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Aims and Objective:
To study the correlation of ECG changes in hypokalemic periodic palsy with serum potassium level.
Material and Method:
Thirty five cases of clinically diagnosed hypokalemic periodic palsy were included in this study admitted to medicine wards of VSS Medical College Hospital, Burla during the period of February 2004 to June 2004. Correlation between electrocardiographic changes i.e PR – interval , QRS – duration, QTc – interval, ST- Segment depression, flattening of T-wave and presence of U-wave and AV block with corresponding serum potassium level was studied.

Secondary causes of hypokalemia were excluded in this study.

ECG Changes of 35 cases are tabulated below with serum potassium level
Se. K+ level in mEq/L Total Cases Prolonged PR interval Presence of U-wave
Mild (3.1 – 3.5) 1 0 1
Moderate (2.6-3) 14 1 14
Severe (<2.5) 20 05 20

There were one (2.9%) cases of mild, 14(40%) cases of moderate and 20(57.1%) cases of severe hypokalemia. At the time of admission all 35 (100%) cases showed flattering of T-wave with presence of U-wave in ECG and prolonged QTc – interval in 32(91.4%) cases. ST –depression was found only 20 (57.1%) cases. Out of 10 cases of AV – block, 6(17.1%) cases had first degree AV-block with prolonged PR interval and 4(11.4%) cases had second degree AV – block.

Out of 10 cases of AV- block 9 (90%) cases had AV-block with serum potassium level 2.5 mEq/L and 1(10%) case had AV block with serum potassium 2.8 mEq/L.

Various types of ECG changes occur in moderate to sever hypokalemia and do not specify level of hypokalemia. However AV – block was present in majority cases of severe hypokalemia and presence of AV – block with other features of hypokalemic ECG changes preclude immediate potassium supplementation before the availability of serum potassium level reports.

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To study the hematological changes in chronic alcoholic liver diseases.

Thirty chronic alcoholic patients were investigated after excluding the patients having pathological diseases of other organs those altering the haematological status. All selected cases had history of alcohol abuse for more than 5 years, all the haematological parameters were compared with the duration and amount of alcohol consumption and the observations were complied and discussed. The significance of mean in comparison to control was done by using student unpaired ‘t’ test. Association of parameters with amount and duration of alcohol consumption was made by calculating correlation coefficient.

Chronic alcoholism was commonly observed in 4th and 5th decades with median age of 44 years.

The mean Hb% was 9.21.3 gm% , macrocytosis (MCV > 96fl) in 56.7% of cases and all cases were normochromic (MCH >27 pg and MCHC>30%). Raised ESR (86.6%), leucopenia (33.33%), thrombocytopenia (30%) were other observations.

Correlation of duration of alcohol consumption with haematological changes revealed a significant decrease in Hb% and increase in ESR and increase in MCV with the duration of alcohol consumption 5 to 10 years and when it is more than 10 years of duration.

S. Bhakta, Sk Lath, SR Pattnaik, BK Barik, B Pradhan , S Tripathy, RC Sethy

Aim and Objective:
Plaque rupture, the commonest cause of acute myocardial infarction(AMI) is associated with raised level of acute phase reactants like C-reactive protein. CP is a marker of atherosclerotic inflammation and insult of myocardial necrosis. In this study serum CRP level in AMI pateitns at the time of hospital admission was correlated with their subsequent in hospital prognosis.

Materials and Methods:
In the present study, 61 AMI patients with varied types of presentation and risk factors were taken. Fifty healthy age and sex matched volunteers were taken as control. Non-cardiac causes, which can raise the CRP level, were excluded from both groups. Blood samples of AMI patients for CRP were sent at the time of their hospital admission. Other cardiac markers like CK-MB and troponin I also estimated for diagnostic purpose as well as to correlate with CRP as a prognostic indicator. Patients were followed up fro complications like LVF, repeat cardiac discomfort, arrhythmia, cardiogenic shock and death.
Raised level of CRP (8.203.86 ms/1 SD) was noted in AMI patients compared with controls (31.195 mg/1 SD). Patients with >6 mg/1 of CRP developed more (82.85%) complications like arrythmia, CCF, pericarditis and repeat chest complications (P<0.001). 11 patients (18%) expired out of them 10 had > 6 mg/1 CRP (91%). More complications observed when CRP levels were raised within 6 hr duration of symptoms (70.83%). In contrast to it other cardiac markers (CK-MB and TROP – I) failed to predict the prognosis within 6 hr duration of symptoms. After 6 hours , prognostic value of CRP and other cardiac markers correlated well.

The serum CRP level on hospital admission is an indicator short term of prognosis of AMI irrespective of the duration of symptoms.

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To study the pentoxyfylline as an adjuvant therapy in treatment of severe falciparum malaria in patients of sickle cell anaemia.

Patients having clinical features suggestive of severe falciparum malaria (according to WHO guidelines) excluding pregnant woman were investigated for sickling test and hemoglobin electrophoresis. Biochemical and haematological investigations e.g hemoglobin concentration, total leucocyte count, differential count, urine for sugar , albumin, red cell , pus cell, hemoglobin, serum for direct and indirect bilirubin, AST, ALT, alkalaine phosphatase, urea, creatinine, sodium and potassium were done on the day of asmission and on 3rd and 8th day. Detailed daily clinical examination was done. Forty cases of severe falciparum malaria with sickle cell disease were studied. Twenty cases treated with quinine and pentoxyfylline and other twenty cases were treated with quinine only.

Patients who received pentoxyfylline and quinine had less duration of unconsciousness, had significant fall of bilirubin concentration as compared to those received quinine only. There was no significant difference in BUN and overall mortality between the two groups.

