Missing competing interests in editorial

In: Sáfadi MAP. Pertussis in young infants: a severe vaccine-preventable disease [editorial]. Autopsy Case Rep [Internet].2015;5(2):1-4. http://dx.doi.org/10.4322/acr.2015.010Due to a desktop publishing error the Editorial was published with the following errors:• Missing competing interests disclosure paragraph.• Wrong section name.On page 4 where you read:FINANCIAL AND COMPETING INTERESTING DISCLOSURENo writing assistance was utilized in the production of this manuscript.You should read:FINANCIAL AND COMPETING INTERESTS DISCLOSUREMAP Safadi has received grants to support research projects and consultancy fees from GlaxoSmithKline(GSK), Novartis, and Sanofi Pasteur.No writing assistance was utilized in the production of this manuscript

Sharing experience through case reports

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Hereditary hemochromatosis

Hereditary hemochromatosis (HH) is the most commonly identified autosomal recessive genetic disorder in the white population, characterized by increased intestinal iron absorption and secondary abnormal accumulation in parenchymal organs, not infrequently accompanied by functional impairment. This entity is associated with mutations of the HFE gene (located on the short arm of chromosome 6 at location 6p22.2; closely linked to the HLA-A3 locus), which encodes the HFE protein, a membrane protein thought to regulate iron absorption by affecting the interaction between transferrin receptor and transferrin

Cardiac Myxoma

Primary cardiac tumors (PCT) are rare, accounting for 0.0017-0.03% in autopsy series,1,2 in contrast to metastatic tumors of the heart, which are 30 times more frequent.3,4 Nearly 75% of PCT are benign and most often represented by a myxoma in 50% of cases in the adult population.5 The World Health Organization defines a cardiac myxoma (CM) as a neoplasm composed of stellate to plump, cytologically bland, mesenchymal cells set in a myxoid stroma.6 Approximately 95% of CMs occurs isolated in a wide range of age. However, they occur more frequently among women in the fifth or sixth decade of life.7-9 For a time, myxomas were believed to arise from endocardial thrombi10 and some evidence suggests an association with Herpes simplex virus 1 infections11; however, their tumoral histogenesis remains unknown. Meanwhile, ultrastructure analysis—added to immunohistochemical investigation—suggests that CM is more likely derived from a pluripotent mesenchymal stem cell or sub-endothelial cell. Chromosomal clonal abnormalities, mostly on chromosome 2, 12, and 17, appear to be implicated in the myxoma formation, although defects on chromosome 1q32, the loss of the Y chromosome, and the telomeric association of chromosome 13 and 15, have also been involved.12-14 CMs are mostly pedunculated and solitary, and arise primarily adjacent to the lamina of the fossa ovalis (corresponding to the embryonic septum primum) and develop in the left atrium in 75% of cases, followed by the right atrium (18%),15 the right and left ventricles (3% in each), and the valves (1%).15-20 Multiple myxomas represent 5% of the cases, half of which are of bilateral origin.21 Although CM is a benign tumor, reports on its malignancy are well-known, which include: (i) local relapse; (ii) local invasiveness; and (iii) distant metastasis.12 The potential for malignant transformation is controversial, despite the publication of some reports of sarcomas arising from CM recurrences.22,23 Clinical manifestations of CMs are protean and may vary from asymptomatic cases (with a tumor < 4 cm) to unexpected sudden death (generally caused by blood flow obstruction or embolization). In most cases, the clinical presentation will depend on the tumor size, mobility, and location. One or more symptoms of the following triad will usually be present: (i) embolic phenomena (present in 30-40% of cases and usually associated with a villous surface of the tumour)24; (ii) intracardiac flow obstruction (present in almost 50% of cases); and (iii) constitutional symptoms (present in 20-60% of cases). In general, the most common signs and symptoms are non-specific and include dyspnea, palpitation (due to atrial fibrillation), lower limbs edema, hepatomegaly, angina, syncope, cough, and pulmonary edema. The constitutional symptoms, characterized by fatigue, fever, myalgia, arthralgia, and weight loss, are probably related to interleukin-6 cytokine production.25 The diagnosis of a CM is mostly done with echocardiography, both transthoracic and transesophageal, which represent the imaging modality of choice, although the latter permits precise information for the scheduling of surgery. Due to the rarity and consequent unfamiliarity of most general practitioners with this entity, CMs are sometimes misdiagnosed. Differential diagnosis should include intracardiac thrombus and other cardiac tumor

Myocardial abscess as a complication of an infected arteriovenous fistula: autopsy report

Myocardial abscess is a severe and life-threatening infectious complication thatis commonly but not exclusively associated with infective endocarditis. It mayalso be developed in necrotic myocardial tissue, post trauma, in septic burnpatients, in transplanted heart, in ventricular aneurysm and post angioplasty.Patients on hemodialysis are prone to bacteremia, and infectious complicationsoccur in 48-73% of cases. Myocardial abscess is a rare complication of aninfected arteriovenous fistula. We present an autopsy report of a hemodialysispatient who had an arteriovenous fistula with a polytetrafluoroethylene graftwhere a local infection developed. The patient presented with fever and toxemia.On post-admission day 2, he unexpectedly suffered sudden cardiopulmonaryarrest and died. The autopsy revealed a myocardial abscess, near a branch ofthe left coronary artery, with septic embolism

Asbestos-related pleural disease

The image shows asbestos plaques on the right parietal pleura of a 58-year-old former shipyard worker who died of acute suppurative bronchitis. He also had cor pulmonale and congestive heart failure. Histologically, pulmonary interstitial fibrosis with asbestos bodies was demonstrated. The pleural plaques consist predominantly of dense collagen. This photograph was taken after removal of the lung with the camera held in the lower right thorax, at approximately the level of the diaphragm, looking up toward the apex of the chest cavity