Daya, H.

Horwitz, M.

Shapiro, N.

English

AJOL - African Journals Online

1008 S.A. TYDSKRIF VIR GENEESKUNDE 12 November 1966duced in hyperthyroid patients by injection of acetyl Bmethyl choline.'Some other points about atrial fibrillation which shouldbe remembered are:(i) In the early stages of the disease it is apt to beparoxysmal in occurrence.(it) It is less well controlled by digitalis than fibrillationin euthyroid patients.(iil) As in this case it may disappear spontaneously asthyroid function returns to normal on medicaltherapy. If it persists, it may be abolished byquinidine.SUMMARYThe association of hyperthyroidism and atrial fibrillationin a 28-year-old man is reported. When methimazoletherapy caused clinical euthyroidism, the atrial fibrillationceased. There was no eVidence of underlying hypertensive,coronary, val~ar or other forms of cardiac disease.Subtotal thyroidectomy wa~ performed and the patient isnow well and at work. It IS sug.g~sted that this case is avery rare example of hyperthyrOIdism causing atrial fibril-lation at so young an age as 28 years.I wish to th~nk Dr. R. 1':lurok, Medic~1 Superintendent ofSomerset Hospital, for pefIDlSSlOn to publish; Dr M Horwitzfor e,;er:wiIling ~ncouragement and adyice; Dr. R. HOffenbergfor hiS mter~t III the ~ase;. the PhySICS Department GrooteSchuu! Hospital .for radioactive studies; and Dr. A. S~mie forrefernng the patient.REFERENCESI. Hoffenberg, R. (1966): Personal co=unication.2. StanbuTY. J. B. and Irvine. \V. G.: Personal communicafo3. Attsehull, M. n. (1945): New Engl. J. Med., 233,265. 1 n.STREPTOCOCCAL PHARYNGITIS AND SYSTEMIC LUPUS ERYTHEMATOSUSM. HORWlTZ, B.Sc., M.D. (CAPE TOWN), M.R.C.P. (LaND.), . SHAPIRO, M.B., B.CH. (RA n), Department ofMedicine, University of Cape Town, AND H. DAYA, M.B., CH.B. (CAPE TOWN), Resident Medical Officer,Somerset HospitalThe aetiology of systemic lupus erythematosus (SLE) re-mains unknown and it is thus conceivable that the causemay differ from case to case. It has been suggested thatthere may be an inherent host abnormality, possiblygenetic, predisposing to abnormal immunological reacti-vity, and that extrinsic factors might precipitate the onsetof clinical features. l ,' The disease has a tendency to acuteexacerbations and Marian W. Ropes' in the WaIter BauerMemorial Issue of Medicine in 1964, considers it impera-tive 'to determine the regime which will lessen the ten-dency to acute exacerbation and hasten remission'.A 17-year-old girl, with a family history of rheumatoidarthritis, developed chronic polyarthritis followed by floridSLE. There was concomitant clinical and bacteriologicalevidence of streptococcal pharyngitis. This associationmight be coincidental and irrelevant but alternatively itcould be the clue to an important precipitating factor inthis particular case of SLE. The purpose of this paper isto report the association, and draw attention to thepossible therapeutic implication of prophylactic penicillintherapy.CASE REPORTA 17-year-old schoolgirl, while studying for her matricula-tion examination, developed chronic p;1lyarthritis in Sep-tember 1965. She did not complain of a sore throat, but inDecember 1965 her throat and tonsils were noted as 'red'and 'inflamed' by her general practitioner and also at themedical outpatient department.Owing to interest in the possible role of streptococci inrheumatology, the investigations inc:uded a throat swab,which was negative, and the serum {,ntistreptolysin-O-titrewhich was found raised to 333 Todd units. The haemo-globin was 10 G /lOO ml., ESR 40 m~l./hr. (Westergren),and the LE screening test was negative. Salicylates im-proved the arthritis, but she began to feel tired, listless,and ill. On 26 January 1966 she was given pheno:\ymethylpenicillin, 250 mg. 6-hourly for 