A Rare Case report on Rheumatic Origin of Severe Tricuspid stenosis

Med Phoenix ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 56-58
Author(s):  
Shankar Laudari ◽  
Kaushal Kishore Tiwari ◽  
Sanket Adhyaru ◽  
Ashish Subedi

Tricuspid stenosis is a very rare valvular disease due to narrowing of the orifice of the tricuspid valve of the heart. It is usually of rheumatic origin which is accompanied by other valvular lesions. Other causes of tricuspid stenosis include carcinoid syndrome, endocarditis, endomyocardial fibrosis, lupus erythematosus, right atrial myxoma, drug induced and congenital tricuspid atresia. Here we report a patient who had undergone percutaneous transluminal mitral commissurotomy (PTMC) followed by mitral restenosis with Severe Tricuspid Stenosis with Severe Tricuspid Regurgitation.  

1970 ◽  
Vol 3 (2) ◽  
pp. 235-238
Author(s):  
MT Rahman ◽  
M Das ◽  
M Ullah ◽  
Z Rahman ◽  
A Hossain ◽  
...  

Tricuspid valve stenosis is a valvular heart disease which results in the narrowing of the orifice of the tricuspid valve of the heart. It’s relatively a rare condition. It is almost always caused by rheumatic fever and is generally accompanied by mitral stenosis.Other rare causes include carcinoid syndrome, endocarditis, endomyocardial fibrosis, lupus erythematosus, right atrial myxoma and congenital tricuspid atresia. Here we describe a patient with history of prior CMC presented with severe Tricuspid Stenosis with Tricuspid Regurgitation (Grade-IV), Mitral Restenosis (Severe), Mitral Regurgitation (grade-1+), Aortic Stenosis (Mild) and Aortic Regurgitation (Grade-2). Keywords: Tricuspid stenosis; Rheumatic heart disease; Valvular heart disease. DOI: http://dx.doi.org/10.3329/cardio.v3i2.9197 Cardiovasc. J. 2011; 3(2): 235-238


1970 ◽  
Vol 27 (1) ◽  
pp. 52-55
Author(s):  
MA Quashem ◽  
Hriday Ranjan Roy ◽  
Md Golam Kibria ◽  
AEM Masharul Islam ◽  
AA Shafi Majumder ◽  
...  

A middle aged man was admitted into National Institute of Cardiovascular Diseases with the complaints of intermittent syncopal attack, dyspnoea, low grade fever and headache. After admission, he was diagnosed as a of case right atrial (RA) myxoma by echocardiography. With all preoperative preparation, he was undergone surgery under general anesthesia with cardiopulmonary bypass (CPB). About 9cm x 7cm myxoma was removed and severe tricuspid regurgitation (TR) was found by regurge test. De Vega annuloplasty of the tricuspid annulus was done. Recovery of the patient was satisfactory with disappearance of all symptoms. DOI: 10.3329/jbcps.v27i1.4245 J Bangladesh Coll Phys Surg 2009; 27: 52-55


2016 ◽  
Vol 11 (1) ◽  
pp. 45-47
Author(s):  
SMG Saklayen ◽  
Rakibul Hasan ◽  
Redoy Ranjan ◽  
Mostafizur Rahman ◽  
Rezwanul Hoque ◽  
...  

Cardiomyopathy is the measurable deterioration of the function of the myocardium for any reason, usually leading to heart failure. Tricuspid regurgitation may result from structural alterations of any one or all of the components of the tricuspid valve apparatus which include the leaflets, chordae tendinae, annulus, and papillary muscles or adjacent right ventricular muscle. We are reporting a case of Cardiomyopathy with tricuspid regurgitation with right heart failure in a 38 years male. Preoperatively he was diagnosed as a case of constrictive pericarditis. Diagnosis of Tricuspid regurgitation with cardiomegaly was confirmed peroperatively. During operatrion tricuspid valve anatomy dimunited and severe tricuspid regurgitation was identified. Grossly dilated RA, RV identified and other anatomy of heart was normal. De-Vega Tricuspid anuloplasty done with pledgeted stich 2-0 polyster. Part of right atrial wall (2X2.5 inch) excised and resected portion sent for histopathology. Postoperative course was uneventful with marked improvement of symptoms.University Heart Journal Vol. 11, No. 1, January 2015; 45-47


2020 ◽  
Vol 10 (2) ◽  
pp. 137-138
Author(s):  
Samiha Haque ◽  
Ishrat Jahan ◽  
Tufayel Ahmed Chowdhury ◽  
Muhammad Abdur Rahim ◽  
Mehruba Alam Ananna ◽  
...  

Rapidly progressive glomerulonephritis is one of the most dramatic and tragic presentations of lupus nephritis (LN) or renal manifestation of systemic lupus erythematosus (SLE). A 35-year-old Bangladeshi gentleman presented with worsening oedema, scanty, high colored, frothy urine and deteriorating renal function. He had puffy face, anaemia, oedema, normal jugular venous pressure (JVP), high blood pressure (150/90 mm Hg), ascites and bilateral pleural effusions. Diagnostic work-up confirmed SLE with class IV LN. His initial response to specific therapy showed improvement Birdem Med J 2020; 10(2): 137-138


2020 ◽  
Vol 8 ◽  
pp. 2050313X2091002 ◽  
Author(s):  
Umut Selamet ◽  
Ramy M Hanna ◽  
Anthony Sisk ◽  
Lama Abdelnour ◽  
Lena Ghobry ◽  
...  