This study shows that simultaneous administration of pentoxyfylline and quinine leads to early recovery from coma and reduction of serum bilirubin concentration . So pentoxyfylline may be useful in severe falciparum malaria in sickle cell disease.

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Study of dyslipidemia in non-diabetic first degree relatives (F.D.R.) of type 2 diabetes mellitus patients.

Forty type –2 diabetes mellitus with forty numbers of their FDR were included in the study. Secondary causes of dyslipidemia were excluded in both groups by history taking, clinical examinations and appropriate laboratory tests. Fasting lipid profile comprising of serum cholesterol, triglyceride and HDL-C were done in automatic analyzer and VLDL-C, LDL-C values were calculated out by using Friedwald equation.

Mean cholesterol, triglyceride and LDL-C values were below normal (i.e. cholesterol < 200mg/dl, triglyceride <150mg/dl and LDL-C < 130 mg/dl) but diabetics showed higher values than FDR and 15% of FDR were having HDL-C values below normal (i.e. <40mg/dl in males and <45 mg/dl in females) 22.5% diabetics and 30% FDR were having cholesterol /HDL C-Ratio > 5, while LDL-C/HDL – C ratio > 3.5 were found in 12.5% of diabetics and 20% of FDR (Atherogenic ratio).

F.D.R. of type 2 diabetes mellitus patients showed very high incidence of low HDL-C level, perhaps prevalence of more of insulin resistance in them, thus predisposing them to atherogenic profile even if they are normoglycemic and this makes a need of creating awareness in them.

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Autoimmune hepatitis – A Case Report
A rare case of cirrhosis of liver following autoimmune hepatitis is reported in a young female patient. The pathophysiology, clinical presentation and management of this condition are reviewed.
Key Words: Autoimmune, cirrhosis, hepatitis
Autoimmune hepatitis (formerly called autoimmune chronic active hepatitis) is a chronic disorder characterized by continuing hepatocellular necrosis and inflammation, usually with fibrosis, which tends to progress to cirrhosis and liver failure. The prominence of extrahepatic features of this disorder supports an autoimmune process in its pathogenesis. Because autoantibodies and other typical features of autoimmune disorder do not occur in all cases, a ‘broader’ more appropriate designation of this type of chronic hepatitis is idiopathic or cryptogenic.
Case Report
A 33 year old female patient came to us with history of amenorrhoea for last 6 months, gradual distension of abdomen for last 3 months, one episode of hematemesis 2 months back and scanty urination for 10 days.
One month prior to admission, the patient was diagnosed provisionally as a case of cirrhosis of liver and sclerotherapy was done for bleeding esophageal varices. Patient was on regular treatment with propranolol 40mg /day, Pantoprazole, Sucralfate and other supportivce drugs. Patient had no further hematemesis after sclerotherapy, but symptoms of progressive liver failure persisted. She is not a known case of DM, HTN, SCD, Pul, TB. There is no history of intake of heparotoxic drugs or joint pain. On examination, the patient was edematous with mild pallor, mild icterus, with a pulse rate of 68/min, regular, BP 110/90 mm Hg, CVS-NAD, chest-bilateral basal fine crepitions, abdomen-moderate ascites with engorged abdominal veins, the 24 hr urine output was 100ml.
Hb% - 8.4%,
TLC – 7,900/mm3, DC-N 80%, E 6%, L-14%
RBS – 104m%
Urine Sugar Nil, Albumin - +
Sr. urea – 5-6%, Sr. creatinine 2mg%
Sr. Na+ - 100 mmol/lt, Sr. K+ - 2.0 mmol/lt
Sr. RA factor – Negative
HbsAg – Negative
LE cell – Negative
Anti nuclear antibody – positive (Odd ratro 1.64), (+ve>1.0)
Anti ds DNA – Borderline positive
S. bilirubin 1` - 0.72mg%
S. bilirubin 30` - 2.11mg%
SGPT – 25IU/lt
SGOT – 62 IU/lt
Sr. Alk. Phosphate – 135 IU/lt
Sr. GGT – 12.2 IU/lt
Sr. Alb – 1.7 gm/dl
Sr. Protein – 6.5gm/dl
A: G ratio – 0.35
USG of abdomen – Ascites with splenomegaly, dilated portal vein
Chest X ray PA view – NAD
Needle biopsy of liver showed portal and periportal mononuclear infiltrate with areas of piecemeal necrosis and fibrosis.
The patient was diagnosed as a case of autoimmune cirrhosis of liver, started on oral prendisolone 30mg/day and other supportive treatment. The patient showed marked improvement after starting oral prednisolone. The condition of the patient was found to be stable on regular follow up since last six months.
Autoimmune hepatitis (AIH) – an inflammatory liver disease of unknown etiology characterized by suppressor – T cell defects and the production of autoantibodies directed against hepatocyte surface antigens. Two main types are recognized according to the presence of circulating autoantibodies.
Type I – After adults or childredn antinuclear antibodies (ANA) and / or
Antismooth muscle antibodies (SMA)
Type II – Affect children
Anti liver/kidney microsomal type I (LKM I) antibodies.
Clinical Features
Predominantly affects young and middle aged women, 25% present with acute hepatitis and features of an autommune disease e.g. fever, malaise, utticarial rash, polyrthritis, pleurisy or glumerulonephritis. The remainder present insidiously or are symptomatic and diagnosed incidentally with signs of chronic liver disease. Amenorrhoea is common.
• Autommune thyroiditis
• Autoimmune hemolytic anemia
• Penicious anemia
• Diabetes mellitus (Type I)
• Ulcerative colitis
• Glomerulonephritis
• HLA AI, B8 and DR3 haplotype
• Abnormal LFT (AST)
• Hypergammaglobulinemia
• +ve for autoantibodies (ANA,SMA orLKM)
• Anemia TIC & TPC (Hypersplenism)
• Liver biopsy : Mononuclear infiltrate of portal and periportal areas with piecemeal necrosis, fibrosis and other features suggestive of cirrhosis.
• An ERCP should be performed to exclude primary sclerosing cholangitis if alkaline phosphatase is disproportionately raised.
Immunosuppression (prednisolone, azathioprine )
Liver transplantation, but recurrence may occur
Prognosis : There is paucity of literature about autoimmune hepatitis among Indian population. The disease however shows variable natural history. Mild cases are marked by remissions and exacerbations, response to immunosuppression being excellent. Overall mortality without treatment is as high as 40%. Moderate to severe cases progress to cirrhosis of liver, hepatic failure and rarely hepatocellular carcinoma. In general, immunosupression remains the mainstay of treatment and treatment often slows down the disease process. Hence early diagnosis and institution immunosuppression is rewarding.
The diagnosis of autoimmune hepatitis requires a high degree of suspicion, thus many cases remain undiagnosed. All cases of hepatocellular failure where no obvious cause like viral hepatitis, alcoholism, ingestion of hepatotoxic drugs etc. are found should be investigated for autoimmune hepatitis.
1. Krawitt E.L: Autoimmune hepatitis. N. Engl. J. Med. 334;897,1996.
2. Czaja A.J. et al. atommne hepatitis; Evolving concepts and treatment strategies. Dig. Dis. Sci. 40; 435,1995.
3. Czaja A.J. et al. Associations between alleles of the major histocompatibility complex and type I autoimmune hepatitis, Hepatology 25; 317, 1997.
4. Johnson P.J. et al. Meeting report; International autoimmune hepatitis group. Hepatology 18:998,1993.

