Introduction: Hypercalcemia is well described in various granulomatous disorders, such as sarcoidosis, tuberculosis, berylliosis, leprosy and fungal infections. However, the association of Paracoccidioides brasiliensis and hypercalcemia is rare: to the best of our knowledge, only two cases have previously been reported, and neither had a clear documentation of the etiology of the hypercalcemia.
Treatment with amiodarone was withdrawn and atenolol was prescribed.The patient started to present worsening of exertional dyspnea. The worsening was associated with the use of atenolol, which was discontinued, and the patient restarted amiodarone, 200 mg/day.The patient was submitted to ergometric test (February 21, 2003). At basal condition, the HR was 124 bpm and BP was 134/98 mmHg; after 2 minutes and 45 seconds of exertion, these parameters were 192 bpm and 158/94 mmHg. He started to present atrial fibrillation and nonsustained ventricular tachycardia during exertion. The symptoms abated; the exertional dyspnea persisted, as well as occasional episodes of palpitations, throughout two years. Subsequently, the dyspnea presented rapid increase, which started to occur even with the patient at rest. After one month, the patient had not improved and sought medical attention.At physical examination (June 3, 2004), the patient presented HR of 98 bpm, 24 breaths per minute, BP of 140/110 mmHg, increased jugular venous pressure, rales in the left hemithorax. Heart assessment disclosed arrhythmic beats, muffled heart sounds and systolic murmur +++/4+ in the aortic area. The liver was palpable at 2 cm from the right costal margin and the patient presented ++/4+ lower-limb edema.The chest X-ray showed an enlarged cardiac area with a round shape. The morphological analysis disclosed an increased P wave, QS in leads I, aVL and Q wave in lead V6. Right atrial overload, electrically inactive lateral area and ventricular repolarization alterations were diagnosed.Laboratory assessment (December 19, 2001) disclosed: hemoglobin -15.5 g/dl; hematocrit -46%; total cholesterol -242 mg/dl; triglycerides -241 mg/dl; fasting glycemia -107 mg/dl and creatinine -1.3 mg/dl. e112
Background: Systemic lupus erythematosus (SLE) is a chronic, multi phenotypic, autoimmune inflammatory disease and renal involvement significantly worsens its prognosis. Apoptosis dysregulation plays a key pathogenic role. Survivin, a protein from the apoptosis inhibitors family, has been considered a promising strategy in cancer therapy and evaluated as one of the regulatory pathways in the scenario of immune-mediated disorders. Objective: This study aims to explore survivin behaviour in SLE patients with lupus nephritis (LN), assessing its potential as a therapeutic and prognostic biomarker. Methods: 297 SLE patients were classified based on the American College of Rheumatology (ACR) 1997 criteria, from 2000 to 2015. In a cross-sectional study, the serum level of survivin was measured by an ELISA test and compared between 200 SLE individuals and healthy controls. In a longitudinal cohort, 97 patients with active LN had the concentration of survinin measured, before and after treatment with cyclophosphamide pulse therapy. Results: The serum concentration of survivin was significantly lower in the SLE group than in healthy controls, regardless of concomitant NL or disease activity. The longitudinal evaluation revealed a significant reduction in survivin serum level after treatment. However, survivin rates were not able to discriminate groups that achieved remission from those that maintained nephritis activity. Conclusion: Our study suggests that survivin levels in SLE patients are lower than in the general population. Even so, its use as a biomarker in SLE seems limited, not reflecting disease activity or response to LN treatment, as in other contexts.
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