10 days, in view of theraised ASO titre. However, her general health continuedto deteriorate with severe tiredness and weakness ano-rexia, loss of weight, and the appearance of an eryt'hema-tous rash on her face. On 9 February left-sided pleurisydeveloped and she was admitted on 17 February. Hermother has chronic rheumatoid arthritis and is known toone of us (M.H.).She looked ill and her temperature was lOO°F. Anerythematous rash was present on the 'butterfly' area ofher face. The proximal interphalangeal and wrist jointswere slightly swollen. The tonsils were enlarged andslightly inflamed. A left pleural effusion was present. Thepulse rate was lOO/min. No other clinical abnormalitieswere noted. The blood pressure was 110/65 rnm.Hg.Urinalysis showed a 1+ proteinuria. .Chest X-ray confirmed the presence of a left pleuraleffusion, with some cardiac displacement to the right. Onaspiration, it was a serous exudate with protein 3-6 G /lOOrnI., scanty polymorphs, but no growth on culture. Anelectrocardiograph showed non-specific T-wave flattening.The ESR was 113 mm./hr. (Westergren), haemoglobin9 G/lOO m!., pev 28%, WBC 2,300/cu.mrn. with 62%neutrophils, 32% lymphocytes, 2% eosinophils, and 4%monocytes. Platelets were 44,OOO/cu.mm. Blood urea was75 mg./100 rnI., serum albumin 4-4 G /lOO ml., serumglob~l~n 2·5 G /100 ml., thymol turbidity 4 units, zincturbIdity 10 units, and gammaglobulins were raised on theelectrophoretogram. Blood culture yielded no growth andsputa were normal. The latex fixation test and the SLElatex agglutination test were negative. Throat swab yieldeda P?or .growth of beta-haemolytic streptococci, sensitive topemcillm, streptomycin, erythromycin, novobiocin, andtetracycline. The antistreprolysin-O titre was 100 Toddunits.Management of SLE. On 18 February she was very ill witha tempera~re of 104°F, and prednisone therapy was com-!Uenced With a dose of 60 mg. daily. Her response andIIDprovement were prompt, dramatic, and progressive and all12 Tovernber 1966 S.A. MEDICAL JOURNAL 1009the clinical abnormalities disappeared. Proteinuria was nolonger detectable after a few days. The pleural effusion wasabsorbed and the ECG became normal. The haemoglobin roseto 11·2 G/100 rnl., WBC to 13,900/cu.mm., and platelets to204,OOO/cu.mm. The ESR fell to 7 mm./hr. (Westergren).Prednisone was reduced to 40 mg. daily from 20 February,to 30 mg. daily from 29 March when she was discharged,then to 20 mg. daily on 28 April, and to IS mg. daily on 23June. She has remained well as an outpatient with a repeatedlynormal ESR. Haemoglobin rose to 14·5 G/IOO m!., and therewas no proteinuria. There were no important side-effects fromprednisone therapy, except a transitory abdominal discomfortin March, which ceased after the addition of antacids. Theimprovement in renal involvement was particularly gratifying.The blood urea remained slightly elevated for 2 months, butfinally became normal (45 mg./IOO m!. on 23 February, 62mg./lOO ml. on 3 March, 54 mg.IIOO ml. on IS March, SImg.IIOO ml. on 22 March, 49 mg./ 100 ml. on 7 April, 40 mg./100 m!. on 21 April, and 29 mg.IIOO m!. on 9 June).ManagemenT of beta-haemolYTic sTreplOcoccal pharyngiTis.Erythromycin. 250 mg. 6-hourly, was given on 24 February for10 days. but throat culture on I March and 7 March vieldeda growth of beta-haemolytic streptococci again, still sensitiveto penicillin, streptomycin, chloramphenicol. tetracycline, ery-thromycin and novobiocin. Phenoxymethyl penicillin wasaccordingly gi\'en, 500 mg. 6-hourly from 11 March for 10days. As an outpatient she continues to receive 250 mg.phenoxynnethyl penicillin b.i.d. in an attempt at prophylaxisagainst recurrence of streptococcal pharyngitis (and subsequentpossible exacerbations of SLE). There have been no signs ofany 'drug reaction' and