Main Article Content

Abstract

Systemic lupus erythematosus (SLE) is an idiopathic autoimmune chronic inflammatory
disease that is unique in its diversity of clinical manifestations, variability of disease’s progression, and prognosis. The disease is characterized by the remission and multiple flare-ups in between the chronic phase that may affect many organ systems.The prevalence of SLE in the US population is 1:1000 with a woman to man ratio of about 9-14:1. At Cipto Mangunkusumo Hospital, Jakarta in 2002, there was 1.4% cases of SLE of the total number of patients at the Rheumatology Clinic. Neuropsychiatric manifestations of SLE (NP-SLE) have a high mortality and morbidity rates. The incidence of NP-SLE ranges 18-61%. Diagnosis of NP-SLE is difficult because there is no specific laboratory examination. Accordingly, in all SLE patients with central nervous system (CNS) dysfunction, additional tests will be necessary to confirm an NP-SLE diagnosis and exclude other causes. Similar to diabetes insipidus, SLE is a systemic disease which affects many organ systems, one being the endocrine system. No data has specified the occurrence rate of diabetes insipidus in SLE patients. This disease arises from a number of factors able to interfere with the mechanism of neurohypophyseal renal reflex resulting in the body’s failure to convert water.3 There are three general forms of the disease, a polydipsicpolyuric syndrome caused by partial/complete vasopressin deficiency (central-diabetes-insipidus/CDI), vasopressin resistance of the kidney tubules (nephrogenic-diabetes-insipidus/NDI), and primary polydipsia. CDI occurs in about 1 in 25,000 persons

Article Details

How to Cite
Pangestu, Y., Wardoyo, A., Wijaya, L. K., SETIYOHADI, B., Albar, Z., Sukmana, N., Budiman, B., Djoerban, Z., Effendy, S., Aziza, L., & Sitorus, F. (2018). Diabetes insipidus in neuropsychiatric-systemic lupus erythematosus patient. Indonesian Journal of Rheumatology, 1(2). https://doi.org/10.37275/ijr.v2i1.24

References

  1. Indonesian Rheumatism Association. Systemic lupus erythematosus
  2. diagnostic and management guidance. [Panduan diagnosis dan
  3. pengelolaan systemic lupus erythematosus] Jakarta: The Association;
  4. West SG. Systemic lupus erythematosus and the nervous system. In:
  5. Wallace DJ, Hahn BH, editors. Dubois’ lupus erythematosus. 6th ed.
  6. Philadelphia: Lippincott Williams & Wilkins; 2002. p.693- 738.
  7. Bryun GA. Controversies in lupus: nervous system involvement. Ann
  8. Rheum Dis. 1995;54:159-67.
  9. Vratsanos G, Kang I, Craft J. Systemic lupus erythematosus. In: Austen
  10. KF, Frank MM, Atkinson JP, Cantor H, editors. Samster’s immunologic
  11. disease. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2001. p.
  12. -90.
  13. Ranakusuma ABS, Subekti I. Diabetes insipidus. In: Noer S, Waspadji
  14. S, Rachman AM, Lesmana LA, Widodo D, Isbagio H, et al, editors.
  15. Text book of internal medicine. [Buku ajar ilmu penyakit dalam] 3rd ed.
  16. Jakarta: Balai Penerbit FKUI; 1996. p. 816-24.
  17. Levine JS, Branch DW, Rauch J. Review article: the antiphospolipid
  18. syndrome. N Engl J Med 2002;346: 752-62.
  19. Setiyohadi B. The management of systemic lupus erythematosus.
  20. [Penatalaksanaan lupus eritematosus sistemik] In: Setiyohadi B,
  21. Kasjmir YI, editors. Complete papers of the 2003 rheumatology
  22. scientific meeting. [Naskah lengkap temu ilmiah reumatologi 2003]
  23. Preceedings of the 2003 Rheumatology Scientific Meeting; 2003
  24. Sept 19-21; Jakarta, Indonesia. Jakarta: Indonesian Rheumatism
  25. Association; 2003. p.154-58.
  26. Gladman DD, Urowitz MB. Clinical feature connective tissue disorders.
  27. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Wisman MH,
  28. editors. Rheumatology. 3rd ed. Edinburgh: Mosby; 2003. p. 1359-75.
  29. Goodnight SH, Hathaway WE. Disorders of hemostasis and thrombosis
  30. a clinical guide. New York: McGraw-Hill; 2001. p. 237-47.
  31. Sanna G, Bertolaccini ML, Cuadrado MJ, Khamashta MA, Hughes RV.
  32. Central nervous system involvement in the antiphospolipid (Hughes)
  33. syndrome. Rheumatology 2003;42:200-13.
  34. Wallace DJ. Severe lupus. In: Hochberg MC, Silman AJ, Smolen JS,
  35. Weinblatt ME, Wisman MH, editors. Rheumatology. 3rd ed. Edinburg:
  36. Mosby; 2003. p. 1415-26.
  37. Baylis PH, Thompson CJ. Diabetes insipidus and hyperosmolar
  38. syndrome. In: Becker K, Bilezikian JP, Bremner WJ, Hung W, Kahn
  39. CR, Loriaux DL, et al, editors. Principles and practice of endocrinology
  40. and metabolism. 3rd ed. Philadelphia: Lippincott Williams & Wilkins;
  41. p. 285-93.
  42. Pivonello R, De Bellis A, Faggiano A, Di Salle F, Petretta M, Di Somma
  43. C, et al. Central diabetes insipidus and autoimmunity: relationship
  44. between the occurrence of antibodies to arginine vasopressinsecreting cells and clinical, immunological, and radiological features in
  45. a large cohort of patients with central diabetes insipidus of known and
  46. unknown etiology. J Clin Endocrinol Metab 2003;88(4):1629-36.
  47. Kajiyama H, Terai C, De Bellis A, Bizzaro A, Bellastella A, Ohta S, et al.
  48. Vasopressin cell antibodies and central diabetes insipidus in a patient
  49. with systemic lupus erythematosus and dermatomyositis. J Rheumatol
  50. ;31:1218-21.
  51. Maghnic M, Altobelli M, Lorgi A, Genovese E, Meloni G, Manca-Bitti
  52. ML, et al. Idiopayhic central diabetes insipidus is associated with
  53. abnormal blood supply to the posterior pituitary gland caused by
  54. vascular impairment of the inferior hypophyseal artery system. J Clin
  55. Endocrinol Metab 2004;89:1891-96.