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Ciprofloxacin resistance in typhoid fever
Abstract: Typhoid fever is widely prevalent in this part of Orissa. After multidrug resistance against the first line drugs chlormphenicol, ampicillin and co-trimoxazole, the emergence of chromosomally mediated quinolone resistance in typhoid fever has become a major concern in its treatment. Treatment failures with ciprofloxacin are being increasingly reported. 156 cases of Typhoid fever were admitted, out of them 802 cases were culture positive i.e. responded to ciprofloxacin. 18 cases did not responded to ciprofloxacin, as chloramphenicol was given in the dose of 50mg/kg for further 7 days. 10 cases responded to chloramphericol. 4 cases each responded to certriaxone and cefixime.
Key Word: Ciprofloxacin, Salmonella typhi, Typoid fever.
Thyphoid fever is endemic in most developing regions, especially the Indian sub continent, South and Central America and Asia.
Thyphoid fever continues to be global health problem, with an estimated 13 to 17 million cases worldwide resulting in approximately 600,000 deaths per year 3. Children <1 year of age appear to be most susceptible to initial infection and to the development of severe disease. The increasing trend in the mortality and morbidity is due to factors like poor nutrition, poor environmental sanitation and inadequate treatment set-up. The standard textbook picture to typhoid fever is an exception rather than the rule. Typhoid fever is a common illness in this part of the state. The high incidence of typhoid fever is a common illness in this part of the state. The high incidence of typhoid fever acquired greater significance because of various spectrum of presentation and emergence of multidrug resistance led us to carry out a detailed study of typhoid fever cases.
Material and method:
All the cases of fever (high grade) admitted to the medical wards of V.S.S. Medical College/Hospital, Burla with a provisional diagnosis of Typhoid fever, during the period of (January 20021 to December 2002) were taken up for the study.
Patients with continuous fever for (more than 400C) for at least 5 days were screened as potential cases for typhoid fever and subjected to thorough clinical and laboratory examination and those satifying at least 4 of the following criteria were taken up as study:
1. Splenomegaly.
2. Relative bradycardia (if within first week)
3. TLC<10,000/cubic mm)
4. Positive Culture (one or more)
a. Blood culture
b. Stool Culture
c. Urine culture
5. Serology
Positive Widal test ‘O’ titre ( 320) or rising ‘O’ titre.
In the present study, diagnosis was made by isolation of Salmonella typhi in 54 cases. Half of the cases who had positive stool culture and all the three cases having positive urine culture had positive blood culture also.
The various complications seen were as follows:
1. Typhoid encephalopathy (12.5%)
2. Pnemonia (2.5%)
3. Myocarditis (2.5%)
4. Gastrointestinal complications in the form of paralytic ileus (5%)

Response to treatment is indicated as follows:

Response No response
(62 cases) (18 cases)

