non-a, non-b (nanb) hepatitisarchive.nmji.in/approval/archive/volume-1/issue-1/editorials-2.pdf ·...

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2 THE NATIONAL MEDICAL JOURNAL OF INDIA VOL I JANIFEB 1988 reviews. So to attract these we decided to rely on a mixture of straightforward patriotism and straightforward bribery (one thousand rupees). To achieve a high standard we have invited eight distinguished doctors to be active members of the editorial board, and each original article and review is assessed by two referees-one Indian and one foreign. This is our first effort. If you like it we would be pleased to hear from you; if you do not we will be grateful if you could write and tell us what you think is wrong and how it might be corrected. This is, after all, The National Medical Journal of lndia-a journal as much your responsibility as it is ours. REFERENCE 1 Sahni P, Pande G K. Smith J. Nundy S. Belter Medical Writing in India. The National Medical Journal of India. New Delhi. 1988. Non-A, Non-B (NANB) Hepatitis Hepatitis due to the NANB group of viruses is not as clearly identified as that due to hepatitis A virus (HA V),I hepatitis B virus (HBV),2 and the delta agent (HDV).3 There is strong evidence to suggest that there are at least three diffe- rent types of human NANB viruses- transmitted by blood transfusion, by coagulation factor administration and by the faecal-oral route. The earliest evidence to suggest the existence of the third type of hepatitis besides infectious and serum hepatitis came through the epidemiological studies of Havens> in 1956. A symposium on viral hepatitis in 1975 at Washington D.C., USA focused the attention of hepatologists on post-transfusion NANB hepatitis. Accumulated evidence three years later confirmed the occurrence of NANB hepatitis due to needle pricks. Further, by 1981 another, but less common, NANB virus was described which was transmitted through the plasma.« The third type of NANB virus transmitted through contaminated water was suggested by two groups of investigators during 1980 and 1982 7 11 Of the three types, i.e., post-transfusion (PTH), post-coagulation factor administration and enteric NANB hepatitis, the first type has been reported mainly from developed countries, the third type is common in developing countries and the second type is infrequent everywhere. About 75-95 per cent of the reported PTH from different countries is due to NANB infection." It is estimated that about ten per cent of the recipients of blood transfusion develop NANB hepatitis. This occurs more frequently with the transfusion of commercial donor blood as compared with that obtained from voluntary donors. The risk of NANB infection is high amongst females and drug addicts. About 10-25 per cent of all patients admitted to hospital with jaundice have been reported to have NANB infection even though the relation- ship between blood transfusion and hepatitis has been demonstrated in a very small proportion of them. PTH caused by NANB is very often anicteric or mild but it is an important cause of chronic liver diseases such as chronic hepatitis and cirrhosis. It may also be associated with liver cancer. Coagulation factor transmitted NANB is infrequent and its incidence amongst patients other than haemophiliacs is not known. Most of the coagulation factor concentrates, anti-haemophilic factor, factor VIII, anti-haernophilic and factor IX complex have been found to transmit NANB infection. Hepatitis due to faecal-oral NANB infection has been commonly reported in epidemic forms. Community outbreaks of this disease have been reported from India, USSR, Japan, Indonesia, Thailand, Burma, Nepal, Bangladesh, Algeria and the Ivory Coast. This problem has been extensively studied in

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Page 1: Non-A, Non-B (NANB) Hepatitisarchive.nmji.in/approval/archive/Volume-1/issue-1/Editorials-2.pdf · The post-blood transfusion NANB virion isreported to be a22to 37nmsized. particle

2 THE NATIONAL MEDICAL JOURNAL OF INDIA VOL I JANIFEB 1988

reviews. So to attract these we decided to rely on a mixture of straightforwardpatriotism and straightforward bribery (one thousand rupees). To achieve ahigh standard we have invited eight distinguished doctors to be active membersof the editorial board, and each original article and review is assessed by tworeferees-one Indian and one foreign.

