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Cardiac Beriberi Bello et al. Diagnostic Pathology 2011, 6:8 http://www.diagnosticpathology.org/content/6/1/8 CASEREPORT Open Access Cardiac beriberi: morphological findings in two fatal cases Stefania Bello, Margherita Neri, Irene Riezzo, Mohammad Shafie Othman, Emanuela Turillazzi, Vittorio Fineschi* Abstract Cardiovascular beriberi is categorized into two main groups, according to its cause: alcoholic and non-alcoholic (dietary). Cardiovascular beriberi can also be divided into a fulminant form (Shoshin beriberi) and a chronic form. Shoshin beriberi is characterized by hypotension, tachycardia, and lactic acidosis and is mainly encountered in non- alcoholic patients in Asian countries, although it has also been seen in alcoholics in Western countries. Due to the complex clinical presentation and to the lack of diagnostic tests, thiamine deficiency is still being missed, especially among non-alcoholics patients. We present two fatal cases of non - alcohol associated cardiac beriberi. An acute myocardial infarction was observed in one case; extensive colliquative myocytolisis (grade 2) was described in the second case respectively. Morphologically, myocardial necrosis and colliquative myocytolysis are the histologic hallmarks of this acute, rare clinical entity. An increase in apoptotic myocytes was demonstrated probably sustaining the cardiogenic shock. Background and oscillopsia for two days. He had a history of gastric Thiamine deficiency (beriberi) has two major manifesta- resection with a Roux-en-Y reconstruction due to peptic tions: dry beriberi (peripheral neuropathy) and wet beriberi ulcer ten months before. He had no history of alcohol (cardiovascular disease), which include Wernicke-Korsakoff or illicit drug use. Clinical examination revealed normal syndrome and lactic acidosis [1]. Deficiency of this vitamin temperature, blood pressure, heart rate and respiration. may be nutritional or secondary to alcohol intoxication. He was well orientated; pupils were equal, round and Thiamine (vitamin B1) is a cofactor of key metabolic reactive to light, with marked nystagmus on lateral gaze. enzymes and thiamine deficiency (TD) may cause altera- He exhibited partial bilateral sixth nerve palsy. He tions in heart metabolism. However, very little is known moves all four extremities but he had difficulty to stand about the effects of TD on the myocardium. Thiamine is and ambulate. No other focal neurological deficit was considered a clinically important factor in heart function, present. Laboratory studies revealed normal serum and its deficiency has been reported to cause heart failure sodium, serum chloridre, serum bicarbonate, and serum [2-4]. Due to the complex clinical presentation and to the creatinine. The liver function tests showed normal lack of diagnostic tests, thiamine deficiency is still being enzymes and serum bilirubin levels with normal missed, especially among non-alcoholics patients [5]. albumin. Electrocardiogram and chest radiograph were We present two fatal cases of non - alcohol associated normal. Magnetic resonance imaging (MRI) and compu- cardiac beriberi. Clinical and cardiac morphologic find- terized tomography (CT) examinations of the brain were ings are described and discussed. not diagnostic. The spinal fluid cultures were reported as negative. In the suspect of TD, serum thiamine level Case presentation measurement was programmed but the vitamin was not Case 1 administered. On the fourteenth day of hospital stay, the Clinical findings patient suddenly experienced chest discomfort, diffuse A 47 year old - man was admitted to hospital since he ST-segment depression in the 12-lead electrocardiogram had been complaining about cefalea, dizziness, diplopia (ECG) with ST-segment elevation in aVR and rapidly evolving congestive heart failure leading to cardiogenic shock with serious hypotension (60/40 mmHg), * Correspondence: [email protected] Department of Forensic Pathology, University of Foggia, Foggia, Italy hypothermia, intense perspiration, and coma. His © 2011 Bello et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Bello et al. Diagnostic Pathology 2011, 6:8 Page 2 of 5 http://www.diagnosticpathology.org/content/6/1/8 Table 1 Case 1: the ongoing arterial blood gas results are shown th 14 day progressive arterial blood gas results pH pCO2 mmHg Lactate mmol/L HCO3 mmol SBE mmol/L 16.36 p.m. 7.032 30 18 7.8 -20.8 17.35 p.m. 7.182 46.2 19 16.8 -10.2 18.02 p.m. 7.24 57.2 21 21.8 -3.1 18.12 p.m. 7.215 47.5 22 24 -3.8 18.54 p.m. 7.107 55.2 27 16.7 -11.3 19.33 p.m. 7.180 41.0 23 14.7 -12.1 20.02 p.m. 7.196 38.4 23 14.4 -12.2 arterial blood showed a significant lactic acidosis