Bilateral Parotid Involvement as the Solitary Metastatic Site from Squamous Cell Lung Cancer

The detection of metastatic disease has major therapeutic and prognostic implications on the management of cancer patients. We report an asymptomatic metastasis from the lung cancer to the intra-parotid lymph node which was detected by the FDG PET scan and subsequently confirmed by fine needle aspiration cytology. The case is unique as solitary metastatic involvement of the parotid from non-head and neck tumors are extremely rare and thus, may be missed during staging evaluation

Pulseless Right Upper Limb: An Unusual Manifestation of Invasive Pulmonary Aspergillosis in Acute Myeloid Leukemia

Abstract Aspergillus is the most common cause of fungal pneumonia in acute leukemia patients receiving chemotherapy or undergoing hematopoietic stem cell transplantation. Despite a high index of suspicion and prompt institution of specific antifungal therapy, it causes significant morbidity and mortality in patients with hematological malignancies. It has to be differentiated from mucormycosis because the treatment differs. Histological confirmation obtained by lung biopsy is ideal, but is difficult to obtain in those patients who often have thrombocytopenia. We report a case of acute megakaryoblastic leukemia with typical manifestations of invasive pulmonary aspergillosis who developed pulseless right arm due to invasion of the right subclavian artery. When total leucocyte counts recovered, patient also developed immune reconstitution inflammatory syndrome and massive pulmonary hemorrhage, which was managed by bronchial artery embolization

Cardiac Amyloidosis: Approach to Diagnosis

Amyloid is an amorphous, fibrillar material formed from various abnormally folded proteins that deposits locally or systemically. Over 95% of cases have been attributed to light chain deposition (AL) or transthyretin deposition (ATTR) amyloidosis. The basic investigations in the evaluation of cardiac amyloidosis include the electrocardiogram, echocardiography and cardiac biomarkers. Echocardiography in a patient with cardiac amyloidosis shows biatrial enlargement, biventricular hypertrophy, diastolic dysfunction, interatrial septal thickening, valvular thickening, a glistening appearance of the interventricular septum, and pericardial effusion. Magnetic resonance imaging can help distinguish amyloidosis from other causes of infiltrative/restrictive cardiomyopathy, from example, sarcoidosis, hemochromatosis, and Fabry disease based on characteristic enhancement patterns in these diseases. The latest Expert Consensus recommends that serum/urine immunofixation electrophoresis along with a serum free light chain assay must be done in all the cases of suspected cardiac amyloidosis. If the light chain assays are positive, we proceed with tissue diagnosis for confirmation of AL amyloidosis. If the screening assays are negative for monoclonal gammopathy, the next step is to obtain cardiac scintigraphy. If the nuclear scan is negative, but the index of suspicion remains high, an endomyocardial biopsy can be done. Once amyloid is demonstrated in histopathologic specimens, it must be typed to distinguish between AL and ATTR. The ideal method for this is tandem mass spectrometry, although this may not be widely available. It has a sensitivity of 88% and specificity of 96% higher than other techniques 23. In resource-poor settings, immunohistochemistry or immunoelectron microscopy can allow this distinction, although with lesser sensitivity

Eosinophilia to endomyocardial fibrosis: Documentation of a case

Endomyocardial fibrosis (EMF) is an important cause of restrictive cardiomyopathy in tropical countries. The etiopathogenesis of EMF remains obscure. The role of eosinophilia in the etiopathogenesis of EMF has been debated extensively, but remains unproven. Accordingly, we present a case wherein a patient with documented eosinophilia and heart failure at the age of three-and-a-half years presented with endomyocardial fibrosis at the age of nine years. Such documentation is important to highlight the central role of eosinophils in the pathogenesis of EMF

Diphtheritic myocarditis: An unusual and reversible cause of heart failure

Diphtheria is a life-threatening infectious disease caused by Corynebacterium diphtheriae. Although the disease is seen infrequently in the postvaccination era, sporadic cases continue to occur. Cardiac involvement, in the form of myocarditis, is the most serious manifestation of diphtheria and is the most common cause of mortality in these patients. The features of diphtheritic myocarditis on cardiac magnetic resonance imaging (MRI) have not been reported previously. In this brief report, we describe the cardiac MRI and histopathologic features on endomyocardial biopsy of a patient with acute heart failure who was later diagnosed to be a case of diphtheritic myocarditis

