Cardiac Manifestations of Sjogren's Syndrome: A Review of Literature.

Sjogren's syndrome (SS) is a chronic inflammatory disorder of the exocrine glands. It is characterized by a lymphocytic infiltrate in the lacrimal and salivary glands causing keratoconjunctivitis sicca and xerostomia. Extra-glandular involvement may be present in about one-third of patients with primary Sjogren's syndrome (pSS). The most commonly affected organs are the thyroid, lungs, gastrointestinal tract, kidneys, skin, and nervous system. Cardiac manifestations of Sjogren's syndrome are rare and not well-described in the current literature. Most of the evidence is present in the form of case reports and small case series. However, recent studies have shown that patients with Sjogren's syndrome (SS) seem to have a greater overall risk of cardiovascular (CV) events. Although not conventionally considered a feature of the disease, cardiac manifestations can lead to increased morbidity and mortality in this patient population. In this review article, we study the association between cardiac diseases and primary Sjogren's syndrome.

Systemic Haemophilus parainfluenzae Infection Manifesting With Endocarditis and Membranoproliferative Glomerulonephritis.

Infective endocarditis (IE) is a potentially fatal disease that is primarily caused by Staphylococci and Streptococci. The HACEK group of bacteria (Hemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae) account for only 1-3% of reported IE cases. IE has long been known to cause glomerulonephritis. The most common histologic patterns seen are crescentic and diffuse proliferative glomerulonephritis. Notably, membranoproliferative glomerulonephritis (MPGN) is one of the less common patterns seen with IE. We present a rare case of MPGN associated with Haemophilus parainfluenzae endocarditis. A 56-year-old male with no significant past medical history presented to a local hospital with complaints of fever, night sweats, dyspnea, diarrhea, and dark urine for about a month. He was found to have a hemoglobin of 4g/dL, requiring multiple transfusions. He also had bilateral pleural effusions and pulmonary edema. In the following days, he had worsening renal function and was transferred to our hospital for further workup. Initial labs showed anemia, thrombocytopenia, and leukocytosis. He had creatinine elevated at 5.28 mg/dL and a low estimated glomerular filtration rate (eGFR) of 12 mL/min/1.73m2. Urinalysis showed proteinuria, urine hemoglobin, urine white blood cells (WBCs), and red blood cells (RBCs). Blood cultures revealed H. parainfluenzae. Transesophageal echocardiogram (TEE) showed large vegetations with perforation of the mitral valve leaflet. Serology showed low complement levels. Renal biopsy displayed a membranoproliferative pattern of glomerulonephritis on light microscopy. The hepatitis panel was negative, as was the autoimmune workup. The patient was diagnosed with MPGN associated with H. parainfluenzae endocarditis. His complex clinical course required mitral valve replacement and aortic valve repair. He completed the course of antibiotics, with improvement in renal and cardiac function.