CONTENTS. Laboratory Findings of Amebic Liver Abscess Mohammad Shafiqur Rahman Patwary, Ghulam Mahmood, MA Latif

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1 CONTENTS Original Articles Rescue Therapy with Omeprazole, Amoxicillin, Clarithromycin and Colloidal 1-4 Bismuth for Helicobacter pylori Infected Patients After Failure of Standard Triple Therapies in Bangladeshi Duodenal Ulcer Patients MG Kibria, M M Rahman, N Islam, M R Khan, MAR Miah, M M R Bhuiyan, M Hasan. Angiographic Correlation with Admission Electrocardiogram in Acute Inferior 5-11 Wall Myocardial Infarction Md. Toufiqur Rahman, Sufia Rahman, KMHS Sirajul Haque, S Azizul Haque Pattern of Changes in the Findings among the Patients Undergoing Diagnostic Endoscopy in the Department of Gastroenterology, IPGM&R and BSMMU in the Last Two Decades A.S.M.A Raihan, M Chowdhury, MA Rahim Miah, T.K Majumder, S.K Sarker, Z Hossain M.Z Rahman, M Hasan Microbial Pathogens and Antibiotic Sensitivity at Intensive Care Unit of BIRDEM: A Retrospective Study Md. Rawshan Ali Basunia, Md. Raziur Rahman, Mohammad Omar Faruq, Farida Huq, Areef Ahsan, Rashedul Hassan, Bakhtiar Ahmed A Study of Relationship between Blood Group and Age Related Cataract S. Ahmed, A. Islam, A.G. Mondal, N.U. Ahmed, Z.R. Bhuyan, M.Husain Efficacy of Oxyphenonium Bromide and Imipramine in Irritable Bowel Syndrome A Prospective Double Blind Randomized Placebo Controlled Study MJ Uddin, RK Banik, MA Kabir, MMR Bhuiyan, MAR Miah, ASMA Raihan, PK Roy, M Hasan Laboratory Findings of Amebic Liver Abscess Mohammad Shafiqur Rahman Patwary, Ghulam Mahmood, MA Latif Fish Oil and Cardiovascular Health Md Toufiqur Rahman, S Azizul Haque, AKM Monwarul Islam, Md Fazlul Haque Case Reports Road to a Diagnosis: A Case Report of an Adult Male with SLE AKM Musa, AKM Shaheen, K Nazimuddin, RSC Sarker, MFA Auroni A Case of Osteopetrosis Presenting with Hydrocephalus and Choanal Atresia A Case Report Shahana A Rahman, Major Jesmine Sultana, Md. Mahbubl Islam, Chowdhury Ali Kawser

2 ORIGINAL ARTICLES RESCUE THERAPY WITH OMEPRAZOLE, AMOXICILLIN, CLARITHROMYCIN AND COLLOIDAL BISMUTH FOR HELICOBACTER PYLORI INFECTED PATIENTS AFTER FAILURE OF STANDARD TRIPLE THERAPIES IN BANGLADESHI DUODENAL ULCER PATIENTS MG KIBRIA, M M RAHMAN, N ISLAM, M R KHAN, MAR MIAH, M M R BHUIYAN, M HASAN. Abstract Helicobacter pylori eradication is the mainstay in the treatment of H. pylori-associated peptic ulcer disease. Current standard eradication therapy consists of two weeks of treatment with a proton pump inhibitor and two antibiotics. Failure rate of anti-h. pylori therapy is 10-20% in western countries and it may be higher in Bangladesh. There is no definite retreatment recommendation. The aim of the study was to assess the efficacy of quadruple therapy consisting of omeprazole, colloidal bismuth, amoxicillin and clarithromycin in patients for whom initial H. pylori eradication using a triple therapy regimen was unsuccessful. Eighteen consecutive patients with H. pylori-associated duodenal ulcer(du), in whom H. pylori eradication attempt with a standard triple therapy had been unsuccessful were included in the study. Failure of initial H. pylori eradication was established with either a positive rapid urease test (RUT) or histology three months after completion of treatment. Rescue therapy consisted of omeprazole (20 mg bid), amoxicillin (1 g bid), clarithro-mycin (500 mg bid) and colloidal bismuth subcitrate (240 mg bid) for two weeks. Healing of DU was assessed three months after the end of treatment and H. pylori eradication was assessed by RUT and histology. Sixteen of the eighteen patients completed the follow-up. The median age was 33 years and the male to female ratio was 5:1. On an intent-totreat basis, the eradication rate was 55.6%, on a per-protocol basis, the eradication rate was 62.5%, ulcer healing was noted to be 81.25%. We conclude that 2-weeks quadruple therapy regimen consisting of omeprazole, amoxicillin, clarithromycin and colloidal bismuth was moderately effective (62.5%) in Bangladeshi patients who failed an initial H. pylori eradication attempt with standard triple regimen. Introduction: Helicobacter pylori infection is now accepted as a major cause of duodenal ulcer 1. Duodenal ulcer is common in Bangladesh. The prevalence of duodenal ulcer was estimated to be 11.98%. 2 Helicobacter pylori is widely prevalent in Bangladesh, with 60% of children being infected by the age three months and 80% being infected by the age of three years. 3 In adults, about 92% have been found to be seropositive for Helicobacter pylori antibody. 4 Successful eradication of H. pylori markedly reduces the risk of ulcer recurrence. 1 International consensus conferences have recommended that H. pylori eradication should be the treatment of peptic ulcer associated with H. pylori. 5,6 In developed countries failure of eradication occur in approximately 10-20% of patients using commonly prescribed regimens. Studies in Bangladesh has shown low eradication rates using different H. pylori eradication regimens and a higher rate of re-infection. 7,8,9,10 In most of the studies, the eradication rate was between 30-64%. 8,9 Bacterial resistance to drugs, various virulence factors of the bacterium, poor compliance, or host factors may contribute to the failure of eradication. Eradication is more difficult when a first treatment attempt has failed, usually because of either poor patient compliance or the development of antibiotic resistance. European H. pylori study group recommends either a second course of triple therapy (selected after consideration of previous treatment and microbial sensitivity or both) or a proton-pumpinhibitor (PPI) based quadruple therapy. 11 A second course of PPI based triple therapy, avoiding Department of Gastroenterology, Bangabandhu Sheikh Mujib Medical University Bangladesh J Medicine 2005; 16 : 1-4

3 Rescue Therapy with Omeprazole, Amoxicillin, Clarithromycin BJM Vol. 16 No. 1 antimicrobial agents against which prior therapy may have induced resistance and avoiding less effective combinations, such as amoxicillin and tetracycline is an alternate approach for retreatment without susceptibility testing. This concept is supported by pooled analysis. 12 However; the optimal strategy for retreatment after the failure of eradication has not yet been established. As failure rate is high in Bangladesh larger proportion of patients will require rescue therapy. Drugs to which H pylori have a low resistance may prove more effective. Of the four drugs used in this trial two were new, which was not used in the previous regimen (Clarithromycin and Colloidal bismuth subcitrate). Furthermore, Clarithromycin being a recent and costly drug in Bangladesh is expected to have high sensitivity against H. pylori. The resistance of H. pylori against Amoxicillin is also reported to be less and it does not develop resistance against Omeprazole and Colloidal bismuth. 13 No study has so far been done in our country concerning the efficacy of a reeradication regimen. The aims of this study were to assess the efficacy and safety of two weeks quadruple therapy with Omeprazole, Amoxicillin, Clarithromycin, and Colloidal bismuth subcitrate as a rescue regimen in a group of DU patients, who have failed to eradicate H pylori after an initial course of three drug regimen as well as to evaluate the rate of ulcer healing in the same group of patients. Materials and Methods: The study was a prospective open clinical trial conducted in the department of Gastroenterology, Bangabandhu Sheikh Mujib Medical University. All adult patients with H. pylori associated DU of 15 to 60 years age have taken part in earlier studies of eradication therapy with different regimens. Those patients who were found to have failed to eradicate H. pylori during their follow-up endoscopy three months after the completion of the previous eradication regimen were included. Patients who agreed to participate in second line treatment after appropriate explanation were then retreated between September 2003 and May Patients who have taken NSAIDS, antibiotics, proton pump inhibitor, H 2 receptor antagonist within four weeks, complicated duodenal ulcer patients (narrowing of duodenal bulb, active bleeding and perforation), patients with erosive gastroesophageal reflux disease, with gastric ulcer, pregnant or lactating woman, patients with concomitant illness and patients with history of previous gastric surgery were excluded. A complete medical history was obtained, physical examination of all the patients were also done. Endoscopy was performed during follow-up three months after their initial eradication attempt to identify the presence of duodenal ulcer and to take biopsy for rapid urease test (CLO), histopathology and staining for Helicobacter pylori. Two biopsies were taken from the antrum and one biopsy from the body of the stomach, one biopsy from antrum was used for CLO test. One biopsy from the antrum and one from the body of the stomach were used for histology. Those who were found to be positive for H pylori either by CLO or by histopathology or both were then retreated with omeprazole (20 mg twice daily), amoxicillin (1 g twice daily), clarithro-mycin (500 mg twice daily) and colloidal bismuth subcitrate (240 mg twice daily) for two weeks Drug compliance was monitored by daily drug intake diary which was maintained by the patient in which the patient was required to mark each dose taken in the day and counting of empty drug packages. (Each dose was supplied in one package).endoscopy was repeated three months after the completion of treatment. Endoscopic healing of ulcer or otherwise was noted and biopsies were taken in the same manner as before the treatment. Eradication is defined as negative rapid urease test with absence of histopathological evidence of H pylori infection. Results: A total 18 patients fulfilling the inclusion criteria were enrolled. H. pylori infection on gastric histology and CLO was found positive in pretreatment samples of all patients enrolled in the study. Two patients withdrew from the study. One had stopped treatment after three days due to intractable side effects. Another patient attended follow up during assessment of compliance but was lost before the second follow up endoscopy for assessment of eradication. Compliance of all the patients who completed the protocol was excellent. Table I Results of Clinical Trial Treatment Result N (%) Cure Rate ITT (10/18) 55.6% PPA (10/16) 62.5% Ulcer Healing (13/16) 81.25% Eradication by RUT (12/16) 75% Eradication by Histology (10/16) 62.5% ITT: Intention To Treat, PPA: Per Protocol Analysis, RUT: Rapid Urease Test 2