Chloramphenicol Ceftriaxone / Cefixime
(10 cases) (4 cases) (4 caaes)
The response to treatment of Salmonella typhi positive in 80 cases were
(a) 62 cases responded to ciprofloxacin
(b) 10 cases responded to chloramphenico.
(c) 4 cases each responded to ceftriaxone / cefixime
Out of 80 cases, 56 were males and 24 were females. Most cases are reported among males than females, probably as a result of increased exposure to infection. Maximum number of cases were seen in the age group of 21 to 30 years. The epidemiological pattern confirm to the pattern found in the present study i.e. occurrence of maximal number of cases in the late summer and early rainy season when sources of water get contaminated by the still prevalent habit of open air defeacation by the side of ponds.
Pyrexia is the sine-qua-non of typhoid. The duration of fever prior to enrolment was 5-30 days. Contrary to the text book picture of stepladder pyrexia, most of our patients had either continuous (47.5%) or intermittent (30%). 45% of cases had modereate grade of fever and 57.5% had associated chills and rigor. The next common presenting symptoms in order of frequency was headache (42.5%), vomiting (27.5%), loose motion (15%), altered sensorium (12.5) and cough (10%).
4 patients presented with features of acute intestinal obstruction, who improved with conservative management contrary to what Patel and Panda had observed in 3.8% of cases 16.
Twenty two cases had moderate anaemia, while six cases had severe anaemia (<6 gn%). Total leucocyte count was within the normal range in most of our series (77.5). Only 8 cases had leucopenia and 16.5% of our cases showed leucocytosis, which signified complications like intestinal perforation and the other was pneumonia.
Widal test was done in all cases of fever. 42.5% of cases showed an initial TO titre of 1:160, 31.2% showed that of 1:320m 23.7% of cases showed titre of 1:80 and 2.5% cases showed low titre 1:40. Out of the 18 cases, where repeat widal test was done, which showed 3 patients having the same titre, while rest patients showed fall in titre.
Out of the 156 cases, isolation of S. typhi was positive in 80 cases including blood, stool and urine culture.
With emergence to multi – dryg resistance to chloramphenicol , ampicillin and co-trimoxazole,drugs like fouoroquinolone and third generation cephalosporins gained importance. In fact, ciprofloxacin became synonymous with typhoid fever. However, a very disturbing trend surfaced in 1992, when news of ciprofloxacin resistance btoke out for the first time in Ukin a one –year old child who acquired the infiction from,India17. In UK, decreased sensitivity against S.typhi i.e MICs ( minimum in hibitory concentrations )of >0.25g/ml for ciprofloxacin was reported to have risen from 2.7%in 1995 to 1998.7
Most clinician in India now believe that efficacy of ciprofloxacin had reduced over the years. In the light of currently available information, the positive fall out of indiscriminate use of ciprofloxacin is return of suspectibility to primary drugs like chloramphenicol.
Out of 80 cultured positive cases, all cases were given ciprofloxacin in the dose of 750 mg twice daily for 10-14 days in adults or 200 mg intravenously twice for 7 days. 62 cases responded and became afebrile on 4-5th day and the test 18 cases did not respond and subsequently changed to chloramphenical ( 50mg/kg )for further 7 days and were afebrile sithin 3-5 days. 4 caseseach responded to third generation cephalosporin (eg. Ceftriaxone, cefixime ).
Typhoid fever remains a common cause of prolonged pyrexial illness in this part of the country. The classical picture given in standard textbooks of m,edicine has become very rare these days. A high index of suspicion is usually necessary to clinch the diagnosis in the absence of culture facilities.
However, in the setting of inappropriate and inadequate treatment with antibiotics in the peripheral hospital, there is increased resistance to MDR strains and also to ciprofloxin. Therefore, close onservation is needed and proper antibiotic should be prescribed to prevent relapse as well as outbreak.
1. Adhikari Pranha M.R. Baliga Srikala, Ciprofloxacin – Resistant Tyhphoid with compoette Response to Cefotaxime. HAPI, 2002;50:428-9.
2. Cammie F, Lesser, Samuel I.Miller Saalmonellsis: typhoid fever, HariPrinciples of Internal Medicine, 2000;Vol I , 15th Edn. Om 970-973.
3. Chande Chhaya, Shrikhande Sunanda, Kapale Sandhanga, Agarwal Seema & Fule R.P. Change in Antimicrobial Resistance pattern of Salmonella Typhi in Central India. Indian J.Mid Res. 2002;115,248-250.
4. Christopher Harlett, Chilvers Edwin, R.Hunter John A.A. et al Salmonela Infection. Davidson Principles and Practice of Medicine, 1999;18th Edn. 123-124.
5. Das Usha & Bhattacharya SS. Multidrug Resistant Salmonella Typhic in Rourkela, Ouissa. Indian J.Patthos. Microbiol; 2000 : 43 (1): 135-138.
6. Dutta T.K. Shanmuganathan C, Kanungo. R.Ghotedar L.H.,Management of typhoid fever –An update. Apicln 2002 ; 12 , 1120 –1123.
7. jesudasan MV, Malathy M, John TJ.Trend of increasing level minimum ceprofloxacin in Salmonella typhi. Ind J Med Res 1996; 103:247-9.
8. Kapil a, Sood S.Dash N R, Das B K, Seth P. Ciprofloxacin in Typhoid fever; The Lancet, 1999;354,164.
9. Luzzatto L.Glucose 6 – phosphate dehydrogenase (G6 PD) dehydrogenase (G6 / PD ). Deficiency. In: Weatherall DJ, Ledingtham JGG, Warell DA (editors), Oxford Textbook of Medicine, 3rd edition, Oxford University, Oxford. 1996; 3: 3537-41.
10. Manson Bahr, Mansons tropical disease 19th Edn.
11. Mathai D Kudva GC, Keystone JS, Kosarsky PE, Jesudasan MV, Lalitha MK, Kaur A, Thomas M, Johan J, Pulimood BM, Short Course Ciprofloxacin Therapy for Enteric fever; JAPI, 1993; 41: 428-430.
12. Multani AS, Mahajan DS, Khurana A, Pal T, Atwal S.To Evalute the Therapeutic Efficacy of Cefixime in quinolones Resistant Typhoid Fever: JAPI, 2002; 50,178.
13. Patel D.K. & Panda R.S. Changing Patterns of Enteric Fever. The Indian Practitioner : Vol XLVI, 1993; 9: 625-630.
14. Threlfall EJ, Ward L.R., Skinner JA, Smith HR, Lacey S, Ciprofloxacin – resistant Salmonella typhi and treatment failure. The Lancet, 1999; 353, 1590-1951.

