WHEN SILENCE TAKES OVER: A CASE OF CATATONIC SYNDROME REVEALING SYSTEMIC LUPUS ERYTHEMATOSUS

PV298 / #813 Case Report Poster Topic: AS23 - SLE-Diagnosis, Manifestations, & Outcomes Late-Breaking Abstract Introduction Systemic lupus erythematosus (SLE) is a complex and potentially serious autoimmune disease. Catatonia is a syndrome characterized by physical and behavioral abnormalities, which can result from psychiatric, neurological, or medical disorders. Attributing catatonia to SLE remains a challenge. Although it is not included in the diagnostic criteria for neuropsychiatric involvement associated with SLE, several cases have been reported in the literature, but only in patients with preexisting, known SLE. We present here a case of catatonia revealing SLE. Case Presentation With Investigation This is a 21-year-old female patient with no significant medical history who presented several days prior to hospitalization with inflammatory arthralgia affecting both small and large joints, complicated by a catatonic syndrome associated with sepsis of pulmonary and urinary origin. This situation led to hospitalization in the intensive care unit for appropriate management. Clinical examination revealed a malar rash, negativism, and mutism. Laboratory results showed normochromic normocytic anemia (hemoglobin at 10.7 g/dl), lymphopenia (690/mm³), a positive direct Coombs test, hypoalbuminemia, elevated alpha-1 globulins, and polyclonal hypergammaglobulinemia on protein electrophoresis (EPP). Autoimmune tests were positive, including antinuclear antibodies (ANA) at 1/160, strongly positive anti-SSA, anti-SSB, and antinucleosome antibodies, as well as positive anti-Sm, antihistone, and antiribosome antibodies, and a borderline anti-RNP. The anti-glycoprotein antibody (Ig M) was strongly positive (58 U/mL). C3 and C4 complement levels were consumed. Hepatic and renal assessments were normal, and 24-hour proteinuria was negative. Serologies for hepatitis B and C viruses, HIV, and syphilis were negative. Thyroid function tests were also normal, as was the pregnancy test (BHCG). A lumbar puncture and cerebral MR angiography were performed, with no abnormalities detected. Deficiencies, toxic, and iatrogenic causes of catatonia were also ruled out. The diagnosis was established as a catatonic syndrome unveiling systemic lupus erythematosus (SLE). The patient was treated with hydroxychloroquine, a methylprednisolone bolus followed by an oral dosage of 1 mg/kg/day, in addition to appropriate antibiotic therapy. After resolution of the infectious episode, a cyclophosphamide bolus was administered. Psychiatric care was provided alongside specific lupus treatment. The clinical outcome was favorable, with notable improvement in the catatonic syndrome, including resolution of negativism, as well as a gradual return of speech and eating. Literature Review Cases of catatonia associated with systemic lupus erythematosus have been reported in the literature, with the majority occurring in patients with a previously diagnosed systemic lupus. Although catatonia is not part of the official neuropsychiatric criteria for systemic lupus erythematosus, this case, along with those described in the literature, suggests that it may represent an important, though rare, manifestation of neuropsychiatric systemic lupus erythematosus (NPSLE). Discussion Distinguishing between NPSLE-induced catatonia and other causes, such as steroid-induced psychosis or antipsychotic-induced catatonia, can be challenging. However, the absence of steroid or antipsychotic use in our patient, alongside improvement with immunosuppressive therapy, strongly suggests that NPSLE was the underlying cause. The neurophysiological mechanisms behind catatonia in NPSLE remain unclear, and further research is needed to clarify these mechanisms and improve diagnosis and management.