BRITISH MEDICAL JOURNAL 31 MAY 1975
`
`Hospital Topics
`
`Recurrent Aphthae: Treatment with Vitamin Bt2,
`Folic Acid, and Iron
`
`D. WRAY, M.M. FERGUSON, D.K. MASON, A.W. HUTCHEON, J.H. DAGG
`
`British Medicalffournal, 1975, 2, 490-493
`
`Introduction
`
`Summary
`
`A series of 130 consecutive outpatients with recurrent
`aphthous stomatitis were screened at the oral medicine
`department, Glasgow Dental Hospital, for deficiencies
`in vitamin BI~, folic acid, and iron. In 2.3 patients (17.7%)
`such deficiencies were found; five were deficient in
`vitamin B1, seven in folic acid, and 15 in iron. Four had
`more than one deficiency. Out of 130 controls matched
`for age and sex 11 (8"5%) were found to have deficiencies.
`The 2~ deficient patients with recurrent aphthae were
`treated with specific replacement therapy, and all 1~0
`patients were followed up for at least one year. Of the 2~
`patients on replacement therapy 15 showed complete
`remission of ulceration and eight definite improvement.
`Of the 107 patients with no deficiency receiving local
`symptomatic treatment only ~3 had a remission or were
`improved. This difference was significant (P<0.001).
`Most patients with proved vitamin Bt~ or folic acid
`deficiency improved rapidly on replacement therapy;
`those with iron deficiency showed a less dramatic
`response.
`The 23 deficient patients were further investigated to
`determine the cause of their deficiencies and detect the
`presence of any associated conditions. Four were found
`to have Addisonian pernicious anaemia. Seven had a
`malabsorption syndrome, which in five proved to be a
`gluten-induced enteropathy. In addition, there were
`single patients with idiopathic proctocolitis, diverticular
`disease of the colon, regional enterocolitis, and adeno-
`carcinoma of the caecum.
`We suggest that the high incidence of deficiencies
`found in this series and the good response to replacement
`therapy shows the need for haematological screening of
`such patients.
`
`University Department of Oral Medicine’and Pathology, Glasgow
`Dental Hospital and School, Glasgow GJ 3JZ
`
`D. WRAY, n.DoS., Research Assistant
`M. M. FERGUSON, M.B., B.D.S., Nuflield Dental Research Fellow
`D. K. MASON, MAX, F.D.S., Professor of Oral Medicine
`
`University Department of Medicine, Wes.tcrn Infirmary, Glasgow
`GII 6NT
`
`A. W. HUTCHEON, M.B., ~,l.S.C.e., Research Fellow
`J. H. DAGG, M.D., F.R.C.P., Consultant Physician
`
`Recurrent oral ulceration, unlike glossitis and angular cheilitis,
`seems to occur infrequently in association with deficiencies of iron,
`folic acid, and vitamin B~v It has also been reported in patients
`with idiopathic steatorrhoea, though again glossitis is more
`common.~ ~ In such cases it may be difficult to establish whether
`the oral lesions are directly due to the underlying disease or
`simply reflect co-existing deficiencies.
`We have examined the relationship between recurrent
`aphthae, specific haematological deficiency, and malabsorption
`in 130 patients presenting consecutively at the oral medicine
`clinic at Glasgow Dental Hospital during the past five years.
`Our findings and the patients’ response to treatment are reported
`here.
`
`Patients and Methods
`
`The 130 patients had suffered from recurrent oral ulceration of the
`aphthous type for periods of six months to 30 years. Their ages
`ranged from 8 to 83 years (mean 38-2 years); 78 were female (mean
`age 40 years) and 52 male (mean age 35-6 years) (table I).
`
`X^aLE I--Age and Sex Distribution of 130 Patients with Recurrent Aphthae
`
`Age (years) :
`
`-9 1-19 -29 -39 --49 -59{-.69 -79 -89
`
`Total
`
`Males ......
`Females .....