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Plasmacytoma, A relatively uncommon presentation
Abstract: We report a case of plasmacytoma in a middle – aged man who subsequently developed multiple myeloma. The pathophysiology, diagnosis and treatment of this condition are briefly reviewed.
Plasma cell disorders are either generalized or localized. Generalized plasma cell proliferation with ostelytic bone lesion and monoclonal component of protein in serum electorphoresis is commonly known as multiple myeloma (M.M.). But 10% of all plasma cell disorders can present as localized plasmacytoma. Plasmacytoma may be two types:
1. Solitary osseous plasmacytoma (SOP)
2. Extramedullary plasmacytoma (EMP)
Usually they present at the age of 50 years, about 20yr before the average of presentation of multiple myeloma2. Though majority of SOP and about 50% EMP can progress to M.M. in long course, but their early detection is very important for the treatment point of view. Local radio therapy with or without chemotherapy can cure these patients.
Case Report:
A 55 yr male was admitted on 25.06.03 with the complaints of swelling over sternal region, noted for last 6 months. It was gradually increasing in size and became painful for last 4 months. He was also complaining of left shoulder pain. For last few days low back pain also started. This pain was nagging in character and increased with movement. His urine output normal, mild wt loss was also associated with it he was mildly anemic and his cardiovascular; CNS and respiratory system had no abnormality. Hepatosplenomegally was absent. His BP was 120/80 and pulse 80/min.
Sternal swelling was firm, mildly tender, nonpulsatile, measuring = 5cm x 9cm x 1.2cm.
On the day of admission FNAC of swelling was done and it reveled plasmacytoma. Serum and urine were sent for M band and Bence Jonce proteins respectively, but both of them were negative. But skull X-ray and Chest X-ray revealed punch out lesions and bone marrow from Rt iliac crest detected plasma cell infiltration (>85%). Hb% was 9.6gm. Urea 18mg% creatinine 1.2mg%. liver function test normal and sedimentation rate 60mm in 1st hr.
Two days after admission, patient fell down in bathroom and the shaft of the humerus and femur were fractured. Plaster cast was done on next day.
Five days after admission, chemotherapy was started with cyclophosphamide 200mg/m2 and predinisolone 80mg/m2 for 54 days along with supportive therapy.
Except mild pain abdomen and chest pain no other complication developed. On follow up after 4 weeks, swellin gover sternum regressed and sternal depression developed at that place due to destruction of mass along withribs instability. No radiotherapy was given.
Solitary plasmacytoma is comparatively an uncommon entity. When the above mentioned patient presented with sternal swelling it gives the suspicion of mediastinal pathology. But firm nature and ultimate FNAC report disclosed it as a plasmacytoma. Early age of presentation (55yrs) and few days H/O of low back pain also point out towards psasmacytoma. But as every patient with plasmacytoma should be a suspected of multiple myeloma, B.M. examination and X-ray skull were done. This led to the diagnosis of the patient as a case of MM. M band negativity in this case tells about non –secretory nature of the tumor,which is more aggressive. This can explain why a patient develops pathological fracture so early. 2 Micro globulin can indicate about the prognosis of the patients, but not in this case due to lack of facility. As this case converted to M.M6, systemic chemotherapy was given instead of local irradiation.
This is a case of plasmacytoma,is rare, it should be considered for any abnormal bony shelling and they should be further followed up to know their progression to multiple myeloma.
1. Meis J.M et al- Solitary plasmacytoma of bone and extramedullary plasma – cytoma: Aclinicopathological and immunological study –Cancer 1987 , 5:1475 –1785.
2. Alexamin R. Localized and indolent myeloma 1980;56:521-526.
3. Dimoponlos MA et al- Curability of slitary bone plasmacytome. J.Clinical Oncology. 1992, 10:587-590.
4. Mouloponlos La et al – MRI in staging of solitary plasmasytoma of bones. J. of cli. Onco. 1993:11:1311-1315.
5. Aviles Aet al – Serum b2 microglobulin in solitary plasmacytoma- Blood 1990: 76 : 1663.
6. Wiltshend E.The natural history of EMP and its relation to solitary myeloma of bone and myelomatosis, medicine 1976;55;217-2383

