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Symptoms of diabetes mellitus in children
Last reviewed: 04.07.2025

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The pre-manifest stages of diabetes mellitus type 1 have no specific clinical symptoms. Clinical manifestation develops after the death of 80-90% of beta cells and is characterized by the appearance of the so-called "major" symptoms - thirst, polyuria and weight loss. Moreover, at the onset of the disease, weight loss is noted, despite increased appetite and increased nutrition. The first manifestation of polyuria may be nocturnal or daytime enuresis. Increasing dehydration causes dry skin and mucous membranes. Fungal and pustular skin diseases often join in; girls may develop vulvitis. The subcutaneous fat layer becomes thinner, tissue turgor decreases. Weakness and fatigue increase, and performance decreases.
In a third of cases, the first clinical symptoms of type 1 diabetes are signs of diabetic ketoacidosis. There are three stages of diabetic ketoacidosis.
- Stage I, ketosis. Against the background of dehydration symptoms, the accumulation of ketone bodies in the body provokes nausea, vomiting, abdominal pain, loose stools (toxic gastroenteritis). In this case, the mucous membranes are bright, the tongue is dry, coated with a thick coating. Rubeosis is characteristic (diabetic blush on the zygomatic arches, above the eyebrows, on the chin), exhaled air has a characteristic smell of acetone.
- Stage II - precoma. Occurs with decompensation of metabolic acidosis against the background of progressive dehydration. The clinical criterion for the onset of stage II is noisy toxic breathing (Kussmaul breathing). As a result of erosive gastroenteritis, abdominal syndrome develops (abdominal pain, tension of the muscles of the anterior abdominal wall, positive symptoms of peritoneal irritation, repeated vomiting). Dryness of the skin and mucous membranes increases, acrocyanosis appears. Blood pressure decreases, tachycardia appears. At the same time, consciousness is preserved, but gradually becomes soporous.
- Stage III - coma. Characterized by loss of consciousness, suppression of reflexes, decreased diuresis, cessation of vomiting, and worsening hemodynamic disorders. Against the background of symptoms of severe dehydration and impaired microcirculation, the patient experiences rare noisy breathing, muscle hypotension, tachycardia, and abnormal heart rhythms. Later, a drop in blood pressure is observed. If timely assistance is not provided, neurological disorders progressively increase. The final stage of CNS depression is coma. The absence or weak reaction of the pupils to light indicates the development of structural changes in the brainstem.
Quite rarely, clinical manifestation of type 1 diabetes mellitus in children ends with non-ketotic hyperosmolar coma, which is characterized by severe hyperglycemia (above 40 mmol/l), absence of ketosis, non-ketotic acidosis, dehydration, and loss of consciousness. In this case, blood osmolality due to hyperglycemia reaches 350 mosm/l and higher. Damage to the hypothalamic thirst center due to high blood osmolality leads to the disappearance of thirst and further disruption of osmoregulatory mechanisms. The reasons for the development of this particular type of coma in children are unknown.
Features of diabetes mellitus in young children
The onset of persistent diabetes mellitus type 1 in children under 6 months is almost never observed. In newborns, a syndrome of transient (transient) diabetes mellitus type 1 is sometimes observed, which begins in the first weeks of life, and spontaneous recovery occurs after several months. It most often occurs in children with low birth weight and is characterized by hyperglycemia and glucosuria, leading to moderate dehydration and sometimes to metabolic acidosis. It is assumed that the insulin response to glucose is reduced, the insulin level in the blood plasma is normal. Transient diabetes is treated with insulin, which is usually discontinued after 2 months with repeated hypoglycemia.
Rare cases of congenital diabetes are caused by a genetic defect in insulin. The defect is a disruption in the leucine-phenylalanine amino acid sequence at position 25.
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