4 BJM Vol. 16 No. 1 Rescue Therapy with Omeprazole, Amoxicillin, Clarithromycin For the intent-to-treat analysis 10 of 18 patients (55.6%) were cured of H pylori infection as determined by histopathology and staining. Considering only the CLO test eradication was 75% whereas combining with histopathology the rate was 62.5%. For the per protocol analysis (PPA, which includes only the 16 patients who completed the treatment regimen for full duration and attended the follow-up assessment) 10 out of 16 patients were eradicated (62.5%). Total 13 (81.25%) patients out of 16 had their ulcer healed. Discussion: Although H. pylori is susceptible to many different antibiotics, successful treatment remains a challenge. Even the most effective regimens available today fail in 5-20% of the patients. Previous trials in Bangladesh has shown that widely used triple therapy with PPI and various combination of antibiotics cured less then 60% of patients with a high rate of recurrence. 6,7,8,9 In this prospective study we have observed the efficacy and safety of two weeks bismuth based quadruple therapy in patients with at least one previous failed eradication attempt. Clarithromycin is thought to have high sensitivity against H. pylori and the resistance of H. pylori against amoxicillin is also reported to be less and it does not develop resistance against omeprazole and colloidal bismuth. 13 Consequently this (OACB) regimen was chosen for this study. In this study eradication rate achieved (55.6% intention to treat and 62.5% per protocol analysis) was not as high as was achieved in the developed countries. Similar study with quadruple therapy in Singapore by Ang and his colleagues has shown the eradication rate of 69.8% (intention to treat). On a per-protocol basis, the eradication rate was 82.2%. 14 Another study by Dore et al in USA reported it to be 95% and 98% respectively 14 whereas with rifabutin based therapy cure rate have been shown to be 76-96%. 16 Lower cure rate of 67% eradication was also observed in a study by Wheeldon et al where the rescue regimen containing Omeprazole, Clarithromycin, Amoxicillin was used for 10 days. 17 The eradication rate obtained in this rescue therapy trial may not representative as the sample size was small in this study. It was not possible to obtain larger sample for such study as attempts for eradication of H. Pylori is not common in this country and consequently there is small group of patients who actually fulfill the inclusion criteria. Low eradication rate in this study may be due to factors which were beyond the scope of this study. Compliance with drug was monitored and found to be good, concomitant use of other medications such as NSAIDs that may adversely influence the healing and eradication was eliminated. Drug sensitivity, bacterial virulence factor and host factors may still be the possible causes of low eradication. Pretreatment assessment of microbial sensitivity to drug was not assessed as culture and sensitivity test for H. pylori is not routinely available in Bangladesh till now. It has been suggested that when susceptibility testing is not available, the best approach may be to try quadruple therapy for 14 days as salvage therapy 15 ; therefore, this approach was adopted in this study. Another factor for low eradication rate may be due to bacterial virulence factors. CagA negative strains have been shown to be a risk factor for treatment failure. 18 However the CagA and VacA status in this study was not known. It is also possible that other virulence factors may be involved in the bacterial response to H. pylori eradication therapy. A large study employing a ranitidine bismuth citrate (RBC) based regimen as the salvage therapy for initial treatment failure has shown excellent results. Based on culture sensitivity results RBC, Amoxicillin, clarithromycin regimen has shown overall cure rate of 99% (PP) and 91% (ITT). 19 We could not use an RBC based regimen because of unavailability of the drug in this region. Further studies are needed to find out factor or factors responsible for the low eradication rate in Bangladeshi patients and a more effective eradication therapy. Newer drugs may be available in future and therapies containing such drugs may become more effective. Till such time a 14 day regimen consisting of Omeprazole 20mg b.i.d, Amoxicillin 1gm b.i.d, Clarithromycin 500mg b.i.d, Colloidal bismuth subcitrate 240mg b.i.d is moderately effective and well tolerated second-line treatment for H. pylori infected patients who have failed standard eradicating triple therapy regimens. References: 1. Suerbaum S and Michetti P. Helicobacter pylori infection. N Engl J Med 2002; 347: Hasan M, Ali SMK, Azad Khan AK. Peptic ulcer in Bangladesh: an endoscopic survey. Gut 1985;16: A Mahalanabis D, Rahman MM, Sarkar SA, Bardhan PK, Hildebrand P, Beglinger C, Gyr K. Helicobacter pylori infection in the young in Bangladesh, prevalence socioeconomic and nutritional aspects. Int J Epidemol 1996; 25: Ahmad MM, Rahman M, Rumi AK, Islam S, Huq F, Chowdhury MF, Jinnah F, Morshed MG, Hasan SM, 3

5 Rescue Therapy with Omeprazole, Amoxicillin, Clarithromycin BJM Vol. 16 No. 1 Azad Khan AK and Hasan M, Prevalence of Helicobacter pylori in asymptomatic Population- a pilot serological study in Bangladesh. J Epidemiol 1997; 7: Howden CW, Hunt RH. Guidelines for the management of Helicobacter pylori infection. Am J Gastroenterol 1998; 93: Bazzoli F. Key points from the review Maastricht Consensus Report, the impact on general practice. Eur. J Gastroenterol Hepatol 2001;13 Suppl.2: Hildebrand P, Brandhar P, Rossi L, Pervin S, Rahman A, Arefin MS, Hasan M, Ahmad MM, Kerieger KG, Terracciano L, Bauerfeind P, Beglinger C, Gyr N, Azad Khan AK, Recrudesceuce and reinfection with H. pylori after eradication therapy Bangladeshi adults. Gastroenterol 2001;121: Rahman MM, Hussein SMB, Ahmed Z, Siddique MAM, Hossain R, Uddin MN, Bhuyan MAB. A prospective study of three different Helicobactr pylori eradication regimens in the treatment of peptic ulcer disease. Bangladesh Armed Forces Medical Journal 2001/2002;29: Rahman MT, Miah MAR, Roy PK, Rasul K. Study of efficacy of 14 days triple therapy will be furazolicdone based regimen (furazolicdone plus cloroxycollie and omeprazole) in the eradication of Helicobacter pylori in Patients wirh peptic ulcer disease in Bangladesh. Bangl J Mede 2003; 14: Khan MR, Rasul K, Hasan M, Helicobacter pylori eradication therapy for duodenal ulcer disease in Bangladeshi patients by two triple drug regimen results of a clinical trial. Bangl J Med 2003;14: European Helicobacter pylori Study Group, Current European concepts in the management of Helicobacter pylori infection. The Maastricht Consensus Report. Gut 1997;41: Hojo M, Miwa H, Nagahara A, Sato N. Pooled analysis on the efficacy of the second-line treatment regimens for Helicobacter pylori infection. Scand J Gastroenterol 2001;36: Graham DY, Antibiotic resistance in Helicobacter pylori: Implications for therapy. Gastroenterol 1998; 115: Ang TL, Fock KM, TM NG, Teo EK, Chua TS, Tan YL. Efficacy of quadruple therapy for Helicobacter pylori eradication after failure of proton pump inhibitor-based triple therapy in Singapore. Chin J Dig Dis 2003; 4: A Dore M P, Graham DY, Mele R, Marras L, Nieddu S, Manca A, Realdi G. Colloidal Bismuth Subcitrate- Based Twice-a-Day Quadruple Therapy as Primary or Salvage Therapy for Helicobacter pylori Infection. Am J Gastroenterol 2002; 97: Perri F, Festa V, Clemente R. Randomized study of two rescue therapies for Helicobacter pylori-infected patients after failure of standard triple therapies. Am J Gastroenterol 2001;96: Wheeldon TU, Hoang TH, Phung DC, Bjorkman A, Granstrom M, Sorberg M. Long term follow up H. pylori eradication therapy in Vietnam: reinfection and clinical outcome. Aliment Pharmacol Ther 2005;21: Marais A, Monteiro L, Lamouliatte H. caga negative status of Helicobacter pylori is a risk factor for failure of PPI based triple therapies in non-ulcer dyspepsia[abstract]. Gastroenterol 1998; 114: A Kearney D J. Retreatment of Helicobacter pylori Infection After Initial Treatment Failure. Am J Gastroenterol 2001;96:

