Thyroxine is an essential hormone in the human body and exerts many effects on the cardiovascular system. The low metabolic state in hypothyroidism causes bradycardia and reduced cardiac contractility leading to reduced cardiac output. Severe bradycardia and atrioventricular (AV) blocks secondary to hypothyroidism have also been reported. We present a case of severe hypothyroidism causing a high-grade AV block which was successfully treated with thyroxine hormone replacement without requiring cardiac pacemaker placement.
We have presented a case of 41-year-old male who presented to the hospital with worsening shortness of breath, fatigue and flu-like symptoms. On admission to hospital, the patient was in severe cardiogenic shock secondary to acute perimyocarditis. He was admitted to the cardiac intensive care unit for close monitoring and aggressive hemodynamic support. Influenza B antigen was detected in nasopharyngeal aspirate and the patient was started on oseltamivir. The patient’s cardiac function improved significantly in few days and he was discharged home in stable condition with normal ejection fraction.
Acalculous cholecystitis (AC) is an inflammation of the gallbladder in the absence of gallstones. There are many risk factors associated with AC. However, this report implicates allopurinol as an inciting agent for a severe systemic drug reaction, i.e., the drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome complicated by AC. We report a Chinese woman who presented on two occasions with a diffuse maculopapular rash, elevated liver enzymes, and upper abdominal pain attributable to acute AC, the second episode of which developed after the reintroduction of allopurinol treatment for gout. The AC complicated the DRESS syndrome during the course of her hospitalization.
In the setting of an increasing incidence of endocarditis in the United States, we report a patient with necrotizing crescentic glomerulonephritis (GN) associated with native valve bacterial endocarditis due to Streptococcus parasanguinis. He was started on appropriate antibiotic treatment and subsequent blood cultures showed no growth. However, due to continuing decline in kidney function, immunosuppressive therapy was started. Despite immunosuppressive therapy and antibiotics, renal function did not improve and chronic hemodialysis was required. Due to rarity of condition, there are no definite treatment guidelines available. Antibiotics, steroids, immunosuppressive agents can be of help in most cases. Further research in this regard may help with early diagnosis and better treatment modalities.
INTRODUCTION:We present a case of a middle-aged female with antiphospholipid syndrome (APS) presenting as atypical pneumonia and alveolar hemorrhage later confirmed to have APS-induced vasculitis.CASE PRESENTATION: 65 years female with APS with positive anti-cardiolipin beta2 glycoprotein antibodies presented to the Emergency Department (ED) with complaints of worsening dyspnea, chronic cough, intermittent fever over the last 2-3 weeks. She had oxygen saturation of 85%, fever of 101 F with rest vitals stable. Lung exam revealed diffuse bilateral crackles. Lab showed pancytopenia. Diffuse non-consolidated bilateral opacities was seen in chest imaging. Few hours later, she developed respiratory failure requiring intubation. She was started on pulse steroid and broad-spectrum antibiotics for atypical pneumonia. Bronchoscopy yielded evidence of hemorrhage. Infectious workup and other serology were negative. She improved clinically & underwent videoassisted thoracoscopic surgery for wedge biopsy of lung before discharge. Biopsy results were followed which showed necrotizing capillaritis with patchy intra-alveolar hemorrhage, hemosiderin-laden macrophages and fibrin.DISCUSSION: APS is an autoimmune condition with persistently elevated antiphospholipid antibodies (lupus anticoagulant, anticardiolipin or anti-B2-glycoprotein-I) commonly manifests with systemic thrombosis. These antibodies may result in pulmonary microvascular injury thus rarely (2%) presents as diffuse alveolar hemorrhage (DAH) [1]. In patients presenting with DAH, underlying etiology can be diagnosed through a detailed history and physical, pertinent serology, chest imaging, bronchoscopy with lavage, and biopsy in case of uncertain diagnosis. Out of 3 major pathological findings in DAH (pulmonary capillaritis, bland hemorrhage, or diffuse alveolar damage), pulmonary capillaritis is closely associated with autoimmune diseases and thus frequently identified in patients with APL (55%); but absence of capillaritis does not rule out APS [1]. Lung biopsy in pulmonary capillaritis may show neutrophilic infiltration of the pulmonary capillary and hemorrhage within the alveoli. Capillaritis may be observed more often than microvascular thrombosis ( 60% vs 11% vs 29% combined) [1]. All patients with capillaritis have strong positive titer of aPL [2]. Diagnosis can be made with biopsy after correlating with clinical presentation, laboratory data along with immunofluorescence studies. Diagnosis is challenging in case of transbronchial biopsy because of small tissue samples [2]. Routine lung biopsy is not required for diagnostic confirmation given the riskbenefit ratio as these patients are at a higher risk of thrombosis or bleeding due to anticoagulation [1, 2].CONCLUSIONS: DAH may be an initial presentation of APS. Typical biopsy findings are sufficient to establish the diagnosis of small vessel vasculitis given the high pretest probabilities.
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