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Leptospirosis with Jarisch-Herxheimer reaction – A case report
We report a reare case of leptospirosis who developed Jurish – Herxheimer reaction after initiation of treatment. The mechanism of this reaction and its pathophysiology are reviewed.
Key words: Jarisch-Herxheimer, Leptospirosis
Lleptospirosis is caused by Leptospira interrogans (e.g. serogroup L. icterohaemorrhagiae). Spread is bny contact with infected rat urine, e.g. while swimming, taking pond bath. They usually present with fever, jaundice, headache, red conjunctivae, tender legs (myositis), purpura, hemoptysis, hematemesis, or any bleeding, Meningitis, myocarditis and renal failure may develop.
Case Report:
A 32 year old male presented in August 2002, with a 7day history of fever, headache, myalgia and nausea. He had always been fit and well. On examination he was hemodynamically stable, pyrexia, and had meningism, and mild abdominal tenderness, without hepatosplenomegaly. Blood tests showed 9.6 x 109/L neutrophils, 125 x 109/L platelets, but no other abnormalities. We started intravenous cefuoxime 1.5gm twice daily and oral doxycycline 100mg twice daily, to cover meningococal, streptococcal, salmonella and other gram negative and typical pathogens. Blood tests 12 hr. later after admission showed urea and creatinine normal aST 110/U/Lt, ALT 176 U/L. Tests for malaria parasite was negative, widal test negative abdominal sonogram revealed no abnormality. Blood for culture and sensitivity was sent.
The patient became increasingly breathless and hypoxaemic. A chest rediograph showed mild cardiomegaly and an electrocardiograph (ECG) showed low voltage with widerspread ST segment changes. A transthoracic echocardiogram showed mold dilation of left ventricle. Pre-existing cardiac or pulmonary disease was considered unlikely in this otherwise healthy male. The patient was started on intravenous dexamethasone, dopamine infusion and oxygen inhalation. His condition improved over next 48 hours. The report ECG and transthroacic echocardiogramon day 5 showed complete resolution of previous abnormalities. He was discharged after finishing a week’s course of the antibiotics, and soon returned to work. He is doing well since then when last seen in Dec. 2002.
We subsequently diagnosed acute leptospirosis by a leptospira spp. 1gM antibody titre of 1:2560, from blood sample taken on day 8 of admission (negative on the first day of hospitalization). The patient’s acute deterioration after antibiotic treatment was probably due to a Jarisch-Herxhemier reaction.
Cardiovascular involvement can occur in both the septicaemic and immune phases of Leptospira infection. Minor ECG changes and pulmonary edema have been reported in the first week of illness, but cardiomegaly is unusual.
The Jarisch Herxheimer reaction is a recognized complication of antimicrobial treatment of spirochaetal infections. Lysed bacteria releasel LPS, triggering release of cytokines including tumour necrosis factor- and iL-6 & 8. Antibiotics, including tetracyclines, -lactams and cephalosporins trigger LPS release from bacteria. LPS induces NO mediated vasodilation resulting in systemic hypotension. LPS can also induce pulmonary hypertension.
Leptospirosis is relatively uncommon condition in this part of Orissa; Milder cases are underdiagnosed.
It is not possible to predict which patients might develop a Jarisch Herxhemier reaction after starting treatment. Physicians should know that this reaction can include systemic gypotension. And acute pulmonary edema and that most patients recover fully with appropriate supportive therapy.
1. Wesely Farr R. leptospirosis, Clin. Infect Dis. 1995; 21:18
2. Friedland JS, Warrell DA. The Jarisch Herxhemier reaction in leptospirosis: possible pathogenesis and review. Rev. Infect. Dis. 1991;13:207-10.
3. Negussie Y, Remick DG, Deforge LE, Kunkel SL, Eynon A, Griffin GE, Detection of plasma tunour necrosis factor, interleukins 6, and 8 during the Jarisch Herxhemier reaction of relapsing fever J. Exp. Med. 1922;175;1207-12.
4. Evans ME, Pollack M. Effect of antibiotic class and concentration of the release of lipopolysaccharide from Escherichia coli. J. Infect. Dis. 1994; 169:471-73.