6 ANGIOGRAPHIC CORRELATION WITH ADMISSION ELECTROCARDIOGRAM IN ACUTE INFERIOR WALL MYOCARDIAL INFARCTION MD. TOUFIQUR RAHMAN 1, SUFIA RAHMAN 1, KMHS SIRAJUL HAQUE 2, S AZIZUL HAQUE 1 Summary: 56 Patients admitted with the diagnosis of acute inferior wall myocardial infarction ( less than 24 hours of chest discomfort and ECG changes), were underwent coronary angiography and having either RCA or LCX occlusion. All the patients were grouped into two, according to the angiographic findings. Group 1 included patients having significant stenosis / occlusion in RCA (Right Coronary Artery) and Group 2 included patients having significant stenosis / occlusion in LCX (Left Circumflex Artery). Significant ST depression in lead avl was more common in the RCA group (p <0.001), with a sensitivity and specificity of 94% and 70%, respectively. Higher ST-segment elevation in lead III than in lead II was found in 80% of the RCA group and in 8% of the LCX group (p <0.001); deeper ST-segment depression in lead avl than in lead I was found in 88% in the RCA group and in 8 % of the LCX group (p <0.001). Both criteria were positive in 70% of the patients in the RCA group and in none of the LCX group (p <0.001), whereas both were negative in 88% of the LCX patients and none of the RCA patients (0 <0.001).. ST-segment depression in lead avl had a high sensitivity for predicting RCA obstruction (94%), but a low specificity (70%). When the ST-segment deviation in leads I and avl was taken into consideration (criteria B), the sensitivity decreased to 80%, but the specificity increased to 94%. The positive predictive values and the negative predictive values were 98% and 85%, respectively. Moreover, when both criteria were positive, there was no LCX obstruction; when both were negative, there was no RCA obstruction. Introduction Coronary heart disease is a major health problem throughout the world and the most common cause of premature morbidity and mortality in western affluent society. Despite steady progress in treatment of cardiovascular diseases people are still dying of these diseases and substantial early mortality remains. 1,2 In the United States as well as in many other countries, cardiovascular diseases remain by far the number one cause of death for both men and women of all ethnic backgrounds and cause the greatest disability.by the year 2020, coronary heart disease (CHD) will hold first place in the World Health Organization s list of leading cause of disability. 2 Coronary heart disease (CHD) has been recognized as one of the important cause of death in our country. AMI is the leading cause of death in Bangladesh in the 4th decade of life. 3 The presentation of acute myocardial infarction is different depending on the coronary artery involved. The Right Coronary artery (RCA) perfuses the sinus node (in 55% patients), the right ventricle, the AV node, the postero-medial papillary muscle, the inferior part of the left ventricle and the posterior and lateral segments. So, ischemia due to occlusion of the RCA leads to ST elevation in the inferior leads. Though usually there is less extensive left ventricular involvement, but the clinical picture may be impressive due to (1) activation of the vagal nervous system and / or (2) ischemia of the sinus and atrioventricular node, leading to sinus bradycardia and delay or block in the AV node (3) right ventricular involvement with cardiogenic shock and (4) ischemia of the papillary muscle, leading to mitral regurgitation. 2,3 The Left Circumflex (LCX) branch perfuses the posterior wall and variably the inferior and lateral segments. In case of predominant posterior wall involvement following occlusion of the left circumflex, abnormalities in ventricular activation occur in the second half of the QRS complex and are therefore difficult to pick up on the 12-lead ECG frequently 1. Department of Cardiology, National institute of Cardiovascular Diseases, Dhaka. 2. Department of Cardiology, BSMMU. Bangladesh J Medicine 2005; 16 : 5-11

7 Angiographic Correlation With Admission Electrocardiogram BJM Vol. 16 No. 1 causing underestimation of the area at risk and under treatment of the patient.the objective of the ECG in inferior wall infarction is to recognize not only the culprit coronary artery (RCA or LCX) but also whether the right ventricle is involved secondary to an occlusion to the RCA proximal to the right ventricular branch. 3 The distinction between an RCA or LCX occlusion can be made by determining the ST segment vector during the acute phase of myocardial infarction. Because RCA occlusion predominantly results in inferoseptal ischemia, the ST segment vector is directed toward lead III, in LCX occlusion the ischemia is located in the inferoposterolateral region leading to an ST segment vector pointing toward lead II. Therefore, in RCA occlusion, ST- segment elevation is greater in lead III than lead II ( resulting in ST-segment depression in lead ² and avl). A greater amount of ST segment depression in avl than in lead I therefore improves the sensitivity in diagnosing an RCA occlusion. In LCX occlusion, lead II will show more ST segment elevation than lead III ( with lead I showing an isoelectric ST segment ). 4,5 Patients presenting with electrocardiographic criteria for inferior wall AMI, the presence of concomitant precordial ST depression was a sensitive sign of LCX occlusion, although not specific. Absence of precordial ST depression had a high negative predictive value in excluding the LCX as the culprit vessel and was not affected by increasing extent of underlying coronary disease. 6,7,8,9,10 Angiographic studies performed in the earlier hours of AMI in patients presenting with ST segment elevation have revealed approximately 90 percent incidence of total occlusion of the infarct related vessel. In contrast to patient with ST segment elevation, those patients who present without ST segment elevation have a much lower incidence of complete occlusion of the infarct related coronary artery. 11,12,13,14 The possibility of treating an acute coronary occlusion by thrombolytic therapy or intra coronary interventions such as percutaneous transluminal coronary angioplasty (PTCA) and stenting makes it necessary to determine rapidly and precisely, which coronary artery is involved, the size of area at risk and the results of the intervention. The larger the area at risk, the more important the attempt to restore or improve perfusion of that area. Considering these, much effort has been put into correlating ECG changes in acute ischemic episode with coronary angiogram. 15 The ECG is non-invasive, affordable, easy and essentially without any known adverse effects. If specific ECG patterns can be recognized, it will be possible to determine the culprit coronary artery and the size of the ventricular area that is jeopardized. 16 Materials and Methods This study was carried out in the Department of Cardiology of National Institute of Cardiovascular Diseases, Dhaka from July 2002 to June Patients admitted with the diagnosis of acute inferior wall myocardial infarction ( less than 24 hours of chest discomfort and ECG changes), defined by the typical chest discomfort, ECG changes and cardiac enzyme changes, were underwent coronary angiography and having either RCA or LCX occlusion. All the patients were grouped into two, according to the angiographic findings. Group 1 included patients having significant occlusion in RCA (Right Coronary Artery) and Group 2 included patients having significant occlusion in LCX ( Left Circumflex Artery). Exclusion Criteria were previous myocardial infarction, Complete left bundle branch block, Left ventricular hypertrophy, Cardiomyopathy, Congenital and valvular heart disease, Acute pericarditis, Acute myocarditis, Patients with contraindications to CAG, Patients dependent on pacemaker. A 12 lead resting ECG was taken on admission. STsegment deviation from the isoelectric line was measured manually to the nearest 0.5 mm in every lead at 0.08 seconds after the J point. A ST segment deviation of >1 mm will be considered significant. The magnitude of ST segment elevation in leads II and III was compared as will be the ST segment depression in leads avl and ². Location of ECG changes Consideration should be given to the maximal amount of ST segment changes-a)inferior leads- II, III, avf ; b)anterior leads- V1-V4; c) Lateral leads-v5,v6, I, avl. Selective CAG was done within one month of hospital admission. The infarct related artery was determined by coronary artery disease resulting in total or subtotal occlusion. Patients with significant stenosis of both the RCA and LCX arteries was excluded.exact evaluation was almost impossible and infact, the lesions were roughly classified into 6 categories: 1.Normal coronary artery 2.Irregularities of the vessel 3.Narrowing of less than 50% 3.Stenosis between 50% and 75% 4.Stenosis between 75% and 95% 5.Total occlusion. The angiographic view of stenosis more than 50% (area > 75%) was considered to be significant. Results A total of 56 patients of acute inferior wall myocardial infarction admitted in coronary care unit of NICVD 6

