its anions normally determine 95% of plasma osmolality.
Very effectively stimulate the secretion of vasopressin through the osmoreceptor sucrose and mannitol. Glucose practically does not stimulate the osmoreceptor, just like urea.
The most reliable evaluative factor in stimulating vasopressin secretion is to determineNa + and plasma osmolality.
The secretion of vasopressin is influenced by blood volume and blood pressure level. These influences are exerted through baroreceptors located in the atria and aortic arch. Stimuli from the baroreceptor travel through afferent fibers to the brainstem as part of the vagus and glossopharyngeal nerves. From the brain stem, signals are transmitted to the neurohypophysis. A decrease in blood pressure or a decrease in blood volume (eg, blood loss) significantly stimulates the secretion of vasopressin. But this system is much less sensitive than osmotic stimuli at the osmoreceptor.
One of the effective factors stimulating the release of vasopressin is nausea, spontaneous, or caused by procedures (vomiting, alcohol, nicotine, apomorphine). Even with incoming nausea, without vomiting, the level of vasopressin in plasma increases 100-1000 times!
Less effective than nausea, but an equally constant stimulus for vasopressin secretion is hypoglycemia, especially spicy. A decrease in the level of glucose in the blood by 50% of the initial level increases the content of vasopressin by 2-4 times in humans, and in rats by 10 times!
Increases vasopressin secretion renin-angiotensin system. The level of renin and/or angiotensin required to stimulate vasopressin is not yet known.
It is also believed that nonspecific stress, caused by factors such as pain, emotions, physical activity, increases the secretion of vasopressin. However, it remains unknown how stress stimulates the secretion of vasopressin - in some specific way, or through a decrease in blood pressure and nausea.
Inhibits the secretion of vasopressin vasoactive substances such as norepinephrine, haloperidol, glucocorticoids, opiates, morphine. But it is not yet clear whether all these substances act centrally, or by increasing blood pressure and volume.
Once in the systemic circulation, vasopressin is quickly distributed throughout the extracellular fluid. Equilibrium between the intra- and extravascular space is achieved within 10-15 minutes. Inactivation of vasopressin occurs mainly in the liver and kidneys. A small part is not destroyed and is excreted intact in the urine.
Effects. The most important biological effect of vasopressin is retaining water in the body by reducing urine output. The point of application of its action is the epithelium of the distal and/or collecting tubules of the kidneys. In the absence of vasopressin, the cell membranes lining this part of the nephron form an insurmountable obstacle to the diffusion of water and soluble substances. Under such conditions, the hypotonic filtrate formed in the more proximal parts of the nephron passes unchanged through the distal tubule and collecting ducts. The specific gravity (relative density) of such urine is low.
Vasopressin increases the permeability of the distal and collecting ducts to water. Since water is reabsorbed without osmotic substances, the concentration of osmotic substances in it increases, and its volume, i.e. quantity decreases.
There is evidence that a local tissue hormone, prostaglandin E, inhibits the action of vasopressin in the kidneys. In turn, non-steroidal anti-inflammatory drugs (for example, Indomethacin), which inhibit the synthesis of prostaglandins in the kidneys, increase the effect of vasopressin.
Vasopressin also acts on various extrarenal systems, such as blood vessels, gastrointestinal tract, and central nervous system.
Thirst serves as an indispensable complement to the antidiuretic activity of vasopressin . Thirst is a conscious sensation of the need for water. Thirst is stimulated by many factors that cause the secretion of vasopressin. The most effective of them is hypertensive environment. The absolute level of plasma osmolality at which the feeling of thirst appears is 295 mOsmol/kg. At this osmolality, the blood normally produces urine with maximum concentration. Thirst is a kind of brake, the main function of which is to prevent a degree of dehydration that exceeds the compensatory capabilities of the antidiuretic system.
The feeling of thirst increases rapidly in direct proportion to plasma osmolality and becomes unbearable when the osmolality is only 10-15 mOsmol/kg above the threshold level. Water consumption is proportional to the feeling of thirst. A decrease in blood volume or blood pressure also causes thirst.