and he (TPN) for 5 days. He underwent abdominal surgery and was immediately given bicarbonate (Table 1). The remained on TPN which was administered without a multi- patient developed hemodynamic instability that was vitamin solution. After 3 weeks of receiving TPN he pre- refractory to vasoactive drugs followed by unrecoverable sented hypotension and tachycardia, confusional state and cardiac asystole. The day after, the laboratory completed agitation. He complained fever, abdominal pain, nausea, and the dosing of the thiamine that resulted equal to vomiting; abdominal local tenderness was present. The clini- 66 nmol/L (n.v. 66 - 200 nmol/L). cal course quickly worsening; on the fourth week of TNP Pathological findings the man suddenly experienced cardiac arrest and unex- At autopsy the body was 175 cm height and 70 kg weight. plained lactic acidosis: pH7.140; pCO2 31.1 mmHg; lactate The heart was normal in size (12×8.5×8 cm) and weight 19 mmol/L; HCO3 11.1 mmol; SBE -18.7 mmol. He was (397 g); the coronary vessels and main branches were nor- immediately administered vasoactive drugs and bicarbonate. mal. Histologically, the heart presented focal myocytes One hour later he died. The dosing of the thiamine resulted necrosis with massive and diffuse polymorphonuclear leu- equal to 60 nmol/L (n.v. 66 - 200 nmol/L). kocytes infiltrate, especially on the anterior left ventricular Pathological findings samples to demonstrate an early myocardial infarction At autopsy the body was 168 cm in height and 70 kg in (Figure 1A-D). The heart showed hyper-contraction of the weight. The heart had a normal shape and was normal myocell with a breakdown of the whole contractile appara- tus with markedly thickened Z-lines and extremely short sarcomeres. This breakdown varied from irregular, pathological and eosinophilic cross-bands consisting of segments of hyper-contracted or coagulated sarcomeres, to a total disruption of myofibrils, the whole cell assuming a granular aspect without visible clear-cut pathological bands. The necrosis was plurifocal, formed by foci ranging from one to thousands of myocardial cells and was found in any cardiac region. Unique bands of 10 to 20 hyper- contracted sarcomeres close to the intercalated disc (paradiscal lesion) were observed too. In addition, the his- tological sections were analyzed with a confocal micro- scopy and confirmed the presence of foci of myocardial contraction band necrosis or coagulative myocytolysis visi- ble in all regions of the heart. These pathological changes were formed by paradiscal and pancellular lesions. The lat- Figure 1 Myocardial findings in case 1. (A) Infiltration of ter were formed by segments of hyper-contracted sarco- polymorphonuclear leukocytes (CD15), without fibrin or meres with scalloped sarcolemma. Normal cells around hemorrhage, into the dead myocardial tissue. (B) hyper-contracted ones assumed a wavy appearance. No Immunohistochemical analysis for the phenotypic characterization evidence of platelet aggregation or other vessel changes or of the cells revealed a positive reaction to the antibody directed against of polymorphonuclear leukocytes (CD15). (C) Confocal laser of interstitial or sarcolemmal alterations existed. microscopy: double immunohistochemical reactions for the phenotypic characterization revealed a positive reaction to the Case 2 antibodies directed against of CD45 (blue reaction) and CD15 Clinical findings (green reaction). (D) Myocyte nuclei labelled by TUNEL assay A 43 year - old man, admitted to an hospital due to a severe (apoptosis) revealed an intensive, wide, positive reaction (brown nuclei). ulcerative rectocolitis, submitted to total parenteral nutrition Bello et al. Diagnostic Pathology 2011, 6:8 Page 3 of 5 http://www.diagnosticpathology.org/content/6/1/8 in size (12×12×6 cm) and weight (410 g). The coronary 2A-D). Myocells with normal nuclei and generalized arteries arose normally; no significant stenosis or throm- myofibrillar disappearance producing an increasing botic occlusion of the coronary segments were detected. vacuolization of myocardial cells without any cellular Plurifocal and interstitial intermyocellular fibrosis due to reaction (grade 2). collagen substitution was evident. Apparently normal Immunohistochemical findings nuclei with myofibrillar disappearance producing an Pathologic features were estimated using histologic increasing vacuolization of myocardial cells until a histo- sections stained by haematoxylin-eosin (H&E) and logic pattern of empty sarcolemmal tubes without any thrichrome stain. In addition, immunohistochemical cellular reaction or signs of healing results. The colliqua-
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