Hamartoma of mature cardiac myocytes: Report of a rare case with review of literature

Hamartoma of mature cardiac myocyte is a benign tumor of the heart. They are characterized by haphazardly arranged hypertrophic cardiac myocytes with variable amounts of intervening fibrosis, mature adipose tissue along with irregularly distributed variable-sized vascular channels. The case presented here had a hyperechoic mass in the left ventricle arising from the midinferior and posterior interventricular septum, infiltrating into the adjacent myocardium. The MRI , histopathology findings and the clinical outcome is presented

Immunohistochemical characterization of glandular elements in glandular cardiac myxoma: Study of six cases

Back ground: Glandular cardiac myxoma has varying clinical presentation with uncertain histogenesis and debatable immunohistochemical profile. Glandular epithelial differentiations are rare phenomenon known to be present as an intrinsic component of the tumor. The origin of the glands has been attributed to epithelial differentiation of a totipotent cardiomyogenic precursor cells or the entrapped foregut rests in the tumor. Materials and Methods: Retrospective study includes six cases of glandular cardiac myxoma collected over a perior of 4 years. Sections were examined to define the histogenesis, histological and immunohistochemical profile of the glandular elements. Results: Incidence of glandular cardiac myxoma was 6.6% with a male to female ratio of 1:2.Mean age was 49.9 years. Left atrium was the commonest site. Five were sporadic and one was familial. Chest pain and dyspnea were the commonest clinical symptoms. Histologically all myxoma showed well formed glandular structures with typical myxomatous area. No atypia, mitosis or necrosis was identified in the glandular elements. Markers in six cases of glandular cardiac myxoma were immunopositive for CK7, CK 19, EMA, CEA, focally for E-cadherin while immunonegative for CK20, Chromogranin, Synaptophysin, calretenin, vimentin, B-catenin, TTF-1 and GCDFP-15 favoring enteric differentiation. Conclusion: Glandular cardiac myxoma is a rare entity which shows characteristics similar to those of classical cardiac myxoma with benign glandular elements showing enteric differentiation. Complete surgical excision is the treatment of choice with good prognosis. It is important to recognize this entity to avoid an erroneous diagnosis of metastatic adenocarcinoma

Allylmethylsulfide, a Sulfur Compound Derived from Garlic, Attenuates Isoproterenol-Induced Cardiac Hypertrophy in Rats

Allylmethylsulfide (AMS) is a novel sulfur metabolite found in the garlic-fed serum of humans and animals. In the present study, we have observed that AMS is safe on chronic administration and has a potential antihypertrophic effect. Chronic administration of AMS for 30 days did not cause any significant differences in the body weight, electrocardiogram, food intake, serum biochemical parameters, and histopathology of vital organs. Single-dose pharmacokinetics of AMS suggests that AMS is rapidly metabolized into Allylmethylsulfoxide (AMSO) and Allylmethylsulfone (AMSO2). To evaluate the efficacy of AMS, cardiac hypertrophy was induced by subcutaneous implantation of ALZET® osmotic minipump containing isoproterenol (~5 mg/kg/day), cotreated with AMS (25 and 50 mg/kg/day) and enalapril (10 mg/kg/day) for 2 weeks. AMS and enalapril significantly reduced cardiac hypertrophy as studied by the heart weight to body weight ratio and mRNA expression of fetal genes (ANP and β-MHC). We have observed that TBARS, a parameter of lipid peroxidation, was reduced and the antioxidant enzymes (glutathione, catalase, and superoxide dismutase) were improved in the AMS and enalapril-cotreated hypertrophic hearts. The extracellular matrix (ECM) components such as matrix metalloproteinases (MMP2 and MMP9) were significantly upregulated in the diseased hearts; however, with the AMS and enalapril, it was preserved. Similarly, caspases 3, 7, and 9 were upregulated in hypertrophic hearts, and with the AMS and enalapril treatment, they were reduced. Further to corroborate this finding with in vitro data, we have checked the nuclear expression of caspase 3/7 in the H9c2 cells treated with isoproterenol and observed that AMS cotreatment reduced it significantly. Histopathological investigation of myocardium suggests AMS and enalapril treatment reduced fibrosis in hypertrophied hearts. Based on our experimental results, we conclude that AMS, an active metabolite of garlic, could reduce isoproterenol-induced cardiac hypertrophy by reducing oxidative stress, apoptosis, and stabilizing ECM components