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Diabetes insipidus in a pediatric patient with systemic lupus erythematosus. A case report

N Tekin1, N Kural, A K Koçak

  • 1Department of Pediatrics, Osmangazi University Faculty of Medicine, Eskişehir.

Insights

Systemic lupus erythematosus (SLE) can affect the central nervous system (CNS), leading to diverse neurological symptoms. This case highlights a rare instance of CNS lupus presenting with diabetes insipidus (DI) in a young patient, successfully treated with immunosuppression and desmopressin.

Area of Science:

  • Neurology
  • Endocrinology
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease with potential for central nervous system (CNS) involvement.
  • CNS manifestations in SLE are diverse and can present with varied clinical neurological disorders.
  • Cerebral involvement in SLE can lead to significant morbidity, necessitating comprehensive diagnostic and therapeutic approaches.

Observation:

  • A 14-year-old female patient presented with clinical features indicative of cerebral involvement secondary to SLE.
  • An unusual complication observed was the development of diabetes insipidus (DI), a condition affecting water balance.
  • The diabetes insipidus demonstrated a positive response to desmopressin, a synthetic analog of vasopressin.

Findings:

  • The presented case illustrates a rare association between SLE-related CNS dysfunction and the development of diabetes insipidus.
  • Effective management involved a combination therapy including high-dose methylprednisolone and cyclophosphamide.
  • This therapeutic regimen successfully ameliorated both the general SLE symptoms and the specific endocrine dysfunction (DI).

Implications:

  • This case underscores the importance of considering endocrine complications, such as DI, in pediatric patients with CNS lupus.
  • The findings suggest that aggressive immunosuppressive therapy can be beneficial for managing both neurological and endocrine manifestations of SLE.
  • Further research into the mechanisms linking CNS lupus and DI may reveal novel therapeutic targets.

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