This is our first effort. If you like it we would be pleased to hear from you; ifyou do not we will be grateful if you could write and tell us what you think iswrong and how it might be corrected.

This is, after all, The National Medical Journal of lndia-a journal as muchyour responsibility as it is ours.

REFERENCE1 Sahni P, Pande G K. Smith J. Nundy S. Belter Medical Writing in India. The National Medical

Journal of India. New Delhi. 1988.

Non-A, Non-B (NANB) Hepatitis

Hepatitis due to the NANB group of viruses is not as clearly identified as thatdue to hepatitis A virus (HA V),I hepatitis B virus (HBV),2 and the delta agent(HDV).3 There is strong evidence to suggest that there are at least three diffe-rent types of human NANB viruses- transmitted by blood transfusion, bycoagulation factor administration and by the faecal-oral route. The earliestevidence to suggest the existence of the third type of hepatitis besides infectiousand serum hepatitis came through the epidemiological studies of Havens> in1956. A symposium on viral hepatitis in 1975 at Washington D.C., USAfocused the attention of hepatologists on post-transfusion NANB hepatitis.Accumulated evidence three years later confirmed the occurrence of NANBhepatitis due to needle pricks. Further, by 1981 another, but less common,NANB virus was described which was transmitted through the plasma.« Thethird type of NANB virus transmitted through contaminated water wassuggested by two groups of investigators during 1980 and 19827•11 Of the threetypes, i.e., post-transfusion (PTH), post-coagulation factor administration andenteric NANB hepatitis, the first type has been reported mainly fromdeveloped countries, the third type is common in developing countries and thesecond type is infrequent everywhere.

About 75-95 per cent of the reported PTH from different countries is due toNANB infection." It is estimated that about ten per cent of the recipients ofblood transfusion develop NANB hepatitis. This occurs more frequently withthe transfusion of commercial donor blood as compared with that obtainedfrom voluntary donors. The risk of NANB infection is high amongst femalesand drug addicts. About 10-25 per cent of all patients admitted to hospital withjaundice have been reported to have NANB infection even though the relation-ship between blood transfusion and hepatitis has been demonstrated in a verysmall proportion of them. PTH caused by NANB is very often anicteric or mildbut it is an important cause of chronic liver diseases such as chronic hepatitisand cirrhosis. It may also be associated with liver cancer.

Coagulation factor transmitted NANB is infrequent and its incidenceamongst patients other than haemophiliacs is not known. Most of the coagulationfactor concentrates, anti-haemophilic factor, factor VIII, anti-haernophilic andfactor IX complex have been found to transmit NANB infection.

Hepatitis due to faecal-oral NANB infection has been commonly reported inepidemic forms. Community outbreaks of this disease have been reported fromIndia, USSR, Japan, Indonesia, Thailand, Burma, Nepal, Bangladesh,Algeria and the Ivory Coast. This problem has been extensively studied in

Page 2: Non-A, Non-B (NANB) Hepatitisarchive.nmji.in/approval/archive/Volume-1/issue-1/Editorials-2.pdf · The post-blood transfusion NANB virion isreported to be a22to 37nmsized. particle

THE NATIONAL MEDICAL JOURNAL OF INDIA VOL 1 JANIFEB 1988 3

India. The mode of transmission of enteric NANB is similar to that of hepatitisA. Adults suffer more than children in epidemics. Pregnant women contract asevere form of the disease and have a higher mortality. There are no reportedchronic sequelae. 10 Superinfection with NANB in Hepatitis B carriers has beenreported to be an important "ause of fulminant at d subacute hepatic failure. II

The diagnosis of all the three types of NANB hepatitis is by exclusion ofinfection caused by HBV, HAV and HDV through appropriate serologicaltests. Attempts to develop a scientific serological test to confirm the diagnosisof NANB virus infection have not yet been successful. Shirachi et al. 12 first pub-lished a report of a double immunodiffusion test for NANB hepatitis. Latercounter-immunoelectrophoresis, immunofluorescence, radioimmunoassayand ELISA techniques have been used to establish sensitive and specificserological tests. It may come as a surprise to many of us that in spite of thephenomenal advances in immunodiagnostic methods for viral diseases NANBhepatitis still remains a diagnosis by exclusion.