8 BJM Vol. 16 No. 1 Angiographic Correlation With Admission Electrocardiogram with less than 24 hour duration of symptom onset, who underwent subsequent angiography and having either RCA or LCX occlusion, were included in this study. All the patients were grouped into two, according to the angiographic findings. Group 1 included patients having significant stenosis / occlusionin RCA (Right Coronary Artery) and Group 2 included patients having significant stenosis / occlusionin LCX ( Left Circumflex Artery). The age of the study population ranged from 25 to 78 years. The mean ± standard deviation age among all was ± years. In group A, the age of patients ranged from 27 to 73 years with mean ± SD of ± years. In group B, the age of patients ranged from 28 to 72 years with mean ± SD of ± years. Table I Age distribution of study population. Age groups Group 1 Group 2 (in years) (RCA), n=44 (LCX), n=12 no. (%) no. (%) (02%) 01 (08%) (18%) 04 (34%) (41%) 05 (42%) ( 18%) 01 (08%) (14%) 01 (08%) (07%) 00 (00%) Total 44 (100%) 12 (100%) Table II Sex distribution of the study population Sex Group 1 Group 2 Total (RCA), (LCX), n=56 n=4 n=12 Male (95%) Female (05%) Among the 56 study population, 53 (95%) patients were male and 03( 05%) were female. Table III Degree of ST segment elevation in inferior leads (Lead II, III and avf). Inferior leads Group- 1 (RCA), Group-2 (LCX), p value n=44 n=12 (ST elevation in mm) (ST elevation in mm) Lead II 4.02 ± ± 1.72 < 0.05, significant Lead III 4.63± ± 1.08 <0.05, significant Lead avf 4.16 ± ± 1.16 > 0.05, ns Table IV ST segment depression in lead 1 ECG findings Group 1 (RCA), n=44 Group 2 (LCX), n=12 p value no. (%) no. (%) ST- (>1mm) 24 (55%) 03 (25%).01 Table IV shows ST segment depression in lead 1 present in 24 (55%) cases in group1 and in 03 (25%) cases in group 2. Table V: ST segment depression in lead avl ECG findings Group 1 (RCA), n=44 Group 2 (LCX), n=12 p value no. (%) no. (%) ST- (>1mm) 41 (94%) 03 (25%) <0.001 Table V shows significant ST depression in lead avl in Group 1 (RCA) in 41cases (94%) 7

9 Angiographic Correlation With Admission Electrocardiogram BJM Vol. 16 No. 1 Table VI Criteria A means higher ST segment elevation in lead III than lead II. ECG findings Group 1 (RCA), n=44 Group 2 (LCX), n=12 p value no. (%) no. (%) ST elevationin lead III > 35 (80%) 01 (08%) <0.001 lead II Table VI shows Criteria A is more seen in Group 1 (RCA) in 35 cases (80%) than in Group 2 (LCX) and it is significant. Tab VII Criteria B means greater ST segment depression in lead avl than lead I. ECG findings Group 1 (RCA), n=44no. (%) Group 2 (LCX), n=12no. (%) p value ST depressionin lead avl > lead ². 39 (88%) 01 (08%) <0.001 Table VII shows Criteria B is more seen in Group 1 (RCA) in 39 cases (88%) than in Group 2 (LCX). Table VIII Criteria A + B Positive means higher ST segment elevation in lead III than lead II plus greater ST segment depression in lead avl than lead I. ECG findings Group 1 (RCA), n=44 Group 2 (LCX), n=12 p value no. (%) no. (%) Criteria A + B Positive 31 (70%) 00 (00%) <0.001 Table VIII shows Criteria A + B Positive is more seen in Group 1 (RCA) in 31 cases (70%) than in Group 2 (LCX). Table IX Criteria A + B negative means absence of higher ST segment elevation in lead III than lead II plus absence of greater ST segment depression in lead avl than lead I. ECG findings Group 1 (RCA), n=44 Group 2 (LCX), n=12 p value no. (%) no. (%) Criteria A + B negative 00 (00%) 11 (88%) <0.001 Table IX Shows Criteria A + B negative is seen only in Group 2 (LCX) in 11 cases (88%). Table X Sensitivity, Specificity and predictive values of different ECG findings to predict occlusion of either RCA or LCX. Sensitivity(%) Specificity(%) Positive predictive Negative predictive value (PPV)(%) value (NPV)(%) ST lead I 55(%) 71(%) 88(%) 29(%) ST lead avl 94(%) 70(%) 93(%) 74(%) ST in V5 -V6 35(%) 76(%) 27(%) 82(%) Criteria A 88(%) 94(%) 98(%) 67(%) Criteria B 80(%) 94(%) 98(%) 85(%) 8

10 BJM Vol. 16 No. 1 Angiographic Correlation With Admission Electrocardiogram Table X shows ST-segment depression in lead ² has a high specificity (71%) for predicting for RCA obstruction but a low sensitivity (55%) and STsegment depression in lead avl has a high sensitivity (94%) for predicting for RCA obstruction but a low specificity (70%). When the ST-segment deviation in leads I and avl was taken into consideration (criteria B), the sensitivity decreased to 80%, but the specificity increased to 94%. The positive predictive values and the negative predictive values were 98% and 85% respectively. Discussion: Myocardial infarction is the major cause of death among patients with coronary artery disease, despite impressive strides in diagnosis and management over the last three decades. It is becoming an increasing important problem in developing countries too. About 50 percent deaths associated with acute myocardial infarction occur within one hour of the event and are attributable to arrhythmia, most often ventricular fibrillation. 4 The major cause of myocardial infarction is atherosclerotic disease of the epicardial arteries. Luminal narrowing due to atherosclerosis, resulting in hemodynamically significant obstruction of blood flow is the major cause of symptoms of coronary ischemia. On top of that, the majority of myocardial infarction occurs as a result of the disruption of arterial lesions that are not hemodynamically significant. 15 Just with the location of the infarct, independent of infarct size and type (Q and non -Q wave), anterior infarction demonstrated a lower left ventricular ejection fraction and higher incidence of congestive heart failure and cumulative cardiac mortality. When patients were evaluated on the basis of both location and type of infarction, those with anterior infarction exhibited a worse hospital course and cumulative cardiac mortality than with inferior infarction. 16 The Electrocardiogram remains a crucial tool in the identification and management of acute myocardial infarction. A detailed analysis of patterns of STsegment elevation may influence decisions regarding the use of reperfusion therapy. The early and accurate identification of the infarct-related artery on the electrocardiogram can help predict the amount of myocardium at risk and guide decisions regarding the urgency of revascularization. Electrocardiographic signs of reperfusion represent an important marker of microvascular blood flow and consequent prognosis. The electrocardiogram is also crucial for identifying new conduction abnormalities and arrhythmias that influence both short-and long-term outcome. 17 Electrocardiogram is the first laboratory performed at the bedside. The technique is relatively cheap, reliable and reproducible. It can be applied serially and when properly interpreted, is the cornerstone of the laboratory diagnosis of myocardial infarction. Coronary angiography films were reviewed by investigators who were blinded to the electrocardiographic findings. The infarct-related artery was determined by the following criteria: coronary artery disease resulting in total or subtotal occlusion of an artery. Patients with significant stenosis in both the RCA and LCX artery were excluded. 25 Patients were divided into two groups according to the culprit artery. The chi-square test was used to compare electrocardiographic differences between groups. All tests of significance were 2-tailed and p values of <0.05 were considered statistically significant. 18 The study population consisted of 56 patients (53 men and 03 women). Age of the study population ranged from 25 to 78 years. The mean ± standard deviation age among all was ± years. In group A, the age of patients ranged from 27 to 73 years with mean ± SD of ± years. Ingroup B, the age of patients ranged from 28 to 72 years with mean ± SD of ± years. Significant ST depression in lead avl was more common in the RCA group (p <0.001), with a sensitivity and specificity of 94% and 70%, respectively. Higher ST-segment elevation in lead III than in lead II was found in 80% of the RCA group and in 8% of the LCX group (p <0.001); deeper ST-segment depression in lead avl than in lead I was found in 88% in the RCA group and in 8 % of the LCX group (p <0.001). Both criteria were positive in 70% of the patients in the RCA group and in none of the LCX group (p <0.001), whereas both were negative in 88% of the LCX patients and none of the RCA patients (0 <0.001). No significant differences were found for significant ST-segment elevation in leads V5 to V6 (33% of the LCX group and 25% of the RCA group, p = 0.3). ST-segment depression in lead avl had a high sensitivity for predicting RCA obstruction (94%), but a low specificity (70%). When the ST-segment deviation in leads I and avl was taken into consideration (criteria B), the sensitivity decreased to 80%, but the specificity increased to 94%. The positive predictive values and the negative predictive 9