Etiology
The development of central forms of diabetes insipidus is based on damage to various parts of the hypothalamus or posterior pituitary gland, i.e. neurohypophysis. The following factors may be the reasons:
infections acute or chronic: influenza, meningoencephalitis, scarlet fever, whooping cough, typhus, sepsis, tonsillitis, tuberculosis, syphilis, rheumatism, brucellosis, malaria;
traumatic brain injuries : accidental or surgical; electric shock; birth trauma during childbirth;
mental trauma ;
pregnancy;
hypothermia ;
tumor of the hypothalamus or pituitary gland : metastatic or primary. Cancer of the breast, thyroid glands, and bronchi most often metastasizes to the pituitary gland. Infiltration with tumor elements in lymphogranulomatosis, lymphosarcoma, leukemia, generalized xanthomatosis (Hand-Schüller-Crispen disease). Primary tumors: adenoma, glioma, teratoma, craniopharyngioma (especially common), sarcoidosis;
endocrine diseases : Simmonds, Sheehan, Lawrence-Moon-Biedl syndromes, pituitary dwarfism, acromegaly, gigantism, adinosogenital dystrophy;
idiopathic: in 60-70% of patients the cause of the disease remains unclear. Among idiopathic forms, hereditary diabetes mellitus, which lasts for several generations, has a noticeable representation. The type of inheritance is autosomal dominant and recessive;
autoimmune : destruction of the hypothalamic nuclei as a result of an autoimmune process. This form is thought to occur among idiopathic diabetes insipidus, in which autoantibodies to vasopressin-secreting cells appear.
For peripheral In diabetes insipidus, vasopressin production is preserved, but the sensitivity of renal tubular receptors to the hormone is reduced or absent, or the hormone is intensively destroyed in the liver, kidneys, and placenta.
Nephrogenic diabetes insipidus is more often observed in children, and is caused by anatomical inferiority of the renal tubules (congenital deformities, cystic degenerative processes), or damage to the nephron (amyloidosis, sarcoidosis, lithium poisoning, methoxyfluramine). or decreased sensitivity of renal tubular epithelial receptors to vasopressin.
Diabetes insipidus clinic
Complaints
for thirst from moderate to painful, not letting go of patients day or night. Sometimes patients drink 20-40 liters of water per day. At the same time, there is a desire to drink ice water;
polyuria and frequent urination. The urine produced is light, without urochromes;
physical and mentalweakness;
loss of appetite,weight loss; possible development obesity if diabetes insipidus develops as one of the symptoms of primary hypothalamic disorders.
dyspeptic disorders from the stomach - a feeling of fullness, belching, pain in the epigastrium; intestines - constipation; gallbladder - heaviness, pain in the right hypochondrium;
mental and emotional disorders: headaches, emotional imbalance, insomnia, decreased mental activity, irritability, tearfulness; sometimes psychosis develops.
menstruation disorders, in men - potency.
Anamnesis
The onset of the disease can be acute and sudden; less often - gradual, and symptoms increase as the disease becomes more severe. The cause may be traumatic brain or mental injuries, infections, or surgical interventions on the brain. Most often, the cause cannot be identified. Sometimes a family history of diabetes insipidus is established.
Flow chronic diseases.
Inspection
emotional lability;
the skin is dry, salivation and sweating are reduced;
body weight can be reduced, normal or increased;
the tongue is often dry due to thirst, the borders of the stomach are lowered due to constant fluid overload. With the development of gastritis or biliary dyskinesia, increased sensitivity and pain on palpation of the epigastrium and right hypochondrium is possible;
the cardiovascular and respiratory systems, the liver are usually not affected;
urinary system: frequent urination, polyuria, nocturia are noted;
signsdehydration of the body, if the fluid lost in the urine is not replenished for some reason - lack of water, conducting a test with “dry eating”, or the sensitivity of the “thirst” center decreases:
severe general weakness, headaches, nausea, repeated vomiting, aggravating dehydration;
hyperthermia, convulsions, psychomotor agitation;
CVS disorder: tachycardia, hypotension up to collapse and coma;
blood thickening: increase in the number of Hb, red blood cells, Na + (N136-145 mmol/l, or mEq/l) creatinine (N60-132 μmol/l, or 0.7-1.5 mg%);
the specific gravity of urine is low - 1000-1010, polyuria persists.
These phenomena of hyperosmolar dehydration are especially characteristic of congenital nephrogenic diabetes insipidus in children.
The diagnosis is made based on classic signs of diabetes insipidus and laboratory and instrumental studies:
polydipsia, polyuria
low specific gravity of urine – 1000-1005
plasma hyperosmolarity, > 290 mOsm/kg (N280-296 mOsm/kg water, or mmol/kg water);
hypoosmolarity of urine,< 100-200 мосм/кг;
hypernatremia, > 155 mEq/L (N136-145 mEq/L, mmol/L).
If necessary, carried out samples :
Test with dry eating. This test is carried out in a hospital setting, its duration is usually 6-8 hours, if well tolerated - 14 hours. No fluid is given. Food should be protein. Urine is collected every hour, and the volume and specific gravity of each hourly portion are measured. Body weight is measured after every 1 liter of urine excreted.