The liver histology in NANB hepatitis is also not helpful in the aetiologicaldiagnosis. Morphological changes are similar to those due to HA V and HBV.The following light microscopic changes, though not specific, have beendescribed mainly in NANB hepatitis: (a) swollen, vacuolated and multilayeredbile duct epithelium, (b) fatty change, (c) piecemeal necrosis, and (d) portalinfiltration with polymorphonuclear cells and lymphocytes.

Three types of structures-tubular, microtubular and sponge-like in-lusions->have been identified in the hepatocytes of patients with NANB hepatitis byelectron microscopic studies. Shikata and his colleagues found that themonoclonal antibody 48-1 reacted with the microtubular structures. Hesuggested that these ultrastructural chang 'S should be considered to bemarkers of NANB viral infection. 13

There has been very little advance on the characterization of NANB viruses.The post-blood transfusion NANB virion is reported to be a 22 to 37 nm sized.particle with an outer shell and a central core. The post-coagulation factorvirion is suggested to be a 22 to 27 nm spherical particle which is probably asmall enveloped RNA virus. 14 Enteric NANB is reported to be a 25 to 27 nmparticle with an outer shell and an inner core. It is suggested to be a RNA virus.Despite difficulties in isolation and characterization of the NANB virus experi-mental models have been successfully developed. The chimpanzee andmarmoset have been infected with human NANB post-transfusion and coagu-lation factor related viruses» and preliminary studies suggest that Rbesusmonkeys may be suitable models for studying enteric NANB infection.

More than two decades have passed since our attention was focused onNANB hepatitis. During this period, techniques to study the viruses haveshown tremendous progress. However, the NANB viruses have eluded scien-tists but there is hope that soon this infection will be better understood and themeans to control it elucidated in the same way as has been done for HBV andHA V infection.

REFERENCESSiegl G. Structure and biology of hepatitis A virus. In: Szmuness W, Alter H J, Maynard J E(eds) Viral Hepatitis. Franklin Institute Press, Philadelphia, 1982; 13-...20.

2 Gerin J L, Wai-knoshih J, Hoyer B H. Biology a.id characterisation of hepatitis B virus. In:Szmuness W, Alter H J, Maynard J E (eds) Viral Hepatitis. Franklin Institute Press Philadel-phia, 1982; 49-56. •

3 Rizzetto M. Biology and characterisation of delta agent. In: Szmuness W, Alter H J, MaynardJ E (eds) Viral Hepatitis. Franklin Institute Press, Philadelphia, 1982; 355..ffl.

4 Tabor E. The three viruses of non-A, non-B hepatitis. Lancet 1985; I: 743-5.5 Havens W P Jr. Viral hepatitis: Multiple attacks in a narcotic addict. Ann lntern Med 1956; 44:

199-203. .6 Hollinger F B. Mosley J W, Szmuness W, et al. Transfusion transmitted viruses study: experi-

mental evidence for two non-A, non-B hepatitis agents. 1 Infect Dis 1980; 142: 4~7.7 Khuroo M S. Study of an epidemic non-A, non-B hepatitis. Possibility of another human

hepatitis virus distinct from post-transfusion non-A, non-B type. lAMA 1980; 68: 818-23.8 Tandon B N, Joshi Y K, Jain S K, Gandhi B M, Mathiesen L R, Tandon H D. An epidemic

of non-A, non-B hepatitis in North India. lnd 1 Med Res 1982; 75: 739-44.

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4 THE NATIONAL MEDICAL JOURNAL OF INDIA VOL I JANIFEB 1988

9 Dienstag J L, Alter H J. Non-A, Non-B hepatitis: Evolving epidemiologic and clinicalperspective. Semin in Liver Dis 1986; 6: 67-81.

