BACKGROUNDTakayasu's arteritis is a rare disease that mainly affects the aorta and its main branches in the form of vascular occlusion. The patient may also present with aortic regurgitation, aneurysm of the aorta or its branches and secondary arterial hypertension. About 13% of patients develop ocular ischemic syndrome which is a rare condition, which is caused by ocular hypoperfusion due to stenosis or occlusion of the common or internal carotid arteries. CASE REPORTA 39-year-old female patient diagnosed with Takayasu's arteritis in 2013. She underwent pulse therapy with cyclophosphamide and methylprednisolone at diagnosis. Maintenance was done with prednisone and methotrexate (MTX). She underwent left internal carotid artery angioplasty in 2014. New pulse therapy regimen with cyclophosphamide 1.2 g/month for 1 year in 2015, due to disease activity (carotid artery restenosis). Maintenance started again with MTX until 2017, when she lost follow-up. She resumed in 2018, during pregnancy, having used prednisone alone. In June 2019, infliximab was started and she continued on this treatment until July 2021. Treatment was switched to tocilizumab in August 2021. Nevertheless, her desease maintained an aggressive evolution with bilateral occlusion of internal carotids and basilar artery. She evolved with bilateral amaurosis and optic nerve atrophy (ischemic neuritis) in addition to low ocular pressure (2 mmHg) due to ischemia of the ciliary body, characterizing ischemic ocular syndrome caused by the disease. CONCLUSIONTakayasu's arteritis is a rare disease that mainly affects young women. Although the initial symptoms are nonspecific, early treatment is of paramount importance to avoid severe forms of the disease, such as the patient described above, who developed several complications, including ocular ischemia and stenosis of the carotid and basilar arteries.
BACKGROUNDInfections are one of the most frequent causes of morbidity, hospitalization and mortality in patients with systemic lupus erythematosus (SLE). Several risk factors for infections in these patients have been identified, such as disease activity, low levels of complement, nephritis, leukopenia, pulse therapy and immunosuppressive therapy. Central nervous system infections are rare in SLE patients, constituting only 3% of all infections, with a predominance of meningitis caused mainly by Cryptococcus neoformans and Mycobacterium tuberculosis. CASE REPORTPatient E.C.A., female, 48 years old, diagnosed with SLE since 1999, with skin, joint and hematological involvement. Previous history of ischemic stroke without motor sequelae, and HTLV-1 infection diagnosed in 2011. Antiphospholipid syndrome was ruled out. Previous use of hydroxychloroquine (suspended due to toxic maculopathy) and azathioprine (suspended in 2019). Belimumab was started in December 2020 due to hematological flare, with a good response. Treatment without corticosteroids was maintained, with the disease in remission. However, in September 2021 was hospitalized with fever associated with a lowered level of consciousness, requiring orotracheal intubation. Cryptococcus neoformans was found in cerebrospinal fluid culture, obtained with an opening pressure of 40 cm H 2 O. Amphotericin B deoxycholate was used initially, with a switch to amphotericin B lipid complex. She evolved with ventilator-associated pneumonia and blood stream infection by Acinetobacter baumannii; with death still in the consolidation phase of treatment for neurocryptococcosis. CONCLUSIONWe report a case of a patient living with HTLV, with predominantly hematological SLE in more than 20 years of evolution, currently undergoing immunosuppressive therapy with belimumab. Although the main risks for neuroinfection in SLE are previous use of high doses of corticosteroids, and high SLEDAI, the case above is unusual, and highlights the need for high suspicion for neuroinfection in patients with SLE and use of immunosuppressants. Furthermore, to the best of our knowledge, this is first case report of neurocryptococcosis complicating treatment with belimumab.
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