`
`[ 1 9 25 10
`
`Total
`
`52
`78
`
`130
`
`The diagnosis was made from the clinical appearance and the
`history using the criteria of Lelmer) The ulcers were typically
`1-4 rnm in diameter, with a grey base and a regular erythematous
`margin. Healing usually occurred in 3-21 days. The ulcers were
`present continuously or with varying periods of remission and
`occurred singly or in crops. Patients with bullae, traumatic ulcers,
`acute ulcerative gingivitis, herpes simplex and zoster, erythema
`multiforme, Reiter’s syndrome, Behqet’s syndrome, and other such
`conditions were excluded, as were those whose condition was related
`to the menstrual cycle.
`A group of 130 controls matched for age and sex was obtained from
`patients attending Glasgow Dental Hospital for routine treatment.
`
`HAEMATOLOGICAL STUDIES
`
`Venous blood was taken from each of the patients and controls at two
`consecutive clinic visits. The serum iron and total iron-binding
`capacity (T.I.B.C.) were measured by an automated method.~ A con-
`sistem iron saturation of the T.I.B.C. of less than 16% was re-
`garded as indieadng iron deficiency.5 "Ilhe serum folate and, later,
`~e whole bh~d fola~e were measured using a teohnique modified
`
`Sandoz Inc.
`Exhibit 1030-0001
`
`JOINT 1030-0001
`
`

`
`BRITISH MEDICAL JOURNAL 31 MAY 1975
`
`491
`
`from ~h~t of Waters and Mollin.~ Folio acid deficiency w~s
`ddagnosed when ~he serum folate was less r~han 2-5 /~g/l or the
`w~hol¢ blood folate was less than 80 t~g/l. Sea’m’n vitamin
`was assa~’ed using Euglena graeilis~ vahies consistendy below
`120 ng/l. being regarded a~ abnormal. Routine haema,totogical
`measurements and blood film examinations were performed using
`standard methods.’
`Patients found to have iron, folic acid, or vitamin Btt deficiency
`wexe havestigated fustier by A.W.H. and J.H.D. to determine ~he
`cause of tgae deficiency and initiate treatment, ia~bsorption was
`diagnosed w~aen .the faec~ fat exceeded 5 g daiiy, w~ten rahe serum
`x’~|ose two hours a£tor a sta~da.rd oral dose related ¢o body weight
`wa~ less ~ban 2-0 rmnol]l (30 mg/100 rrd), and xchen intestinal
`clumping of barium was seen on follow-tl~rough examirmtion. In
`two patients w~tlh malabsorption intestinal biopsy failed for teoh-
`nieal reasot~s; in a~other five cases, diagnosed as ad~t coeliac
`disease, ~ntestit,ml biopsy cor~ffrmed the presence of subtotal villous
`atrophy. A clinical response followed the introc~u~tion of a gluten-
`free diet in these patients. Pernicious anaemia wns diagnosed on
`(cid:128)he .basis of blood and bone marrow findings, histamine-fast
`ac&lorhydria, t~e presence of gastric parietal cell antibodies,
`charaoteristic Scthil.ling test result,’~ and a therapeutic response to
`vitamin
`
`TREATMENT
`
`Patients with vitamin Bta deficiency were given 1000 vtg hydroxo-
`cohalamin intramuscularly followed by a further 1000 vtg every two
`months. Folic acid was taken by mouth in doses of 5 mg thrice daily
`during follow-up. Iron was also taken only by mouth and given con-
`tinuously for at least six months. During treatment all patients used a
`zinc chloride/zinc sulphate mouthwash (B.P.C.). Triamcinolone
`0-1% in dental paste (B.P.U.) or hydrocortisone lozenges (B.P.C.)
`were also used for symptomatic relief.
`In assessing the response to treatment, complete absence of ulcers
`for at least one year after treatment constituted a remission, and only
`occasional ulcers after treatment (one to six a year) constituted a
`definite improvement.
`
`Results
`
`HAEMATOLOGICAL DEFICIENCIES
`
`Altogether 23 patients with recurrent aphthae (17-7%) were found to
`be deficient in iron, vitamin B~z, or folic acid compared with 11
`(8.5%) of the controls. This difference was significant (P<0.025).