Grade: the absence of significant dynamics in the specific gravity of urine in two subsequent portions with a loss of 2% of body weight indicates a lack of stimulation of endogenous vasopressin.
Test with intravenous administration of 50 ml of 2.5% solutionNaCl within 45 min. In diabetes insipidus, the volume and density of urine do not change significantly. In psychogenic polydipsia, an increase in plasma osmotic concentration quickly stimulates the release of endogenous vasopressin and the amount of urine excreted decreases and its specific gravity increases.
A test with the administration of vasopressin drugs - 5 units IV or IM. With true diabetes insipidus, health improves, polydipsia and polyuria decrease, plasma osmolarity decreases, and urine osmolarity increases.
Differential diagnosis of diabetes insipidus
Based on the main signs of diabetes insipidus - polydipsia and polyuria, this disease is differentiated from a number of diseases that occur with these symptoms: psychogenic polydipsia, diabetes mellitus, compensatory polyuria in chronic renal failure (chronic renal failure).
Nephrogenic vasopressin-resistant diabetes insipidus (congenital or acquired) is differentiated on the basis of polyuria with primary aldosteronism, hyperparathyroidism with nephrocalcinosis, malabsorption syndrome in chronic enterocolitis.
With diabetes
Table 22
With psychogenic polydipsia
Table 23
|
Sign |
Diabetes insipidus |
Psychogenic polydipsia |
|
common reason |
Infections, traumatic brain injuries (including surgical) |
Gradual Psychotrauma, psychogenic stress |
|
Presence of a tumor |
Pituitary tumors, sarcoma, lymphogranulomatosis, etc. |
Absent |
|
Osmolarity: | ||
|
Test with dry eating (no more than 6-8 hours) |
No dynamics |
The amount of urine decreases, specific gravity and osmolality normalize |
|
How you feel during this test |
Worsens, thirst becomes painful |
Condition and well-being are not affected |
|
Test with i.v. injection 50 ml 2.5% NaCl |
The amount of urine and its density without dynamics |
The amount of urine decreases and the specific gravity |
|
Feeling better, polydipsia and polyuria decrease |
Feeling worse (headaches) |
Central (hypothalamic pituitary) with nephrogenic diabetes insipidus
Table 24
|
Sign |
Central diabetes insipidus |
Nephrogenic diabetes insipidus |
|
Traumatic brain injuries, infections, tumors. |
Family; hyperparathyroidism; taking medications - lithium carbonate, demeclocycline, methoxyflurane |
|
|
Test with intravenous administration of 5 units of vasopressin |
The state of health improves, polydipsia and polyuria decrease. Plasma osmolality , and urine osmolality |
No dynamics |
|
Changes are detected in the urine |
None |
Albuminuria, cylindruria |
|
Blood creatine | ||
|
Arterial hypertension |
BP often |
Treatment of diabetes insipidus
Etiological : for tumors of the hypothalamus or pituitary gland - surgery, or radiation therapy, cryodestruction, administration of radioactive ytrium.
For infectious processes - antibacterial therapy.
For hemoblastoses – cytostatic therapy.
Replacement therapy – drugs that replace vasopressin:
Adiuretin(synthetic analogue of vasopressin) intranasally, 1-4 drops in each nostril 2-3 times a day; Available in bottles of 5 ml, 1 ml - 0.1 mg of active substance;
Adiurecrin(extract of the posterior lobe of the pituitary gland of cattle). Available in powder form. Inhale 0.03-0.05 2-3 times a day. The duration of action of one inhalation is 6-8 hours. During inflammatory processes in the nasal cavity, the absorption of adiurecrine is disrupted and its effectiveness is sharply reduced;
RP:adiurecrini0.05Dsd№30.S. inhale through the nose, ampoules 1 ml;
Pituitrin. Release form 5 units of activity. Water-soluble extract of the posterior lobe of the pituitary gland of cattle. 5 units (1 ml) are administered 2-3 times a day intramuscularly. Often causes symptoms water intoxication(headaches, abdominal pain, diarrhea, fluid retention) and allergies;
DDAVP(1 deamino-8D-arginine-vasopressin) – a synthetic analogue of vasopressin;
diuretics of the thiazide group(Hypothiazide, etc.). Hypothiazide 100 mg per day reduces glomerular filtration, Na + excretion with a decrease in the amount of urine. The effect of thiazide diuretics is not detected in all patients with diabetes insipidus and weakens over time;
Chlorpropamide(oral glucose-lowering drug) is effective in some patients with diabetes insipidus. Tablets of 0.1 and 0.25. Prescribed in a daily dose of 0.25 in 2-3 doses. The mechanism of antidiuretic action is not fully understood; it is assumed that it potentiates vasopressin, at least with minimal amounts in the body.