a subsequent throat swab was nega-tive. Amistrep:olysin-O titre in June was 100 Todd units.DlSCUSSIOlAlthough LE cells were not demonstrated, the clinical andlaboratory features were typical of SLE, including highpyrexia, polyarthritis, pleurisy with effusion, erythematousrash on the 'butterfly' area of the face, abnormal electro-cardiogram, renal involvement with proteinuria and slightazotaemia, anaemia, leucopenia, thrombocytopenia, andvery high ESR. Prednisone therapy led to a rapid andcomplete clinical and laboratory remission and the main-tenance dose in June was 15 mg. daily.When first seen at medical outpatient department inDecember 1965, 3 months after the onset of chronicpolyarthritis, which resembled early rheumatoid arthritis.she did not complain of a sore throat. However, observersnoted redness of the pharynx and tonsils and the anti-streptolysin-O titre was raised to 333 Todd units. InFebruary 1966 when she was admitted with florid SLE,the antistreptolysin-O titre had fallen to 100 Todd units.There was thus proof of recent infection by beta-haemo-lytic streptococci. The throat swab at medical outpatientdepartment was negative, but on and after admission cul-tures yielded beta-haemolytic streptococci on 3 occasions.Combining these clinical and bacteriological observations,the presumptive site of the streptococcal infection whichraised the antistreptolysin-O titre was the pharynx.The suggestion is being propounded that the strepto-coccal pharyngitis and the development of SLE wereneither coincidental nor fortuitous in this case, but thatthe streptococcal pharyngitis was the actual initiator ofthe SLE. She has a potential genetic 'soil', as her motherhas rheumatoid arthritis, and perhaps the streptococcalpharyngitis acted as the 'seed', the situation being analo-gous to that in rheumatic fever, and this possibly initiatedthe cl inical manifestations of SLE.Textbooks of medicine contain statements such as'patients may relate the onset of SLE to a local infection','and 'upper respiratory infections sometimes precede theinitial appearance of symptoms',' but give no more specificdetails. Moore and Lutz,' in a review of SLE in 1955.mentioned that 'an ordinary sore throat may have preci-pitated the illness', but also provide no further details.Ropes' accepts 'infections' as one of the major factorswhich can precipitate the onset of the initial attack ofSLE. On the other hand, authorities such as Dubois andTuffanelli,' Talbott and Moleres Ferrandis,' and McGeeHarvey er al.s are either unconvinced or unimpressed bythe possible role of infections as initiators of SLE.In thi case, it is not being suggested that the strepto-coccal pharyngitis acted as a non-specific 'infective stress'.It is rather postulated that the streptococcal pharyn-gitis acted as a specific initiator of SLE just as it is thespecific initiator of rheumatic fever in other patients.Rheumatic fever and SLE have pathological relationshipsand are sometimes classified together as 'connective tissuediseases' or 'collagen diseases'. Rantz er at: did investigateantistreptolysin-O titres in 6 cases of SLE in 1952, andfound them normal, but they do not state at what stageof the disease the investigations were done. If the first anti-streptolysin-O titre had not been requested in this casewhen she was still an outpatient before her admission,then its evanescent rise would have been mis ed.In 1953'0 LE cells were found in concentrated hepari-nized marrow preparations from 3 patients with severepenicillin reactions, and Kark and Pollak" include penicil-lin among the drugs best avoided in SLE. In this case.chronic polyarthritis and impaired general health werealready present before the first course of oral penicillinwas given at medical outpatient department, so