`Of the 23 patients 15 were deficient in iron (four having iron deficiency
`anaemia and 11 iron deficiency without anaemia), seven in folic acid
`(four showing the characteristic morphological changes in blood and
`bone marrow and three showing no such changes), and five in vitamin
`Bts (all with evidence of megaloblastic change in the bone marrow but
`two having apparently normal peripheral blood). Four patients had
`more than one deficiency (table II).
`Of the 11 deficient controls, seven were deficient in iron, only one
`showing overt anaemia. Three had reduced blood folate levels and
`one had latent Addisonian pernicious anaemia. No control had more
`than one deficiency. Thus iron and folio acid deficiencies were over
`twice as frequent in the patients as in the controls, and vitamin B~
`deficiency was five times more common in the patients than in the
`controls.
`
`RESPONSE TO TREATMENT
`
`Fifteen of the 23 patients (65 %) showed complete remission and eight
`(35%) definite improvement. Of the remaining 107 non-deficient
`patients, who received only local treatment, 12 (11%) had a complete
`remission and 20 (19%) were improved. Only 30% of the non-
`deficient patients, therefore, showed a response comparable to that
`of the 23 deficient patients (P< 0.001).
`Four of the five patients with vitamin atz deficiency were promptly
`relieved of symptoms and remained free of ulcers during follow-up;
`the fifth was definitely improved (table III). Of the seven patienis
`with folio acid deficiency, six were completely relieved of ulcers and
`remained symptom-free during follow-up and one was much im-
`proved. Of the 15 patients with iron deficiency, eight showed remis-
`sion and seven were definitely improved after iron therapy. Three of
`
`the iron-deficient patients had co-existing folio acid deficiency,
`however, and one had ascorbic acid deficiency; they had received
`folio acid and ascorbic acid respectively with remission of symptoms
`before iron theral~ was instituted. In addition, one iron-deficient
`patient underwent resection of a eaecal adenocarcinoma. Of the
`remaining 10 patiems with uncomplicated iron deficiency, five were
`cured and five definitely improved with iron replacement alone
`~table III),
`
`TAI;L~ II--Defidotdes:Found in 23Patients zoith Recurrent Aphthae
`
`No,
`
`Iron
`Deficiency
`
`Folic Acid
`Deficiency
`
`Vitamin Bx,
`Deficiency
`
`F.
`M.
`M.
`F.
`F.
`F.
`F.
`F.
`F.
`M.
`F.
`F.
`M,
`F.
`M.
`M.
`M.
`F.
`V.
`F.
`F.
`F.
`F.
`
`(+)
`(+)
`(+)
`(+)
`(+)
`
`(+)
`+
`(+)
`(+)
`(+)
`
`+
`+
`(+)
`+
`(+)
`
`15
`
`+
`(+)
`+
`
`+
`(+)
`
`C+)
`
`+
`+
`+
`
`(+)
`
`7
`
`5
`
`Total
`
`Symbols in parantheses in this and tables III and IV indicate latent deficiency--
`that is, deficiency without anaemia or detectable blood film abnormality.
`
`TABLE lI1--Re$ponse to Replacement Therapy
`
`Case
`No.
`
`Iron
`Deficiency
`
`Folic Acid Vitamin B,,
`Deficiency
`Deficiency
`
`Remission
`
`Marked
`Improvemenl
`
`+
`
`(++)
`(+)
`
`(+)
`
`+
`+
`+
`
`(+)
`
`+
`+
`+
`+
`+
`
`+
`
`+
`+
`+
`+
`+
`+
`
`+
`
`+
`
`+
`
`+
`
`+
`+
`+
`
`+
`+
`
`AETIOLOGY OF DEFICIENCIES
`
`We attempted to define with greater accuracy the cause of the
`deficiencies in the 23 patients (table IV). Seven (30%) were shown to
`have a malabsorption syndrome, which in five proved to be adult
`coeliac disease (gluten enteropathy). In addition, four patients were
`found to have Addisonian pernicious anaemia, one was found to have
`idiopathic proctocolitis, one had diverticular disease of the colon,
`one had Crohn’s disease (regional enterocolitis), and one had an
`adenocarcinoma of the caecum.