11 Angiographic Correlation With Admission Electrocardiogram BJM Vol. 16 No. 1 values were 98% and 85%, respectively. Moreover, when both criteria were positive, there was no LCX obstruction; when both were negative, there was no RCA obstruction. These results did not change with the variation of the obstruction site along the coronary artery (proximal vs distal). 19 Occlusion of the LCX artery is difficult to diagnose using the standard 12-lead electrocardiogram. Because the posterolateral and inferoapical segments of the left ventricle are supplied by the LCX, their involvement in LCX occlusion is expected. Radionuclide studies show that thallium defects in the posterolateral segments are relatively specific for LCX AMI, whereas defects in the posterobasal segment are seen with equal frequency in RCA AMI. Indeed, the lateral limb leads are highly significant in inferior wall AMI. The avl lead faces the highlateral segment of the left ventricular wall, and is the only lead truly reciprocal to the inferior wall. ST-segment depression in lead avl is a sensitive early electrocardiographic sign of inferior wall AMI and showed that ST-segment depression in leads I and avl was observed only during RCA occlusion. 20 It was reported that ST-segment depression in lead I is significantly less common with LCX-related AMI that with RCA related AMI. These studies did not compare the relative magnitude of ST-segment depression in the 2 leads, as was performed in this study. In the case of RCA infarction, the ST-segment depression in leads avl and I represents reciprocal changes that are more prominent in the true reciprocal lead, avl; in LCX AMI, the high posterolateral and apical segments are ischemic, therefore the ST-segment depressions in these leads are canceled out and an even ST-segment elevation can appear. Standard lead III is oriented to the right inferior segment, whereas lead II is oriented principally to the left inferior segment and also tends to be oriented to the inferior region of the left lateral or superior wall of the left ventricle. Consequently, lead III is more influenced by RCA-related AMI, whereas lead II is more influenced by LCX-related AMI. By comparing the magnitude of deviations of the STsegment in different leads (avl to I and II to III), it became possible to overcome the limitation who could not differentiate RCA occlusion from distal LCX occlusion. Conclusion This study indicates that it is possible to predict the culprit artery in inferior wall AMI using the readily obtainable measures on the admission electrocardiogram. A higher ST-segment elevation in lead III than in lead II and a deeper ST-segment depression in lead avl than in lead I are sensitive and specific markers for RCA related AMI. The ECG is non-invasive, affordable, easy and essentially without any known adverse effects. If specific ECG patterns can be recognized, it is possible to determine the culprit coronary artery and the size of the ventricular area that is jeopardized. As a result of the present study, observations can be used in order to test the predictive values in patients who may have multi vessel disease. References: 1. ACC Clinical Data Standards, American College of Cardiology Key Data Elements and Definitions for Measuring the Clinical Management and Outcomes of Patients With Acute Coronary Syndromes, A Report of the American College of Cardiology Task Force on Clinical Data Standards (Acute Coronary Syndromes Writing Committee), J Am Coll Cardiol, 2001; 38( 7): Alexander RW, Pratt CM, Ryan TJ & Roberts R. Diagnosis and Managements of patients with Acute Myocardial Infarction, Hurst s THE HEART, 10 th ed, McGraw-Hill, New York, USA; 2001 : Antman EM & Braunwald E. Acute myocardial Infarction, Heart Disease: A Textbook of Cardiovascular Medicine, 6 th ed, W.B. Saunders Company, Philadelphia, Pensylvinia, USA; 2001 : Assali A, Sclarovsky S, Herz I et. al. Comparison of patients with inferior wall acute myocardial infarction with versus without ST- segment elevation in leads V5 and V6. Am J Cardiol; : Baim DS & Grossman W. Coronary Angiography, Grossman s Cardiac catheterization, Angiography, and Intervention, 6 th ed, Lippincott Williams and Wilkins, Philadelphia, USA Bairey CN, Shah PH, Lew AS, Hulse S, Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction. AM J Cardiol; 1987 ; 60: Bayes de luna A. International cooperation in world cardiology: The role of the world Hearts Federation. Circulation 1999; 99: Birnbaum Y., Hasdai D., Sclarovsky S., Herz I., Strasberg B. & Rechavia E. Acute myocardial infarction entailing ST-segment elevation in lead avl: electrocardiographic differentiation among occlusion of the left anterior descending, first 10

12 BJM Vol. 16 No. 1 Angiographic Correlation With Admission Electrocardiogram diagonal, and first obtuse marginal coronary arteries Am Heart J 1996; 131 (1): Birnbaum Y, Solodky A, Herz I, Kusniec J, Rechavia E, Sulkes J & Sclarovsky S. Implications of inferior ST- segment depression in anterior acute myocardial infarction: Electrocardiographic and angiographic correlation, Am Heart J, 1994; 127: Brinbaum Y, Sclarovsky S, Marger A, Strusberg B, Rechavia E. ST-segment depression in avl: a sensitive marker for acute inferior myocardial infarction. Eur Heart J 1993; 14: Blank H, Cohen M, Schlueter GV, Karsh KR, Rentrop KP. Electrocardiographic and coronary angiographic correlation during acute myocardial infarction. Am J Cardiol; 1984; 54: Braat SH, Brugada P, Wellens HIJ. Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. Br Heart J 1983;49: Chan AW, Solankhi N, Webb JG, Dodek A, Gaziano M & Carere RG. Correlation of ST-segment depression and coronary anatomy during acute coronary occlusion, Can J Cardiol, 2001; 17( 3): Chou TC Knilans TK. Myocardial Infarction, Myocardial Injury, and Myocardial Ischemia; Electrocardiography in Clinical Practice, 4 th ed. W.B. Saunders Company, Philadelphia, Pensylvinia, USA, 1996; Hasdai D, Birnbaum Y, Herz I, Sclarovsky S, Mazur A, Solodky A, ST segment depression in lateral limb leads in inferior wall acute myocardial infarction. Eur Heart J 1995;16: Herz I, Assali AR, Adler Y, Solodky Y, Sclarovsky S. New Electrocardiographic Criteria for Predicting Either the Right or Left Circumflex Artery as the Culprit Coronary artery in inferior wall acute myocardial Infarction. Am J Cardiol 1997, 80: Huey BL, Beller GA, Kaiser DL, Gibson RS, A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion. J Am Coll Cardiol 1988;12: Sapin PM, Musselman DR, Dehmer GJ & Wayne EC. Implications of Inferior ST-segment. Elevation Accompanying Anterior Wall Acute Myocardial Infarction for the Angiographic Coronary Artery Morphology and Site of Occlusion, Am J Cardiol, 1992; 69: Schamroth L. An Introduction to Electrocardiography, 7 th ed, Blackwell Science Ltd., Oxford, London1992; Stone PH, Raabe DS, Jaffe AS, Gustafson N, Muller JE, Turi ZG, et al. Prognostic Significance of Location and Type of Myocardial Infarction: Independent Adverse Outcome Associated With Anterior Location J Am Coll Cardiol 1998;11:

13 LABORATORY FINDINGS OF AMEBIC LIVER ABSCESS MOHAMMAD SHAFIQUR RAHMAN PATWARY 1, GHULAM MAHMOOD 2, MA LATIF 3, Abstract: A prospective cross-sectional study was undertaken to evaluate the laboratory finding of amebic liver abscess. 50 patients of liver abscess were admitted in medicine unit of Sher-E- Bangla Medical College Hospital, Barisal, during the period of May 1998 to December Out of these 35 (70%) patients having amoebic liver abscess. Majority patients (58.8%) were in 5 th and 6 th decade. 88.6% were male and 11.4% were female. Ultrasonographicaly 94.3% had solitary lesion and 83% involved right lobe of the liver. 65.7% had ESR more than 40 mm in 1 st hour and 71.43% had Hb level below 12 gm/dl. Neutrophilic leucocytosis was present in 71.43%patients. Aspirated materials from liver abscess showed characteristic anchovy sauce in 97.14%cases. In aspirated materials, red blood cell present in 71.43% and trophozoite of EH present in 20% cases. Stool examination reveled presence of cyst of EH in 28.57% cases. Introduction: Amoebic liver abscess is the commonest extraintestinal form of amoebiasis. Its diagnosis has improved significantly with the availability of ultrasound 1,2 in combination with clinical and serological criteria 3. Formerly amoebiasis was believed to occur principally in tropical countries, for this reason amoebic abscess of the liver was commonly called tropical abscess. An amoebic abscess of the liver arises as a result of the spread of Entamoeba histolytica from the primary site of infection, the large bowel, via the portal vein. Compromised host defence may be important in allowing the establishment of hepatic infection with subsequent abscess formation. The abscess is usually solitary and in the right lobe, and men are more commonly affected than women. Diagnosis requires a high index of suspicion. Right upper quadrant pain, fever and tender hepatomegaly are the predominant clinical feature 4. Ultrasonography and other imaging techniques are useful in confirming the presence of abscess 5. Confirmation of the amoebic abscess needs serological test and response to treatment. Some authors employ initial routine diagnostic fine needle aspiration to exclude pyogenic abscess 4. Identification of amoebic antigen in the aspirate is a more reliable investigation but is not used frequently 6. Most amoebic abscesses of the liver respond to medical management and metronidazole is the amoebicide of choice 4. Materials and Methods: It was a prospective cross -sectional study done in different medicine unit of Sher-E-Bangla Medical College Hospital, Barisal during the period of May 1998 to December During this period 35 cases of amoebic liver abscess was found. The diagnosis of amoebic liver abscess was done on the basis of clinical symptoms, characteristic sonographic findings, leucocytosis, characteristic appearance of needle aspiration fluid, (anchovy sauce), cytological and protozoal study of aspirated material & stool examination. They were treated with metronidazole 2.4 gm/day in divided doses and other measures including needle aspiration. Results: Total of 35 cases of amoebic liver abscess were evaluated in this study. Table-1 shows maximum age incidence was in the 5 th decade followed by 6 th decade with relatively infrequent in other age groups. Table I Age distribution Age in years No. of patients Percent > Total % 1. National Institute of Cardiovascular Diseases, Dhaka. 2. Professor, SBMCH, Barisal. 3. Professor, SBMCH, Barisal. Bangladesh J Medicine 2005; 16 : 32-35