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A rare case of disseminated rhinosporidiosis is reported in a young male patient. The pathophysiology, clinical feature, diagnosis and management of this condition are reviewed.
Key words: Rhinosporidiosis, Rhinosporidium Seeberi
Rhinospordiosis is a chronic granulomatous disease characterized by production of polyps or other manifestations of hyperplasia on mucous membrane surfaces, the etiologic agent being Rhinosporidium seeberi. The disease was First describe d by seeber (1900) in Argentina. This noval pathogen commonly affects mucosa of nose, eye and upper aero-digestive tract of men and animals. Isolated deep seated Rhinosporidiosis is rare. Diagnosis is mainly based on clinical suspicion and histopathological confirmation. At present, no existing medical treatment cures the disease and excision of the mass with cauterization of the base is considered as treatment of choice.
Case Report
A 35 year old male patient came to us with history of multiple swellings all over the body (Fig-1) for last one year, distension of the abdomen for last 2 months and loss of appetite for last 20 days.
The patient came to us for loss of appetite. He was not a known case of DM, HTN, SCD, Pul TB. On examination, the patient was chchectic with mild pallor, noi icterus, with a pulse rate of 84/minute, regular, BP-100/80 mmHg, CVS-NAD, Chest:-NAD, Abdomen: No hepatosplenomegaly or engorged abdominal veins. There were multiple subcutaneous swellings ranging from size 1 1cm to 5 7cm.
DC:-N-82%, L-17%, E-01%
FBS:-106 mg%
ESR:- 5mm in 1st hr,
Sr. Urea –30 mg%
Sr. Creatinine :- 1.43 mg%
Urine – NAD
HbsAg –Negative
Anti-HCV:- Negative
ELISA for HIV- Negative
S.Bilirubin – 0.6 mg%
SGPT :-51 IV/It.
SGOT :-41 lU/Lt
Sr.Alk. phosphatase :-221 lU/Lt
Sr. Albumin: 2.9 gm%
USG of Abdomen:- Normal
Chest X-Ray PA view –Normal
Biopsy study of subcutaneous swelling: Large numbers of spherules (size –10-200 um) in a stroma of connective tissue and capillaries. The spherules contain thousands of endospores.
The patient was diagnosed as a case of disseminated rhinosporidiosis. The patient was stared with tab Dapsone 100 mg/day & Vit-B complex. On regular follow up since last 6 months, the size of subcutaneous swelling were regressing.
Discussion :
RHINOSPORIDIOSIS is a chronic granulomatous disease characterized by production of polyps or other manifestations of hyperplasia on mucous membrane surfaces. The etiologic agent is Rhinosporidium seeberi.
Historical review:
Most of the early studies of rhinosporidiosis were made in India and Ceylon where the disease occurs frequently. Sporadic case have been detected and studied in many parts of the world. The systematic position of R. seeberi is still uncertain. Most investigators consider it has not been isolated in culture.
Clinical Types:
Friable, highly vascular, sessile or pedunculated polyps may appear on almost any mucosal surface, and rarely secondary lesions are found on skin, probably as aresult of autoinoculation by scratching. Lesions of the mucosae often spread by extension beyond the mucocutaneous border.
Primary lesions appear most often on the nasal mucosa and are accompanied by painless itching and a profuse mucoid discharge. The lesion is at first flat and sessile. Later hyperplastic growth greatly exceeds lateral extension of the lesion so that a polypoid mass much larger than the peduncle develops. The polyp may extend from the neres into the pharynx or externally over the lip and may reach weight of 20grams. It is friable and bleeds freely after trauma. Its surface is mucoid and papillate or so lobulate that its surface suggests that of a cauliflower. The color varies from pink to purplish red, and close examination of thesurface mayh reveal minute white sports which are the mature sporangia of the fungus. Lesions are found also on the larynx, Penis vagina, rectum and skin.
Lesions of the eye may cause symptoms similar to those produced by a foreign body, lacrimation or photophobia. Growth of the polyp may cause eversion of the lid. Lesions on th eskin being as papillomas and become warty with inclusions of myxomatous material. They are relatively painless except when on the sole of the foot and when they become so large as to be uncomfortably heavy. Dissemination to visceral organs is rare.
Differential diagnosis:
Typical lesions of rhinospordiosis can be recognized usually by the pink to purple colour, friable consistency and the presence of barely visible white sporangia within the polyp. Atypical lesions or those in unusual anatomical sites must be differential from warts, condylomata and hemorrhoids.
Little is known about the immunology of rhinosporidiosis.
On the examination of the gross tissue, unless rhinosporidiosis has been suggested by the clinician, or by the history of the patient’s geographic residence, the pathologist may consider the specimen an ordinary nasal polyp. The correct diagnosis can usually be made without difficulty on examination of routine H and E stained slide. Under the scanning lens of the microscope, although the polypoid structure may be evident, the histopathologic pattern differs greatly from tht of the common nasal polyp. The most striking feature is the presence in the stroma or epidermis of numerous sharply defined globular cysts which usually vary from 10 to 200  in diameter. Some of the cysts may be partly collapsed, assuming a semilunar shape. In contrast to the loose, edematous, myxomatous stroma of the ordinary nasal polyp, the stroma in rhinospordiosis is rather dense. There is a chronic inflammatory reaction in which neutrophils, plasma cells and lymphocytes are prominent. In contrast to the usual nasal polyp. Eosinophils are inconspicuous. Occasionally purulent microabscesses occur.
The cysts of all size have a sharply defined chitinous appearing wall. In a large maturing cyst the wall alone may be 5  thick. Histologically, rhinosporidiosis should be differentiated, specially in immuno-suppressed persons with other fungal infection like Coccidioides immitis.
Differential incidence: Although rhinosporidiosis is seen most often in children and young adults, it occurs at any age. No racial difference in susceptibility are recognized. The disease is seen much more frequently in men than in women, but the extent to which this difference is related to greater frequency or severity of exposure is difficult to evaluate. Infections are seen most often in labourers and in those with frequent exposure to water of streams and pools.
Geographic distribution:
Rhinosporidiosis is found must often in India and Ceylon, but it is reported also from the East Indies, the Malay, States, the Philippines, Iran, South Africa, Italy, England, Scotland, Southern United States, Mexico, Cuba, Argentina, Brazil and Paraguay.
Source of infection:
The disease is not contagious, and sources of infection are exogenous. The frequent history of prior extended to water of pools and rivers and the occurance of multiple cases among those members of a group of workmen most intimately and repeatedly exposed to water source suggest the R. seeberi has a natural habitat in water. Rhinosporidiosis was observed in workmen who dived under water to bring up san din buckets, but not in their associates who carried the sand from the water’s edge. It has been suggested that water insects or fish may be hosts of the fungus.
Laboratory diagnosis:
Direct examination of the surface of the polyp may reveal the subsurface position of sporangia which are white and so large (up to 350  in diameter) that thery can be seen with naked eye. Dissection of sporangia or excision and microscopic examination of tissue confirms the diagnosis. Culture is not successful, and the inability of R. seeberi to grow on artificial media, as well as some peculiarties about its reproductive cycle in tissues, have raised the question whether it is actually a fungus.
It is resembles in general appearance and in manner of sporulation some species of synchytrium, which are obligate parasites of plants, and which produce characteristic galls on the host plant. Animal inocultion is not helpful in diagnosis. Although R.seeberi is found in natural infections of horses, mules and cows, experimental infections usually do not succeed. Recently molecular methods like polymerase chain reaction are being developed for diagnosis.
Rhinosporidiosis should be suspected or considered in all cases of swellings of nose, nasopharynx and skin. Although disseminated Rhinosporidiosis is very rare, still remains a possibility and requires a different mode of treatment. Presently the medical treatment of Rhinosporidiosis is not satisfactory and requires further study and research.
1. Caldwell, G.T. and Roberts, J.D.: Rhinosporidiosis in the United States J.A.M.A. 1938; 110,1964.
2. Karunaratne W.A.E.: Rhinosporidiosis in Man, London, Athlone Press, 1964.
3. Weller, C.V. and Riker, A.D.: Rhinosporidiosis in Man, London, Athlone Press, 1964.
4. Weller, C.V. and Riker, A.D.: Rhinosporidiosis seeberi Am.J.Path, 1930,6,721-732.
5. Baron, E.J., Peterson, L.R. Finegold, S.M. New, Controversial difficult-to-cultivate or non-cultivate etiological agents of disease in Bailey and Scott’s Diagnostic Microbiology, 9th Edition, Mosby, st.Louis, Baltimore, Boston, 1994; p-585.
6. Gori, S. Scasso, A.: Cytologic and differential diagnosis of rhinosporidiosis: Acta Cytologica, 1994: 38(3):361-366.
7. Saha, S.NB., Mondal, A.R. Bera, S.P., Das S., and banerjee, A.R.: Rhinosporidial infection in West Bengal – Calcutta based hospital study. Indian Journal of Optolaryngology & Head Neck Surgery – 2001:53(2):100-104