`
`ROLE OF LOCAL TREATMENT
`
`All 130 patients were given local symptomatic treatment. Most
`received a zinc chloride/zinc sulphate mouthwash (B.P.C.) and were
`given topical steroids if this proved ineffective. Though steroids
`are beneficial,* to clinical improvement continues only if treatment
`is maintained,~t and in no case have the ulcers been eradicated)~ In
`
`Sandoz Inc.
`Exhibit 1030-0002
`
`JOINT 1030-0002
`
`

`
`492
`
`this series when a patient was given specific replacement therapy such
`local treatment was stopped. Any lasting clinical improvement seen
`in the 23 deficient patients was thus unlikely to have resulted from
`local treatment.
`
`TABLE Iv--Associated Conditions in Patients with Deficiencies
`
`No. I
`
`Iron I Fslic Acid ]Vitamin
`Deficiency ]
`, Deficiency Deficiency
`
`Associated Condition
`
`I
`2
`3
`4
`
`6
`7
`8
`9
`I0
`II
`12
`13
`14
`15
`16
`
`18
`19
`2O
`21
`22
`23
`
`+
`
`(+++)
`(+)
`
`+
`
`(+)
`(+)
`(+)
`(+)
`(+)
`
`(+)
`
`+
`
`(+)
`
`(+)
`
`Malabsorption, adult coeliac disease
`Malabsorption
`Malabsorption, adult coeliac disease
`Malabsorption, adult coeliac disease
`Malabsorption, adult coeliac disease
`Malabsorption
`Diverticular disease of colon
`Adenocarcinoma of caecum
`Malabsorption, adult coeliac disease
`Pernicious anaemia
`Pernicious anaemia
`Pernicious anaemia
`Latent iron deficiency
`Iron deficiency anaemia
`Latent iron deficiency
`Crohn’s disease
`Idiopathic proctocolitis
`Latent pernicious anaemia
`Iron deficiency anaemia
`Ascorbic acid deficiency
`Latent iron deficiency
`Iron deficiency anaemia
`Latent iron deficiency
`
`Discussion
`
`In all but three of the 23 deficient patients oral ulceration was
`the only presenting complaint, and the underlying haematological
`abnormality or gastrointestinal disease was found only on further
`investigation. Of the other three patients, one had been known
`to have idiopathic proctocolitis for three years, one had Crolm’s
`disease, and the third had a history of treatment for coeliac
`disease in childhood; even in these cases the clinical picture was
`dominated by oral ulceration. In most cases, therefore, asso-
`ciated haematological deficiency or gastrointestinal disease
`would have remained unsuspected without further investigation.
`Indeed, many of the deficiencies were themselves latent
`(table II)--that is, they had produced no recognizable abnor-
`malities in the peripheral blood; screening by peripheral blood
`examination alone would have been thus insufficient to detect
`an underlying abnormality in these patients.
`Deficiencj of vitamin Bts is not generally recognized as a
`cause of recurrent aphthae, though isolated cases have been
`reported.t3 t4 Four patients with Addisonian pernicious anaemia,
`one at the latent stage, were diagnosed in this series. A fifth
`patient had slight vitamin Bts deficiency associated with adult
`coeliac disease, though his main deficiency was in fslic acid.
`Other causes of vitamin B,s deficiency were not found. In
`the patients with pernicious anaemia there was a particularly
`striking response to treatment; three had permanent remissions
`after replacement and one had marked improvement.