14 BJM Vol. 16 No. 1 Laboratory Findings of Amebic Liver Abscess Table-II Sex distribution Sex No. of patients Percent Male Female Total % Table-II shows male suffered more than female. The ratio between male and female is 8:1. 31 (88.57%) cases were male and 4 (11.43%) were female. Table-III Ultrasonogram findings No. of abscess No. of patients Percent Single Multiple Table-VI Hemoglobin of patients Hb in gm/dl No. of patients Percent > < Total Table VI shows 24 (68.57%) cases had hemoglobin level below 12 gm/dl. Table-VII Total count of white blood cell of patients WBC per c.c.m No. of patients Percent , ,001-14, ,001-20, >20, Total Table-IV Lobe distribution in ultrasonogram Lobe No. of patients Percent Right Left Table III & IV shows 33(94.29) patients had single abscess and 29 (82.86%) patients had right lobe involvement in ultrasonogram of hepatobilliary system. Table-V Erythrocyte sedimentation rate of patients ESR mm in 1st hour No. of patients Percent > Total Table-V shows an increased erythrocyte sedimentation rate was noted in 35 (100%) cases of which 24(68.57%) cases had ESR above 40 mm (Westergreen method) Table-VIII Neutrophil count of patients Neutrophil No. of patients Percent <60% % % >85% Table -VII and VIII shows the total count of white blood cell to /c.cm was the major feature in 30 (85.72%) patients and 24 (68.57%) cases showed neutrophilic leucocytosis. Table-IX Aspirated material from liver abscess Features No. of patients Percent Anchovy sauce Turbid / hazy Tissue debris RBC Trophozoite of EH Table -IX shows characteristics of aspirated material from liver abscess % cases showed anchovy 33

15 Laboratory Findings of Amebic Liver Abscess BJM Vol. 16 No. 1 sauce, RBC present in 71.43% cases % cases demonstrate trophozoite of EH and culture negative in 100% cases. Discussion: Amoebic liver abscess is a very common disease in our country due to low socioeconomic condition and poor knowledge in hygiene. Amoebic liver abscess diagnosed by clinical findings ultrasonographic findings, characteristics of aspirated material, culture sensitivity and protozoal study of aspirated material from liver abscess and stool examination. This study was done to evaluate laboratory finding in amoebic liver abscess. In this study amoebic liver abscess is more frequent in the 5 th decade (37.14%). Quaderi et al. 7 showed highest incidence in 4 th decade (45.7%). Males dominated over the females. Higher proportion of males may be due to the fact that males are more prone to contact infection as they frequently take meals outside. Though Harinasuta et al 8 reported that history of dysentery was obtained in only 56% cases of liver abscess. In this study 20% had history of dysentery and stool examination revealed cyst of Entamoeba histolytica in 28.57% cases. Quaderi et al 7 reported cyst of Entamoeba histolytica in 17.14% cases. Pleural effusion found in 5.71% cases but Quaderi et al 7 found in 17% cases. Anemia was seen in majority of the cases (71.43%). About 68.57% cases had haemoglobin below 12 gm%. Anaemia cannot be attributed solely to hepatic abscess. Malnutrition, chronic small bleeding from gastro-intestinal tract and associated helminthic infection may be responsible in most cases % cases show polymorph nuclear leucocytosis. This is consistent with Islam 9 and Rahman 10 studies. Increased erythrocyte sedimentation rate as noted by Wilmot 11, and Rahman 10 was a constant finding, and markedly high values were seen in advanced cases. In this study erythrocyte sedimentation rate more then 40 mm in first hour was recorded in 68.57% cases. The vegetative form of amoebae were noted in 20% cases in aspirated material from liver abscess, consistent with Rahman 10 study (20%) and Quaderi et al 7 study (8.57%). Tropozoites are usually scanty in the amoebic pus drown at the first setting as they are more abundant at the periphery of the abscess cavity 12. They are also difficult to be seen because of the nature of the background in cover slide presentation. Jaundice was seen in 14.29% cases. Islam 9 stresses that presence of jaundice should create suspicion about the diagnosis of hepatic amoebiasis. On the other hand Kamat et al 13 recorded jaundice in 28% of their cases and Powell 14 and Viranuvaatti 15 attribute this hyper bilirubinaemia due to a large abscess on the biliary tract. However Kamat et al 13 attribute jaundice due to hepatocellular damage, as there were not associated with characteristic high values of alkaline phosphatase. The jaundice in liver abscess may be produced by large- scale destruction of liver cells due to abscess formation and associated hepatitis in the adjoining area. Mechanical obstruction of the biliary canaliculi by the abscess 16 is probably not a significant factor. Ultrasound study revealed, 94.29% cases had solitary lesion and involved right lobe of liver in 82.86% cases. It was consistent with Sharma et al 17 study, they showed 89.8% cases had solitary lesion and 85% cases involved in the right lobe of liver. Conclusion: Amoebic liver abscess is commonly encountered in Bangladesh. It is commonly affect adult male. Pleural effusion and jaundice were less common feature. High ESR, low haemoglobin, neutrophilic leucocytosis, solitary right lobe abscess in ultrasound, anchovy sauce aspirated material were dominated lab findings. Tropozoites of EH in pus and cyst of EH is stool may be helpful in diagnosis of amoebic liver abscess through not dominant findings. References: 1. Ralls PW, Colletti PM, Quinn MF, Halls JI. Sonographic findings in hepatic amebic abscess. Radiology 1982; 145: Abul-khair MH, Kenawi MM, Korashy EA, Arafa NM. Ultrasonography and amoebic liver abscess. Ann Surg 1981; 193: World Health Organization Expert Committee. Amoebiasis. Tech Rep Ser 1969; 42: Ribney FJ. Amoebic liver abscess. Br J Surg 1990; 77: Ralls PW, Barnes PF, Radin DR, Colletti P, Halls J. Sonographic features of amebic and pyogenic liver abscesses: a blinded comparison. AJR 1987; 143: Gandhi BM, Irshad M, Acharya SK et al. Amoebic liver abscess and circulating immune complexes of Entameba histolytica proteins. Am J Trop Med Hyg 1989; 39: Quaderi MA, Rahman MS, Rahman A, Islam N. Amoebic liver abscess and clinical experiences with tinidazole in Bangladesh. J Trop Med Hyg 1978; 81:

16 BJM Vol. 16 No. 1 Laboratory Findings of Amebic Liver Abscess 8. Harinasuta T, Bannag D, Jaroonkesma N et al. Amoebic liver abscess in Thailand. 8th Int Cong Trop Med & Malaria Islam N. Amoebic liver abscess and amoebic hepatitis. Medicine To-day 1969; 3(1): Rahman MT. Study on variation in clinical presentation of liver abscess. Dissertation, BCPS Wilmot AJ. Clinical amoebiasis. In: Davidson SS editor. The principle and practice of Medicine. 7 th ed. Oxford: Blackwell Scientific Publication; Rustgi AK, Richer JM. Pyogenic and amebic liver abscess. Med Clin North America 1989; 73: Kamat GR, Jojhri BS, Pathah VP et al. Role of liver function tests and electrophoretic pattern of serum proteins in diagnosis and prognosis of amoebic liver abscess. J Trop Med Hyg 1968; 71: Powell SJ. Clinical aspects of amoebiasis. Medicine Today 1970; 4(1): Viranuvatti V, harinasuta T, Plengvanit V et al. Am J gastroenterology 1963; 39: Rab SM, Alam N & Hoda AN. Amoebic liver abscess: Some unique presentation. Am J Med 1967; 43: Sharma MP, Dasarathy S, Sushma S, et al. Long term follow-up of amoebic liver abscess: Clinical and ultrasound patterns of resolution. Tropical Gastroenterol 1995; 16(3):

