|Year : 1987 | Volume
| Issue : 1 | Page : 29-31
Study of Coxsackie B viral infections in chronic pancreatitis patients from Kerala.
JJ Shanmugam, VV Balakrishnan, MM George, KT Shenoy
J J Shanmugam
|How to cite this article:|
Shanmugam J J, Balakrishnan V V, George M M, Shenoy K T. Study of Coxsackie B viral infections in chronic pancreatitis patients from Kerala. J Postgrad Med 1987;33:29-31
|How to cite this URL:|
Shanmugam J J, Balakrishnan V V, George M M, Shenoy K T. Study of Coxsackie B viral infections in chronic pancreatitis patients from Kerala. J Postgrad Med [serial online] 1987 [cited 2022 Dec 7 ];33:29-31
Available from: https://www.jpgmonline.com/text.asp?1987/33/1/29/5312
During the last decade many reports were seen in the literature correlating viral infections with acute pancreatitis. In the late 1960s, Gamble et al reported high titres of Coxsackie B viral antibody in juvenile on set diabetes than among the non-diabetic patients. Yoon and Co-workers isolated Coxsackie B4 virus from the pancreas of a boy with acute diabetes mellitus. There are many more reports associating Coxsackie B viral infections with diabetes mellitus.,, Here, we describe our preliminary findings obtained with the study of Coxsackie B viral infections in chronic pancreatitis patients from Kerala state.
MATERIAL AND METHODS
Paired sera samples were collected from nine patients with clinically confirmed chronic pancreatitis and admitted to the Gastroenterology Unit of the Medical College Hospital. Trivandrum. The diagnosis of chronic pancreatitis was established on the basis of plain X-rays of the abdomen showing the presence of pancreatic calculi. Paired sera samples were collected with an interval of 14 to 28 days for viral antibody studies. All paired sera were stored at-20° C without the "addition of any preservatives, until tested for viral antibodies. Coxsackie B viral antibodies against all six types (B1 to B6), were titrated in VERO cell lines by means of neutralisation test. The standard strains of Coxsackie B viruses and their specific immune sera were supplied by the Director, WHO Regional Reference Laboratory for Enteroviruses, Statens Serum Institute, Copenhagen, Denmark and the VERO cell line from the National Institute of Virology, Poona. The procedures followed for viral antigen preparation, calculation of TCID50 and the neutralisation test for antibody detection were as per the method of Grist et al.
Six out of nine patients showed neutralising antibody against one or more of B1 to B6 Coxsaekie viruses. Only one patient showed neutralising antibody against three types of Coxsaekie viruses-B1, B2 and including highest titre against Coxsaekie virus [Table 1]. Two out of patients showed rise in antibody titre against Coxsaekie B viruses-from 1 : 40 to 1 : 80 against B2 and from 1 : 160 to 1 : 320 against B3 virus in their first second sera samples, respectively. All other four patients showed only 1 : 10 antibody titres in both first and second sera samples. The details of the results obtained neutralisation test for antibodies against six types of Coxsaekie B viruses are given in [Table 1].
The present study has revealed that of nine patients with chronic pancreatitis were suffering from Coxsaekie B viral infections during the period of study or earlier. Two patients have shown high antibody titres against coxsaekie B2 and B5-1 : 80 and 1: 320. Our findings Coxsaekie B viral infections are higher than the report of Di Pietro et al and less than that of Ray et al-51.2% and 90.9% respectively. The serological evidence Coxsaekie B virus infections in acute pancreatitis patients as reported by other workers,,, ranged from 5.2% to 90.9%, with an initial testing dilutions ranging from to 1 : 32.Hence, wide variations in positivity rate of Coxsaekie B virus infections may be partly due to the differences in the testing dilutions. Even with an in testing dilutions of 1:32, Di Pietro et al could obtain 51.2% of positivity, while Arnesjo et al1 using 1:5 initial testing dilutions reported the same antibody only in 19.8% of patients' sera tested. Our findings have revealed that six out of nine patients showed NT antibodies against one or more Coxsackie B viruses-ranging from 1:10 to 1 : 320. Two patients have shown two fold sero-conversions against Coxsackie B2 and B5 viruses [Table 1]. Since four-fold increase of viral antibody litres were not found, there is no evidence of current Coxsackie B viral infections in any of the patients studied. The present preliminary findings have revealed the high prevalence of Coxsackie B viral infections in chronic pancreatitis patients. Since the numbers of cases studied are few, much emphasis cannot be made on the present findings. Whether the Coxsackie B viruses have any etiological association with the genesis of pancreatitis is yet to be studied in detail including the animal experiments using viruses isolated from the pancreatic specimens of the patients. The present findings, therefore, call for further studies by means of follow up of more number of patients, including the virus isolation attempts from pancreatic specimens, in order to understand the possible association of Coxsackie B or other viruses with the genesis of pancreatitis.
The authors are thankful to the Indian Council of Medical Research for the financial support, to the Director of S.C.T.I.M.S.T. for the permission to carry out the study, and to the Director of WHO Regional Reference Centre for Enteroviruses, Statens Serum Institute, Copenhagen, Denmark for the supply of the standard Coxsackie B viruses and the specific viral antisera.
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