Equis ISSN 2398-2977

Systemic lupus erythematosus-like syndrome

Synonym(s): SLE

Contributor(s): Ruth Morgan

Introduction

  • Very rare.
  • Cause: a multi-systemic autoimmune disease. Possible genetic factors but no heritability established. Has features of both systemic lupus erythematosus and discoid lupus erythematosus, but lupus cells have not yet been identified in the horse.
  • Polysystemic auto-immune disease with multiple and variable signs in several or many organs or structures.
  • Wide range of auto-antibodies.
  • Signs: main signs in skin. Variable from mild limb edema to multiple organ failure - multiple organ involvement including liver, kidney, serosal surfaces.
  • Diagnosis: difficult to diagnose. Some cases have a high titer of anti-nuclear antibody. No lupus cells identified in horses yet.
  • Treatment: corticosteroids, aurothioglucose.
  • Prognosis: very poor.

Pathogenesis

Etiology

  • Autoimmune.
  • Failure of regulating mechanisms that sustain self-tolerance:
    • Auto-antibodies to an unpredictable array of nuclear and cytoplasmic components that are neither organ nor cell specific.
    • Range of antinuclear antibodies grouped in 4 categories - antibodies to:
      • DNA.
      • Histones.
      • Non-histone proteins bound to RNA.
      • Nuclear antigens.
      • Detected by specific direct immunofluorescence tests on tissue biopsies.
  • IgG, IgM and complement C3 found at th epidermal-dermal junction and around small blood vessels.
  • Possible response to viral or bacterial infections, changes in environment, drugs, stress, extreme temperatures.
  • Endocrine implications possibly involved (not defined).
  • Possibly drug response-related in some cases.
  • SLE-like syndrome is a complex disorder of multifactorial origin resulting from interactions between genetic, endocrine, environmental and iatrogenic factors that cause activation of T-helper cells and B cells that result in the secretion of several species of auto-antibodies.
  • Each causative factor may be necessary for the condition to develop but not enough for clinical expression of the disease and the relative importance of each factor varies with individuals.

Predisposing factors

General
  • Not known for horses but drugs are often implicated (possibly with/without justification).

Specific

  • Viral/bacterial infections possibly involved.

Pathophysiology

  • Unknown.

Timecourse

  • Acute onset is possible.
  • Signs may be slow to develop.
  • Progressive with deterioration over weeks to months.
  • Variable remissions and relapses occur at irregular intervals and with unpredictable extent.

Diagnosis

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rosenkrantz W (2013) Immune-mediated dermatoses. Vet Clin North Am Equine Pract 29, 607-613 PubMed.
  • Gershwin L J (2005) Antinuclear antibodies in domestic animals. Ann N Y Acad Sci 1050, 364-370 PubMed.
  • Geor R J, Clark E G, Haines D M et al (1990) Systemic lupus erythematosus in a filly. JAVMA 197, 1489 PubMed.
  • Manning T & Sweeny C (1986) Immune mediated equine skin disease. Comp Cont Educ Pract Vet 12, 979-984 VetMedResource.

Other sources of information

  • Day M J (2010) Systemic Lupus Erythematosus in Domestic Animals. In: Systemic Lupus Erythematosus. 5th edn. Eds: Lahita R G, Tsokos G, Buyon J & Koike T. Academic Press, Elsevier. pp 437-451. ISBN: 978-0-12-374994-9.


ADDED