17 CASE REPORTS ROAD TO A DIAGNOSIS: A CASE REPORT OF AN ADULT MALE WITH SLE AKM MUSA 1, AKM SHAHEEN 2, K NAZIMUDDIN 3, RSC SARKER 4, MFA AURONI 5 Abstract: A 36-year-old diabetic male from Shariatpur, Bangladesh was admitted into BIRDEM Hospital with fever, weakness and burning micturation with severe anaemia. He was initially thought to be a case of septicaemia and haematological malignancy. He was ultimately diagnosed as a case of autoimmune haemolytic anaemia and secondary antiphospholipid syndrome due to systemic lupus erythematosus and treated accordingly. The way he ultimately evolved into a case of SLE during the hospital course was very interesting. A relevant review on SLE, especially its haematological manifestation was done. Introduction: SLE is a chronic multisystem autoimmune disease that characteristically involves many organ systems and associated with serological aberrations, particularly the presence of autoimmune antibodies. The prevalence of SLE varies worldwide. In North America and northern Europe, it is about 40 per 1,00,000 population 1. It is primarily a disease of young adult woman. Female: male ratio is 9:1 between menarche and menopause, 3:1 in young and old 2. In Bangladesh the prevalence is about 1.12% and F: M ratio is 19:1 [Revealed in 1996 over a 18 months period study done in the Rheumatology clinic of IPGM&R (now BSMMU)]. Criteria to distinguish SLE from other connective-tissue diseases have been established by the American College of Rheumatology in , which were updated in where one immunological criteria (False positive VDRL) was replaced by positive antiphospholipid antibody test. These criteria are intended to provide a degree of diagnostic certainty primary for research purposes. It is often possible to be reasonably confident about a diagnosis of SLE on less strict clinical grounds. According to number of criteria present the Rheumatologists classify these cases as possible (2 criteria), probable (3 criteria), definite (4 criteria) and classic (more than 4 criteria) 5. Among the 11 criteria 6 criteria are obvious from the history and physical examinations (malar rash, discoid rash, photosensitivity, oral ulcer, arthritis, neurological disorders) but the rest 5 criteria (serositis, renal disorders, haematological disorders, immunological and antinuclear antibody) needed laboratory confirmation. So it is sometimes very difficult to diagnose SLE in a patient present with less obvious manifestations. Here we describe a 36 year old male who presented initially with nonspecific clinical features like fever, anaemia and symptoms of UTI but subsequently developed haematological features of SLE and antiphospholipid syndrome without any other major common organ involvement. Case History: A 36 year old diabetic male from Shariatpur, Bangladesh was admitted into BIRDEM Hospital because of dysuria, continued fever, fatigue and vomiting of 3 weeks duration. There was no history of abdominal, chest or joint pain or rash and history of travel to Hill Tracts. He was treated with Ofloxacin, Mefenamic acid, and amitriptyline. On examination, he was severely anaemic, dehydrated, with pulse rate of 100/min, temperature 103 F and blood pressure 100/70.Thyroid and lymph nodes were not palpable. There was tenderness in suprapubic region on deep palpation of abdomen; 1. Assistant Professor, Department of Internal medicine, BIRDEM and Ibrahim Medical College. 2. Registrar, Department of Internal medicine, BIRDEM and Ibrahim Medical College. 3. Associate Professor and Consultant, Department of Internal medicine, BIRDEM and Ibrahim Medical College. 4. Medical officer, Department of Internal medicine, BIRDEM. 5. Department of Internal medicine, Honorary Medical officer, BIRDEM. Bangladesh J Medicine 2005; 16 : 41-43

18 Road to a Diagnosis: A Case Report of an Adult Male with SLE BJM Vol. 16 No. 1 but liver and spleen were not palpable. His GCS was 11/15. Examination of respiratory, cardiovascular, and locomotor system did not reveal any abnormality. The provisional diagnosis was DM, septicaemia due to UTI, and severe anaemia. The possibilities of malaria and haematological malignancies were considered. After sending routine investigations the patient was treated symptomatically with I/V Normal saline, Metoclopramide, Inj. Ceftriaxone followed by Tab.Domperidone, Tab.Ranitidine. He was put on diet control for his diabetes as the random blood sugar was 9.5 mmol/l.the initial blood examination showed an Hb: 5gm/dl, ESR: 140 mm in 1 ST hour, TC: 9200/cmm, DC: N-64%, L-24%, M-7%, E-5%, Platelet count , Blood urea-19mg/dl, S.creatinine-1.3 mg/dl. S.electrolyte, SGOT, SGPT, Alk Phosphatase was normal but S. billirubin was 2.1 mg/dl. Urine R/M/E, ECG, X-Ray chest P/A view and USG of whole abdomen also showed no abnormality. Blood for MP and ICT for malaria were also negative. The PBF comment was anisochromia with anisocytosis with neutrophilia and thrombocytopenia. Suggestive of combined deficiency anaemia probably compensated. We transfused 3 units of packed cell initially, which raises the Hb to 8.4mg/dl on 7 th day of admission. As the fever continues, we repeat the CBC, which shows normal TC, DC, but platelet count reduced from to Among other routine investigations blood and urine C/S showed no growth, triple antigen was not significant. On 5 th day of the admission patient developed pain and swelling in the right calf muscle and Duplex venous study showed DVT in right calf muscle. We thought that the DVT was due to prolonged immobilization and after sending aptt and prothrombin time we started low molecular wt. heparin. The aptt and prothrombin were found to be normal. Leg pain improved within 4 days of drug therapy. We started insulin as his diabetes became uncontrolled. Bone marrow aspiration was done on 9 th day of the admission and the report was erythroid hyper plasia with megaloblastic changes suggestive of combined iron and folate/vit B12 deficiency anaemia without any evidence of malignancy. Iron profile and serum Vit B12 level found normal. In the clinical course on 2 nd week we found palpable lymph node on left axial which was about 2cm in diameter, firm, nontender, not matted & free from underlying structure and overlying skin. Lymph node biopsy shows follicular hyperplasia. In the meantime repeat PBF, Hb% was done along with reticulocyte count, which shows Hb%-8.6mg/dl, reticulocyte count, -1.5% and PBF again suggestive of combined deficiency anaemia probably compensated. Endoscopy upper GIT was normal as was stool for OBT and Hb electrophoresis. The patient s liver and spleen become just palpable. Fever and anaemia persists despite the broadspectrum antibiotic he was getting. On 20th day of admission Hb% was found to be 7.9 gm/dl and the reticulocyte count-4.5%. Both direct and indirect Coomb s test was negative. 7days latter Hb% falls to 5.6gm% with normal TC, DC and high ESR of 150mm in 1 st hour. Finally we came to a conclusion that there is definitely a haemolytic process going on which is causing the rapid decline of Hb%. We repeat reticulocyte count, PBF and Coomb s test showing reticulocyte count- 15%, PBF definitely suggestive of a haemolytic process and the direct Coomb s test positive. So our diagnosis was autoimmune haemolytic anaemia and to find the cause ANA and anti-ds-dna were done; both found positive. Antiphospholipid antibody was also found positive latter on. Final diagnosis: Diabetes mellitus with autoimmune haemolytic anaemia and secondary Antiphospholipid syndrome due to SLE Treatment: Patient was given the following treatment during his hospital stay: Anti-emetic, Ceftriaxone, and Blood transfusion, Low molecular weight heparin followed by Warfarin, Ranitidine, Folic acid, Prednisolone and short acting insulin. Outcome: Patient becomes completely afebrile after 8 days of steroid therapy. His Hb% became 10.7 gm/ dl. Patient improved a lot clinically and discharged with advice on 38th day of admission with following treatment & advice: Short acting insulin, Tab. Prednisolone 60 mg daily with advice of tapering, Tab. Ranitidine 150 mg. twice daily, Tab. Folic acid 5 mg daily, and Tab. Warfarin 5 mg daily. Follow up: 2 weeks after discharge leg swelling completely disappeared, Hb%-16 gm/dl, Platelet , ESR18 mm in 1 st hour, Reticulocyte count- 4.5%, and Prothrombin time: control-13 sec, patient- 15.5, INR

19 BJM Vol. 16 No. 1 Road to a Diagnosis: A Case Report of an Adult Male with SLE Discussion: Our patient presented with continued fever, severe anaemia and symptoms of UTI. UTI was excluded as the Urine R/M/E and urine C/S was normal as was the TC. For the cause of fever, we could not found any source of infection anywhere. So the cause of the fever must be due to SLE as the fever subsided completely with Steroid. As for the severe anaemia, initially we thought that it might be primarily a blood disorder, which was strengthened further by subsequent development of lymphadenopathy and hepatosplenomegaly. But the CBC, PBF, bone marrow and lymph node biopsy do not support any haematological conditions like aplastic anaemia, leukemia or lymphoma. When Hb% begun to fall rapidly despite repeated blood transfusion and without any evidence of external or internal bleeding, diagnosis of haemolysis (intravascular or extravascular) came to our mind. As the naked eye examination does not show any smoky nature of urine (which occurs in intravascular haemolysis) we came to the conclusion that the haemolysis must be extravascular (in the spleen). That s why PBF, reticulocyte count and Coomb s test were done repeatedly and finally gave us the autoimmune nature of haemolysis. To find the cause of autoimmune haemolysis, ANA and anti ds-dna were done and found positive. In a study it is found that 10% of patients with SLE will have a severe haematological crisis at some point during the course of their disease (6.6% haemolytic anaemia and 3.3 % thrombocytopenia) and a further 10% will have a mild haematological disturbance requiring close followup. The study also found that a significant proportion of patients had their haematological crisis at diagnosis or within the first year of diagnosis of SLE 6. ANA test is most sensitive and found in 95% of SLE patient 7. Anti ds-dna is more specific and found in 60% of patient 8. But when both are found positive the certainty of diagnosis SLE approaches 90% 9. Thus though the clinical manifestation of this patient did not fulfill the diagnostic criteria of SLE, immunological criteria helped us to diagnose this case as SLE. After the diagnosis of SLE was established, we did the antiphospholipid antibody test to find out the cause of DVT. It was found positive. So the antiphospholipid antibody syndrome was diagnosed. A recent consensus statement provides simplified criteria for the diagnosis of the antiphospholipid syndrome 10. A patient with the antiphospholipid syndrome must have at least one of the two clinical criteria (vascular thrombosis or complication of pregnancy) and at least one of two laboratory criteria (anticardiolipin or lupus anticoagulant antibody). Our patient has venous thrombosis and positive antiphospholipid antibody. Other prominent manifestations of the antiphospholipid antibody syndrome include thrombocytopenia (in 40 to 50 % of patients), haemolytic anaemia (in 14 to 23 %) livedo reticularis (in 11 to 22%) Antiphospholipid antibody syndrome may be primary (not associated with other disease) or secondary (when associated with SLE or other autoimmune diseases). In a study it has been shown that antiphospholipid antibody syndrome may develop in % patient with both SLE and antiphospholipid antibody after 20 years of followup. 12, 14 Conclusion: The diagnosis of SLE was difficult at first in our case as the patient presented with haematological manifestation along with features of infection. As SLE can masquerades many haematological manifestations especially autoimmune disorders we should always do screening test like ANA and not hesitate to diagnose SLE when other typical physical features (photosensitivity, malar rash, discoid rash, oral ulceration, arthritis,) are not present. Early diagnosis, treatment, followup and counseling for a multisystem disease like SLE may prevent more sinister complication of this disease. References: 1. Hochberg MC. Systemic lupus erythematosus. Rheum Dis Clin North Am.1990; 16: Hahn BH: Pathogenesis of systemic lupus erythematosus. In: textbook of Rheumatology. Volume 2. WB Saunders; 2001: Tan EM, Cohen AM, Fries JF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982;25: Hochberg MC: Updating the American college of Rheumatology revised criteria for the classification of systemic lupus erythematosus (Letter) [see comments]. Arthritis Rheum 40:1725, Schur PH: Clinical features of SLE.In Kelly WN, Harris ED, Ruddy S, Sledge CB (eds): Textbook of Rheumatology. Philadelphia, WB Saunders, 1989, pp