10 Joshi Y K, Tandon M, Babu S, Sariu S, Tandon B N, Chatnrvedi V C. Follow-up of anepidemic of non-A, non-B hepatitis. Liver 1984; 4: 338-9.

11 Tandon B N, Gupta H, Irshad M, Joshi Y K, Chawla T C. Associated infection with non-A,non-B virus as possible cause of liver failure in Indian HBV carriers. Lancet 1984; II: 1130-1.

12 Shirachi R,Shiraishi H, Tateda A, Kikuchi K, Ishida N. Hepatitis c antigen in non-A non-Bpost-transfusion hepatitis. Lancet 1978; II: 853-{j.

13 Shikata T. Serial liver biopsy study in chimpanzees infected with non-A, non-B agents. ActaHep.tologica Japonica 1986; 27: 1507-13.

14 Bradley D W, McCaustland K A, Cook E H, Schable C A, Ebert J W, Maynard J E. Post-transfusion non-A, non-B hepatitis in chimpanzees. Physiochemical evidence that the troubleforming agent is a small enveloped virus. Gastroenterology 1984; 88: 773-9.

15 Feinstone S M, Alter H J, Dienes H P, Purcell R H. Studies on non-A, non-B Hepatitis inchimpanzees and marmosets. In: Szmuness W, Alter H J ,Maynard J E (eds) Viral Hepatitis.Franklin Institute Press, Philadelphia, 1982; 295-304.

Intensive Respiratory Care in India

Respiratory care came of age in the West about twenty-five years ago but stillremains a struggling neonate in India. The purpose of intensive respiratory careis to manage patients with acute respiratory failure, acute on chronic respira-tory failure and to help critically ill patients who have diseases that can lead torespiratory failure. Conditions producing acute respiratory failure not onlyinclude acute disease primarily involving the lungs but also cover a wide area ofgeneral medicine, surgery and obstetrics. Thus, diseases of the central nervoussystem, in particular neuromuscular paralysis, can lead to hypoventilation andrespiratory failure in patients with normal lungs. Many other problems includ-ing shock, sepsis, crush injuries and fulminant tropical infections such astetanus, pyogenic meningitis and malignant malaria can also produce 'pulmo-nary injury' and necessitate intensive respiratory care and support.

In a country as poor and as densely populated as India, where the incidenceof acute infections involving the lungs is still high, the proportion of critically illpatients in a medium-sized hospital is often large. Most critically ill patientswill, at one time or another, need respiratory care. Some patients requiring lessintensive care can be managed in a ward, but there are many who require inten-sive care and need the expertise and equipment that only a well-equipped unitcan provide. But our commitment towards respiratory care units lacks a senseof priorities. One does not decry the setting up of coronary care units, eventhough more often than not these mushrooming units are merely status symbolsthat adorn hospitals. But it is sad to witness neglect of the maintenance ofproper ventilation and adequate lung function in a critically ill individual. Mostcoronary care units ignore the basic fact that the heart and lungs work as asingle inter-related unit, so that acute pump failure leads to respiratory failure,and acute severe hypoxia from a respiratory problem can adversely affect theheart. Ventilator support with a high concentration of inhaled oxygen is thusessential to a patient with severe acute pump failure or to a patient withfulminant pulmonary oedema. The use of such support should be prompt andearly and not as a gesture of apology to a dying patient.

Respiratory care units in the West are special units that have been designedto primarily look after patients with serious respiratory problems. This is anunnecessary luxury in our country as it would entail the duplication of medicalexpertise and equipment and would lead to an impossible strain on the fewavailable well-trained nurses in the field. Special Intensive Respiratory CareUnits Gust as special care units for separate organs or systems) also have aninherent disadvantage in relation to patient care that cannot be easilyovercome. In any critically ill individual, whatever the initial cause and nature