Drug-induced lupus erythematosus has features distinct from primary systemic lupus erythematosus. It can occur with a wide variety of agents that result in the generation of anti-histone or other types of antibodies. Systemic manifestations of drug-induced systemic lupus erythematosus may include renal dysfunction due to circulating immune complexes or due to other immune reactions to the culprit medication(s). Acute interstitial nephritis occurs due to DNA–drug or protein–drug complexes that trigger an allergic immune response. We report a patient who developed acute kidney injury, rash, and drug-induced systemic lupus diagnosed by serologies after starting chlorthalidone and amiodarone. A renal biopsy showed acute interstitial nephritis and not lupus-induced glomerulonephritis. It is important to note that systemic lupus erythematosus and acute interstitial nephritis can occur together, and this report highlights the role of the kidney biopsy in ascertaining the pathological diagnosis and outlining therapy in drug-induced lupus erythematosus.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1188.2-1189
Author(s):  
A. Martins ◽  
D. Santos Oliveira ◽  
F. R. Martins ◽  
M. Rato ◽  
F. Oliveira Pinheiro ◽  
...  

Background:Induction of autoantibodies is frequently observed in patients treated with TNF-α antagonist and the possible development of drug-induced lupus erythematosus (DILE) remains a matter of concern. The prevalence of DILE secondary to anti-TNF-α therapy is estimated around 0.5-1% and clinical features include arthritis/arthralgia, rash, serositis, fever, myalgias, cytopenias, among others. According to the literature, DILE secondary to anti-TNF-α agents differs in several ways from the clinical and laboratory findings typically associated with classic DILE.Objectives:To estimate the incidence of induction of antinuclear antibodies (ANA) and DILE in a monocentric cohort of patients with spondyloarthritis and psoriatic arthritis treated with anti-TNF-α agents. To describe the clinical and laboratorial features and outcomes of patients with DILE.Methods:We performed a retrospective analysis of patients with spondyloarthritis and psoriatic arthritis treated with anti-TNF-α agents, from our University Hospital, who have been registered on the Portuguese Rheumatic Diseases Register (Reuma.pt) between July 2001 and December 2020. Patients with positive ANA (titer > 1/100) before the anti-TNF-α therapy were excluded. Because specific criteria for the diagnosis of DILE have not been established, we considered the diagnosis in case of a temporal relationship between clinical manifestations and anti-TNF-α treatment and fulfillment of ACR/EULAR 2019 classification criteria for SLE. In patients with DILE, clinical features, laboratory findings, systemic therapies and outcome after discontinuation of medication were collected from reuma.pt and medical records. For the clinical and demographic predictors, continuous variables were analyzed using a two-sided t-test and categorical variables using a Fisher’s exact test. P-value <0.05 was considered statistically significant.Results:In the spondyloarthritis group, 290 patients were included (44.8% females, mean age at diagnosis of 33.3 ± 11.5 years and mean disease duration of 15.1 ± 10.4 years) and in the psoriatic arthritis group, 116 patients were included (50.0% females, mean age at diagnosis of 40.1 ± 11.0 years and mean disease duration of 13.1 ± 6.8 years). In our study, we observed high serology conversion rates (positive ANA in 67.9% and 58.6% of patients with Spondyloarthritis and Psoriatic Arthritis, respectively), with similar conversion rates between different anti-TNF drugs. Three patients with spondyloarthritis (1.0%) and 1 patient with psoriatic arthritis (0.9%) developed DILE. Etanercept was the causative agent in 2 cases, infliximab and adalimumab in 1 case, each. Peripheral arthritis (new onset or abrupt worsening) occurred in 2 patients, serositis in 1 patient, constitutional symptoms in 2 patients, subnephrotic proteinuria in 1 patient, lymphopenia in 2 patients and hypocomplementemia in 1 patient. Specific treatment was prescribed to the 4 patients (oral corticosteroids) and they achieved complete recovery. After anti–TNF-α treatment interruption, no patient had recurrent disease. We observed that patients with DILE had a significantly longer disease duration (> 8.4 years; p=0.04) and a significantly longer duration of therapy with anti-TNF (> 4.0 years; p=0.04) when compared to patients without DILE.Conclusion:Despite the frequent induction of autoantibodies, the development of DILE secondary to anti–TNF-α agents is rare. Our study demonstrates an incidence rate similar to other studies reported before. The clinical and laboratorial characteristics of our patients with DILE attributable to anti–TNF-α agents differ significantly from DILE due to more traditional agents, as is described in literature. Overall, patients in this study had mild disease that improved after therapy discontinuation, without recurrence of the disease. It seems that a longer disease duration and a longer period under anti-TNF-α therapy may increase the risk of DILE development.Disclosure of Interests:None declared


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