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The incidence of venomous snakebites is high in rural areas where people are engaged in agricultural activities & are in the habit of sleeping on the floor. About 40,000 people die each year from venomous snake bites (worldwide).Death can be prevented if diagnosis & management is made early in the course. Thus a high degree of clinical suspicion, a timely diagnosis & management is life saving in these cases as it happened in this case report.
Acute onset of pain abdomen in previously healthy young male adults who were sleeping on the floor, without any history of bite, were successfully treated & cured based on high index of clinical suspicion with appropriate antivenom therapy.
Key words : Venomous snake bite , Clinical suspicion, Acute abdomen, Timely diagnosis & management
Snakebite is common in rural areas. Venomous snakenites of the families like Elapidae (Cobra, Krait ) & Viperidae (Viper) are verycommon. Clinical symptoms & signs vary with the species of snake & the amount of envenocation. Fang marks , local swelling , echymosis, blistering , necrosis , are seen at the site of bite in viper bites. Bleeding & clotting disturbances, DICC, ARF , shock are also seen inm veperbites. (Krait ) local signs are absent & the neurotoxic symptoms mostly appear within 1-2hrs after the bite (15min.-15hrs). Blurring of vision , ptosis , dysphagia, Opthalmoplegia, paralysis of muscles of respiration, alteration of consciousness, coma, convulsion occur.
But a patient with a venomous snake bite presenting with features of Acute abdomen has not been reported in neurotoxic bites except in cases of viper & colubridae bites so far. Therefore acute pain abdomen with neurotoxic signs & symptoms should prompt one to suspect snake bite & to exclude other causes of Acute pain abdomen with neurological signs , so that appropriate therapy (ASV, Neostigmine) & supportive measures can be life sving.
Case report
(1) A young male adult about 26 years tushed in to the casualty O.P.D. in early morning with complaints of acute pain abdomen, vomiting , difficulty in deglutition for 6 hrs. Family History : Similar symptoms in his mother who died 1 month back. No other specific complaint was reported by his relatives except for some weakness & frothing from mouth. For this he was treated at Sundergarh district hospitas as a case of acute pancreatitis & was referred to V.S.S Medical College, Burla as patient deteriorated,. For further evaluation & management.
Examination revealed:
Average Body built, drowsy ptosis, frothing from mouth, Restlessness because of severe pin abdomen.
Pulse – 82/min, regular,
BP – 140/90 mmHg
R.R – 20/min, Thoracoabdominal type , No pallor, Icterus, Cyanosis, Lymphadenopathy
Chest – Clinically NAD
P/A – Revealed diffuse tenderness & rigid abdomen , No organomegaly.
Bowel sounds absent – No evidence of freefluid.
CNS – Conscious, drowsy, difficulty in speech & deglutition ( both liquied + solid ) bilateral ptosis was present
No sensory, motor deficit
No meningeal sign
Plantar ( B/L Flexor )
After about 5 min. of admission in the casualty O.P.D., Surgery consultation was done who excluded any surgical, cause of acute abdomen. Necessary investigations were done immediately , which revealed DC – N80 ,E1,L18,M1, TLC- 10,200/Cumm, HB % - 11.6gm %ESR-20mm,1st hr, BI.Urea-40 mg %Sr.Cr.-0.8mg%,Sr.Na+ -137m mol/L,Sr.K+=2.6M MOL/l,Sr.LIPASE- 180 I.U./L, Whole Blood Clotting test neg. , PT – N Sr. Amylase –27UL,St. X-ray Abnormal, U.S.G. Abd. – NAD , ECG – Normal except for the presence of U. waves due to hypokalemia, chest X- ray – NAD.
The patient was finally diagnosed provisionally basing on minimal Neurotoxic sogns & symptoms as a suspected case of neurotoxic snake bite & was treated with (150ml) i.e. 15 vials of Antisnake Venom (ASV), Inj. Atropine 0.6mg I.M. Followed by Inj. Neostigmine (0.5mg) I.V. every 30 minutes for 5 doses, and repeated at 6 hrly. Other supportive care included Nil orally. Throat suction, Broad spectrum antibiotics, I.V. fluids, Hydrocortisone, Symptomatic treatment of pain & vomiting. Hypokalemia was corrected by I.V. kc! Infusion.
With the above treatment after about 2 hours, the patient’s condition started improving gradually with dimunution of pain abdomen, disappearance of ptosis, dysphagia & the patient was symptom free after 2 days & was discharged from the hospital.
(2) Interestingly another young male of 21 years with definite history of Krait bite also presented after one month with the chief complaint of pain abdomen & on examination had features of neurotoxic signs & symptoms & improved with ASV, atropine, Neostigmine. This substantiates further the fact that acute pain abdomen may be a presenting symptoms in Neurotoxic (krait) bites.
Snake bite is common in rural areas. Agricultural workers, hunters, & people sleeping on the floor are at risk as are evident in these cases. History of snake bite may not be present in some cases especially those bitten by krait (Neurotoxic venomous snakes) & fang marks & local signs may not be present. Signs such as early morning ptosis, dysphagia & pain abdomen should prompt one to highly suspect snake bite (Neurotoxic) & to start treatment as early as possible for a good outcome.
A delay in clinical suspicion & diagnosis & thus institution of proper therapy would have proved fatal in the case like his mother who died one month back with similar symptoms without h/o snake bite & without antivemin therapy: could be due to same environment of snakebite.
Acute abdomen like presentation in neurotoxic snake bites is not yet reported in literature. However this case report suggests that Acute abdomen can be a presentation of snake bite & high clinical suspicion & appropriate therapy may save life.
1. Manson’s Tropical diseases – 20th Edition.
2. Hodge III D, Snake bites. In Emergency medicine Eds. May HL, Little Brown Company, Boston, 2nd Edition 1992, 925-928.
3. Reid H.A. Snake bite in tropics British Medical Journal, 1968 3 (614): 359-362.

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