`Fslic acid deficiency as a cause of recurrent aphthae is not
`general!y accepted, though several cases of fslic acid deficiency
`with oral ulceration have been reported,x~ x s Isolated cases of
`idiopathic steatorrhoea with oral ulceration have also been
`reported.S 11 Farmer2O found fslic acid ineffective for treating
`unselected cases of recurrent aphthae, and Sircus et al.st also
`found folic acid of no benefit in (five or six) randomly selected
`patients with ulcers. There were seven patients with fslic acid
`deficiency in this series, all associated with underlying mal-
`absorption states, mostly adult coeliac disease. Fslic acid
`replacement alone produced a complete cure in five of these and
`a marked improvement in two. In one of the two patients who
`had had recurrent aphthae for 30 years complete cure did not
`occur with replacement therapy alone but promptly followed
`the institution of a gluten-free diet (case 2, table IV).
`The dramatic response to vitamin 912 and fslic acid in those
`patients in whom such a deficiency was adequately shown suggests
`a direct role for these substances in the pathogenesis of recurrent
`
`BRITISH MEDICAL IOURNAL 31 MAY 1975
`
`aphthae. The role of iron deficiency is much less clear, though
`recurrent ulceration has been described rarely among the
`oral manifestations of iron deficiency.22 Eleven patients with
`latent iron deficiency and four with overt iron deficiency
`anaemia were diagnosed in this series. In four of these patients
`co-existing deficiencies were present, and treatment of these
`rather than iron therapy was probably responsible for the
`clinical improvement. A further patient with iron deficiency
`improved after resection of an adenocarcinoma of the caecum.
`Of the remaining 10 patients with uncomplicated iron deficiency,
`five had a complete remission and five markedly improved; the
`poorer response of the iron-deficient patients to specific replace-
`ment therapy may reflect the greater difficulty in reconstituting
`body stores with iron as compared with repacement of fslic acid
`and vitamin Bls. Indeed, three of these 10 patients still had a
`saturation of the T.I.B.C. in the iron-deficient range after
`several months of iron therapy.
`The 23 deficient patients on replacement therapy showed a
`significantly better response to treatment than the 107 patients
`without such deficiencies. These 130 patients, however, may
`not have been representative of all patients with recurrent
`aphthae. Hospital patients tend to have severe recurrent oral
`ulceration and to have been referred because they presented a
`problem in management to their general dental or medical
`practitioners. Possibly, therefore, the prevalence of underlying
`disorders in an unselected group of patients with recurrent oral
`ulceration would be lower than in this series. Interestingly,
`however, the age and sex distribution of our patients was closely
`similar to the series of hospital outpatients with recurrent
`aphthae described by Sircus.2t
`Isolated cases of steatorrhoea associated with recurrent
`aphthae have been reported.~ 1~ In our series, the incidence of
`malabsorption and gluten enteropathy was strikingly high--
`5.3% of the whole series and 30.3% of the group with proved
`haematological deficiencies; the estimated prevalence of coeliac
`disease in central Scotland is only 0.054%.22 Apart from one
`patient who was known to have had coeliac disease in childhood,
`this diagnosis was unsuspected before investigation. In most
`cases the ulcers responded to replacement therapy alone, though
`in one (case 2) complete cure did not occur until a gluten-free
`diet was instituted.
`Oral ulceration is associated with various gastrointestinal
`disorders, especially Crohn’s disease, ulcerative colitis, and
`idiopathic proctocolitis,s4-2s In this series, Crohn’s disease
`(case 16) and idiopathic proctocolitis (case 17) were diagnosed
`before the appearance of recurrent aphthae, though the latter
`dominated the clinical picture; both patients responded well to
`iron therapy. Case 8 was an elderly woman who presented with
`recurrent aphthae and was found to be iron deficient. Physical
`examination showed a mass in the right iliac fossa, subsequently
`confirmed to be an adenocarcinoma of the caecum. Removal of
`the lesion and iron treatment brought about a definite improve-
`ment in the ulcers.
`The precise role of iron, vitamin Bt2, or fslic acid deficiency
`in the pathogenesis of recurrent aphthae is speculative. Though
`atrophic glossitis and angular stomatitis have long been recog-
`nized as complications or iron deficiency, attempts to correlate
`these changes with depletion of iron enzymes such as cyto-
`chrome oxidase in buccal mucosa have been unsuccessful.~s 3 s
`Iron enzyme studies in recurrent aphthae will be reported later.