To avoid hypoglycemia and hyponatremia, it is necessary to control the level of glucose and Na + in the blood.
(“diabetes”) is a disease that develops when there is insufficient release of antidiuretic hormone (ADH) or a decrease in the sensitivity of the kidney tissue to its action. As a result, there is a significant increase in the amount of fluid excreted in the urine, and an unquenchable feeling of thirst occurs. If fluid losses are not fully compensated, then dehydration of the body develops - dehydration, the distinctive feature of which is concomitant polyuria. Diagnosis of diabetes insipidus is based on the clinical picture and determination of the level of ADH in the blood. To determine the cause of the development of diabetes insipidus, a comprehensive examination of the patient is carried out.
ICD-10
E23.2
General information
(“diabetes”) is a disease that develops when there is insufficient release of antidiuretic hormone (ADH) or a decrease in the sensitivity of the kidney tissue to its action. Violation of the secretion of ADH by the hypothalamus (absolute deficiency) or its physiological role with sufficient formation (relative deficiency) causes a decrease in the processes of reabsorption (reabsorption) of fluid in the renal tubules and its excretion in urine of low relative density. In diabetes insipidus, due to the release of a large volume of urine, unquenchable thirst and general dehydration of the body develop.
Diabetes insipidus is a rare endocrinopathy that develops regardless of the gender and age group of patients, most often in people 20-40 years old. In every 5th case, diabetes insipidus develops as a complication of neurosurgical intervention.
Classification
Complications
Diabetes insipidus is dangerous due to the development of dehydration of the body in cases where fluid loss through urine is not adequately replenished. Dehydration is manifested by severe general weakness, tachycardia, vomiting, mental disorders, blood thickening, hypotension up to collapse, and neurological disorders. Even with severe dehydration, polyuria persists.
Diagnosis of diabetes insipidus
Typical cases allow one to suspect diabetes insipidus by unquenchable thirst and the release of more than 3 liters of urine per day. To assess the daily amount of urine, a Zimnitsky test is performed. When examining urine, its low relative density is determined (<1005), гипонатрийурию (гипоосмолярность мочи - 100-200 мосм/кг). В крови выявляются гиперосмолярность (гипернатрийемия) плазмы (>290 mOsm/kg), hypercalcemia and hypokalemia. Diabetes mellitus is excluded by determining fasting blood glucose. In the central form of diabetes insipidus, a low level of ADH is determined in the blood.
The results of the test with dry eating are indicative: abstaining from drinking liquids for 10-12 hours. With diabetes insipidus, weight loss of more than 5% occurs, while maintaining low specific gravity and hypoosmolarity of urine. The causes of diabetes insipidus are clarified by X-ray, psychoneurological, and ophthalmological examinations. Space-occupying lesions of the brain are excluded by performing an MRI of the brain. To diagnose the renal form of diabetes insipidus, ultrasound and CT scan of the kidneys are performed. Consultation with a nephrologist is necessary. Sometimes a kidney biopsy is required to differentiate renal pathology.
Treatment of diabetes insipidus
Treatment of symptomatic diabetes insipidus begins with eliminating the cause (for example, a tumor). For all forms of diabetes insipidus, replacement therapy with a synthetic analogue of ADH, desmopressin, is prescribed. The drug is administered orally or intranasally (by instillation into the nose). A prolonged preparation of pituitrin oil solution is also prescribed. In the central form of diabetes insipidus, chlorpropamide and carbamazepine are prescribed, which stimulate the secretion of antidiuretic hormone.
The water-salt balance is corrected by infusion of saline solutions in large volumes. Sulfonamide diuretics (hypochlorothiazide) significantly reduce diuresis in diabetes insipidus. Nutrition for diabetes insipidus is based on limiting protein (to reduce the load on the kidneys) and sufficient consumption of carbohydrates and fats, frequent meals, and an increase in the amount of vegetable and fruit dishes. As for drinks, it is recommended to quench your thirst with juices, fruit drinks, and compotes.
Forecast
Diabetes insipidus, which develops in the postoperative period or during pregnancy, is often transient (transitory) in nature, idiopathic - on the contrary, persistent. With appropriate treatment there is no danger to life, although recovery is rarely recorded.
Recovery of patients is observed in cases of successful removal of tumors, specific treatment of diabetes insipidus of tuberculosis, malaria, and syphilitic origin. When hormone replacement therapy is prescribed correctly, the ability to work is often preserved. The least favorable course of the nephrogenic form of diabetes insipidus in children.
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