20 Road to a Diagnosis: A Case Report of an Adult Male with SLE BJM Vol. 16 No S.M.Sultan, S. Begum and D.A.Isenburg. Prevalence, patterns of disease and outcome in patients with systemic lupus erythematosus who develop severe haematological problems. Rheumatology 2003; 42: Silva C & Isenberg DA. Aetiology and pathology of systemic lupus erythematosus. Hospital Pharmacist 2001; 8: Rahman MA & Isenberg DA. Autoantibodies and lupus nephritis. In Lewis EJ, Schwartz MM & Korbet SM (eds) Lupus Nephritis, pp 1-21.Oxford: Oxford University Press, Steven M. Edworthy. Clinical manifestation of systemic Lupus Erythematosus. In: textbook of Rheumatology. Volume 2. WB Saunders; 2001: Wilson WA, Gharavi AE, Koike T, et al. International consensus statement on preliminary classification criteria for definite antiphospholipid syndrome: report of an international workshop. Arthritis Rheum 1999; 42: Asherson RA, Khamashta MA, Ordi-Ros J, et al. The primary antiphospholipid syndrome: major clinical and serological features. Medicine (Baltimore) 1989; 68: Alercün-Segovia D, Pérez-Vázquez ME, Villa AR, Drenkard C, Cabiedes J. Preliminary classification criteria for the antiphospholipid syndrome within systemic lupus erythematosus. Semin arthritis Rheum 1992; 21: Vianna JL, Khamashta MA, Ordi-Ros J, et al. Comparison of the primary and secondary antiphospholipid syndrome: a European multicenter study of 114 patients. Am J Med 1994; 96: Petri M. Epidemiology of the antiphospholipid antibody syndrome. J Autoimmun 2000; 15:

21 A CASE OF OSTEOPETROSIS PRESENTING WITH HYDROCEPHALUS AND CHOANAL ATRESIA - A CASE REPORT SHAHANA A RAHMAN 1, MAJOR JESMINE SULTANA 2, MD. MAHBUBL ISLAM 3, CHOWDHURY ALI KAWSER 4 Introduction: Many bone dysplasias display increased bone density; most of which are rare 1. Osteopetrosis and pyknodysostosis in this category of bone dysplasias, result from defective bone resorption. Osteopetrosis is a heterogeneous group of rare hereditary diseases characterized by osteoclast dysfunction resulting in diffuse symmetric skeletal sclerosis 2. Alberges Schonberg first described Osteopetrosis in 1904 and Karshner in 1926 as cited by Halim et al 3. The precise nature of the osteoclast dysfunction in this disorder is unknown. There is persistence of primary calcified cartilaginous matrix with an apparent failure of resorption by osteoclast 4. Remodeling of bone is defective and cortical compact bone is poorly differentiated as the marrow space fails to form 2. This disorder presents in several forms. The autosomal recessive congenital form is severe, often fatal and presents in early infancy 5. The problem is not unknown in our country and is reported in local journal as well 3. Still we find it of academic interest to report a case of Osteopetrosis presenting with choanal atresia and progressive hydrocephalus. We also want to update the available information regarding Osteopetrosis. Case Report: RA, a 2 months old baby girl born to a consanguineous parents (1 st cousin) was admitted in the paediatric ward of Bangabandhu Sheikh Mujib Medical University Hospital with the complaints of recurrent respiratory tract infection and noisy breathing since birth and crying during handling of right arm for 14 days. She also had history of irregular fever since 2 nd week of her age. She was treated with several broad spectrum antibiotics since her birth but was never all right. RA came from a middle class family, born normally in a hospital at term. Her mother was on regular antenatal check up. The pregnancy period was uneventful excepting antenatal diagnosis of twin pregnancy. She was the second twin. First twin died immediately after birth due to respiratory distress. She had a five years old elder brother who was a normally growing healthy boy. RA was very ill-looking and dyspnoeic. She was moderately pale, febrile with apparently large head. Anterior fontanel was wide open and bulged. There was significant generalized lymphadenopathy. Her nutritional status was poor (weight below 10 th centile and supine length below 3 rd centile) but occipitofrontal circumference was above 50 th centile (39.5cm). Right upper arm was swollen, hot and very tender. Respiratory rate was 68/minuite with suptrasternal, intercostal and subcostal recession. Inspiratory stridor was present and coarse crepitations were present all over both the lung fields. Moderate hepatosplenomegaly was present which were firm and nontender. Nasogastric tube could not be introduced, and subsequently RA was diagnosed to have choanal atresia by otolaryngologists. Serial OFC measurements showed progressive increase of head size. Within 10 days of admission, OFC increased to 41.0 cm, which was above 97 th centile. Complete blood count showed low haemoglobin (9.0 gm/dl) and high total count (22X10 9 /L) with lymphocyte predominance. Serum calcium, phosphate and alkaline phosphatase was 8mg/dl (low), 3.8mg/ dl (normal) and 267 U/l (normal) respectively. Moderate dialatation of lateral ventricles were found in the ultrasonography of brain. Bronchopneumonic features were found in the chest radiography. Skeletal survey was done which showed generalized increased bone density. Skull base bones appeared sclerotic and thickened (Fig 1). Long bones showed generalized increased density with obliteration of medullary cavity and metaphyseal enlargement. Bone within bone appearance was present in both the femur (Fig 2). A fracture was present at the mid-shaft of the right humerus with exuberant callus formation (Fig 3). 1. Professor, Department of Paediatrics, Bangabandhu Sheikh Mujib Medical University (BSMMU) 2. Paediatrician, CMH, Dhaka. 3. Paediatrician, Department of Paediatrics, BSMMU 4. Professor, Department of Paediatrics, BSMMU Bangladesh J Medicine 2005; 16 : 45-48

22 A Case of Osteopetrosis Presenting with Hydrocephalus BJM Vol. 16 No. 1 Fig.- 1: Sclerotic and thickened skull base bones Fig.-3: Fracture at the mid shaft of right humerus with exuberant callus formation. RA was treated symptomatically with intravenous broad spectrum antibiotic, oxygen inhalation, suction, nasal drop and oro-gastric feeding. Consultation was done with Otolaryngolosist and neurosurgeon. But due to very poor general condition of the patient, invasive intervention for choanal artresia and hydrocephalus was not possible. Genetic counseling was done with the parents. In spite of all measures, RA expired after 12 days of admission at the age of 2 months and 18 days. Fig.-2: Long bones showing generalized increased density with obliteration of marrow cavity and metaphyseal enlargement. On the basis of history, clinical findings and investigation results, RA was diagnosed as a case of autosomal recessive malignant infantile Osteopetrosis (MIOP) with choanal artresia, progressive hydrocephalus, right humerus fracture and broncho-pneumonia. Discussion: Osteopetrosis is rare human genetic disorder, presents is several forms: severe and recessive form also known as malignant infantile Osteopetrosis (MIOP) 6, relatively benign and dominant form, and an autosomal recessive form associated with renal tubular acidosis, mental retardation and carbonic anhydrase II deficiency 4. To date, the only gene whose inactivation is known to be responsible for osteopetrosis is that encoding carbonic anhydrase type II 6. Recent advances in genetics have shown that some patients affected with MIOP have inactivating mutations in a sub unit of the vacuolar 46