`Defects of cell-mediated immunity have recently been
`reported in iron-deficient patientsflt z2 but attempts to show
`infection as a fundamental cause of aphthae have not been
`convincing.
`The oral ulceration which occurs with fslic acid antagonist
`drugs such as methotrexate is also well recognized and responds
`to topical folinic acid; interestingly, Dreizen et al)s induced
`oral ulceration in marmosets by feeding them a diet free of fslic
`acid though changes in the cells of the tongue and buccal mucosa
`analogous to those found in the’Sblood and bone marrow have
`been reported in vitamin Bt, deficiency.2~-~3 The DNA con-
`tent of buccal mucosal ceils, however, has been found to be
`
`Sandoz Inc.
`Exhibit 1030-0003
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`JOINT 1030-0003
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`
`BRITISH MEDICAL JOURNAL 31 M~V 1975
`
`493
`
`normala: and it is uncertain by what precise mechanism
`deficiency of vitamin Bt2 may be implicated in the pathogenesis
`of recurrent aphthae. It seems clear from our study, however,
`that treatment of demonstrable deficiencies of folic acid or
`vitamin B~ is likely to result in a permanent cure of such ulcers;
`the role of iron seems less well defined.
`It was not possible by clinical examination of the ulcers to
`separate patients with an underlying deficiency or disease from
`those with no such abnormality. Our findings, therefore, have
`significant implications for the management and treatment of
`patients with recurrent aphthae. Since there is a one in five
`chance of patients with persistent recurrent aphthae having
`some form of haematological deficiency or malabsorption
`syndrome, all patients presenting in this way should undergo
`haematological screening.
`
`References
`
`Cooke, W. T., Peaney, A. L. P., and Hawkins, C. F., Quarterly Journal of
`Medicine, 1953, 22, 59.
`Shear, M., and Kramer, S., Journal of the Dental Association of South
`Africa, 1964, 19, 324.
`Lelmer, T., "Recurrent oral ulceration and Beh~et’s syndrome; patho-
`logical, immunological, and clinical study," M.D. thesis, University of
`London, 1968.
`Young, D. S., and lticks, J. M.,Journal of Clinical Pathology, 1965, 15, 98.
`Bainton, D. F., and Finch, C. A.~ American Journal of Medicine, 1964,
`37, 62.
`Waters, A. H., and Mollin, D. L.,Jonrnal of ClinicaIPathology, 1961, 14,
`335.
`Dacie, J. W., and Lewis, S. M., Practical Haematology, 4th edn. Oxford,
`Churchill, 1970.
`
`Schilling, R. F.,Journal of Laboratory and Clinical Medicine, 1953, 42, 860.
`Sircus, W., British Medical Journal, 1959, 2, 804.
`Cooke, B. E. D., and Armitage, P., British MedicalJournal, 1960, 1, 764.
`Truelove, S. C., and Morris-Owen, R. M., British MedicalJournal, 1958,
`1~ 603.
`Graykowski, E. A., et al., Journal of the American Medical Association,
`1966, 196, 637.
`Hj#rting-Hansen, E., and Bertram, U., British DemalJonrnal, 1968, 125~
`266.
`Walker, J. E. G., British Journal of Oral Surgery, 1973, 11,165.
`Low, G. C., Quarterly Journal of Meaicine, 1928, 21~ 523.
`Manson Bahr, P., and Willoughby, H., Quarterly Journal of Medicine,
`1930, 23, 411.
`Stephanini, M., Medicine, 1948~ 27~ 379.
`Rodriguez-Molina, R., Annals of Internal Medicine, 1954, 40, 33.
`Dreizan, ~., Levy, B. M., and Bernick, S., Journal of Dental Research,
`1970, 49, 616.
`Farmer, E. D., Dental Practitioner, 1958, 3, 177.
`Sircus, W., Church, R., and Kelleher, J., Quarterly Journal of Medicine,
`1957, 26, 235.
`Waldenstrrm, J., Acta Mediea Scandinavlca, 1938, Suppl. No. 90, p. 380.
