| Abstrakt: |
Diabetes insipidus is a rare endocrinological disease and occurs in 2–4 per 100,000 pregnancies. Diagnosis of gestational diabetes insipidus is very difficult because it develops against the background of physio logical mechanisms that accompany pregnancy: thirst threshold decreases leading to polydipsia and plasma osmolarity decreases causing hypotonic polyuria. Understanding of pathophysiology of the disorder is very important for further management of these vulnerable patients. A 32-year-old patient at 36 weeks of gesta-tion, primigravida, was referred to an endocrinologist with complaints of polyuria (6.5 l/day), nocturia — up to5 times, severe polydipsia. At12 weeks of gestation, there was a risk of abortion for prevention of which the patient received progesterone 100 mg intravaginally twice a dayuntil 34 weeks. She has a history of subacutethyroiditis, with no family history of endocrine pathology. Physical examination revealed a decrease in skin turgor, blood pressure 110/85 mm Hg. Heart rate 115 bpm, weight 71 kg (body mass index 26.9 kg/m2). The patient was at high risk of developing preeclampsia. Laboratory data: analysis of urine according to Zimnitsky: volumeper day — 6.8 l, specific gravity in portions: 1.012; 1.008; 1.010; 1.005; 1.012; 1.014; 1.010.Total blood count,total urine test, serum sodium and potassium, liver function tests, level of thyroid-stimulating hormone, free thyroxine, thyroid peroxidase antibodies and morning free cortisol level were normal. The patient was administereddesmopressin 10 μg intranasally twice daily. Six weeks after delivery, desmopressin was stopped and she had no further evidence of polyuria, polydipsia or nocturia. [ABSTRACT FROM AUTHOR] |