`McCrae, W. M.,Journal of Medical Genetics, 1969, 6, 129.
`McCarthy, P., and Shldar, G., Archives of Dermatology, 1963, 88~ 913.
`Issa, M. A., British Dentalffournal, 1971, 130~ 247.
`Kyle, J., Grohn’s Disease. London~ Heinemann Medica’l, 1972.
`Varley, E. W., Oral Surgery, 1972, 33~ 570.
`Verbov, J. L., British Journal of Dermatology, 1973, 88, 517.
`Jacobs, A.,Journal of Glinlcal Pathology, 1961, 14~ 610.
`Dagg, J. H., et al., British Journal of Haematology, 1966, 12, 331.
`Higgs, J. M., and Wells, R. S., British Journal of Dermatology, 1972, 86,
`Suppl. No. 8, p. 88.
`Joynson, D. H. M., et al., Lancet, 1972, 2, 1058.
`Graham, R. M., and Rheault, M. H., Journal of Laboratory and Clinical
`Medicine, 1954, 43, 235.
`Boen, S. T., Aeta Medica Scandinavica, 1957, 159, 425.
`Boddington, M. M., Journal of Clinical Pathology, 1959, 12, 229.
`Boddington, M. M., and Spriggs, A. I., Journat of Glinical Pathology,
`1959~ 12, 228.
`Atkin, N. B., Boddington~ M. M., and Spriggs, A. I., Nature, 1962, 195~
`394.
`
`Letter from . . . South Australia
`
`Birth Pangs of Medibank
`
`PHILIP RHODES
`
`British Medicalffournal, 1975, 2, 493-494
`
`Medibank is the major excitement on the medical scene. It is
`the strange name of the new health service funded from govern-
`ment taxes. The new system will begin on 1 July but such are
`the complexities of Australian government and politics that,
`though Medibank will begin on that day, it will only be effective
`in South Australia, Tasmania, and Queensland. The first two
`have Labour governments in tune with the federal government
`of Mr. Gough Whitlam, and Queensland has a fiery premier who
`does not like the central government, but who is willing to take
`any generosity which is handed out to his state. The states with
`the largest populations, New South Wales, Victoria, and
`Western Australia, have not yet decided whether to join the
`national scheme. There have been political cries for rejecting
`the scheme outright, and one or two of the leaders of the
`opposition parties have tentatively tried to use the issue to force
`a general election.
`
`Faculty of Medicine, University of Adelaide, Adelaide, South
`Australia
`PHILIP RHODES, F.R.C.S., F.S.C.O.G., Dean
`
`Mr. Whitlam has let it be known that he would be delighted
`to accept this part!cular challenge. He is sure he would win.
`Nevertheless, he does not want an election at all and wishes to
`run his full term. The last election was not long ago, and
`though the people appear to be heartily sick of the national state
`politicians with their posturings, vapourings, and attempts to
`drum up causes for no other purpose than to harass their
`opponents, there seems to be no desire to go through all the
`paraphernalia of an election this year. Meanwhile, there is the
`usual anxiety that the politicians fiddle as the country rushes to
`perdition, mainly because of inflation.
`The present system of health care is essentially one in which
`the patient pays the doctor on a fee-for-item-of-service basis. The
`doctor can charge what he likes, but usually sticks to the rates
`agreed nationally. The padent pays the fee, and if he is insured
`he can recover almost all of it. The insurance funds are separate
`from those of government. They function well for those who can
`afford to insure. The rates of premium are fiat ones, and they
`cover whole families, or only a single person. The poorer
`sections of the community, therefore, inevitably pay a larger
`percentage of their disposable income in health insurance than
`the richer. And the Medibank advertising stresses that over one
`million people in the country are not covered by health insurance.
`They gamble on remaining healthy, for if they fall ill they may
`have to face enormous bills. Even if they go into hospital to
`avoid paying a general practitioner’s fee they still have to pay
`
`Sandoz Inc.
`Exhibit 1030-0004
`
`JOINT 1030-0004