it isunnecessary to incriminate penicillin in the pathogenesisof the SLE. When she was an inpatient, the second courseof penicillin therapy was only undertaken after muchconsideration, but was considered justifiable as the strepto-coccus was persisting in the pharynx in spite of erythro-mycin therapy. It did not cause any drug reaction orexacerbation of SLE, which continued to improve andremit during prednisone therapy.These considerations are not merely of theoreticalinterest. If streptococcal pharyngitis recurs in patients whohave had rheumatic fever, it is well known that there is ahigh incidence of recurrence of rheumatic fever, and hencethe value of prophylactic penicillin therapy in such cases.So, by analogy, phenoxymethyl penicillin is being con-tinued indefinitely in this case as an attempted prophylaxisagainst recurrences of streptococcal pharyngitis and thepossible serious exacerbations of SLE. This proceduremight constitute a major beneficial factor in her unknownprognosis.CONCLUSIONStreptococcal pharyngitis was detected in close relationshipto the onset of a case of SLE. The antistreptolysin-O titre wassignificantly raised to 333 Todd units. There was prompt andcomplete response to prednisone therapy which is being main-tained. It is postulated that the assnciation is not merelvcoincidental, but of significance, analogous to the role o'fstreptococcal pharyngitis in rheumatic fever. The beta-haemo-lytic streptococcus may have been the 'seed' on a genetically-determined 'soil' with a family history of rheumatoid arthritis.LEPTOSPIROSIS IN CAPE TOWNR. I. SAMSON, M.B., CH.B. (CAPE TOWN), Department of Medicine, University of Cape Town and Somerset HospiTal,'D T. S. PILLAY, M.B., CH.B. (CAPE TOWN), Somerset HospitalS.A. TYDSKRIF VIR GE 'EESKU 'DE1·9Conjugated bilirubin(mg. '100 ml.)]7·87-4441·2093·112 ovember 1966TABLE 1Total bilirubin(mg./100ml.)248·6591·5143·5052·00·5Dare30/ 9/654/10/659/10/6519/10/6526/10/651/l1/658/11/6511/11/6519/ I 1/65Foundation helped to ensure the continued study and docu-mentation of the possible role of streptococci in rheumatology.REFERENCESI. Burch. P. R. J. and Rowetl. N. R. (1965): Amer. J. Med., 38, 793.2. Beeson, P. B. and McDermott, W. (1963): Cecil.£oeb Textbook 0;Medicine, Illh ed. Philadelphia: W. B. Saundets.3. Ropes. M. W. (1964): Medicine (Baltimore). 43, 3 .4. Harrison, T. R. (1962): Principles 0; lmemal Medicille, 4th ed. NewYork: McGraw-Hill.5. Moore, J. E. and Lutz. W. B. (1955): J. Chron. Dis., I, 297.6. Duhois. E. L. and Tuffanelli, D. L. (1964): J. Arner. Med. Assoc.,190, 104.7. Talhott, J. H. and Moleres Ferrandis, R. (1956): Col/agen Diseases.London: Grune & Stratton.8. McGee Harvey, A., Shulman, L. E.. Tumulty. P. A .. Conlev, C. L.and Schoenrich, E. H. (1954): Medicine (Baltimore). 33. 291.9. Rantz, L. A.. Dicaprio, J. M. and Randatl, E. (1952): Amer. J.Med. Sci .. 224, 194.10. Walsh, J. R. and Zimmerrnan, H. J. (1953): Blood. 8. 6-.11. Kark, R. M. and Potlak, V. E. (1962): Arthr. and Rheum., 5, 524.112 units. SGOT 79 units. Blood urea 106 mg./lOO ml.Serum electrolytes: serum sodium 125 mEq. I., serum potas-sium 3 mEq./I., serum chloride 98 mEq./I., serum bicarbonate30·3 mEq./1.X-ray of the chest showed diffuse calcific foci throughoutthe lung fields with fibrosis, especially at the <.pices and a largebullae at the right apex.There were no acid-fast bacilli present in the sputum andthe blood Wassermann reaction was negative.In view of the association of jaundice, purpura, andpolymorphonuclear leucocytosis, leptospirosis wassuspected on admission. On 30 September 1965, leptospiralagglutination titre was 1/10,000 for Leptospira icterohae-morrhagica. Urine microscopy and guinea-pig inoculationwere negative.ManagementInitially, he was managed with the regime for livt:rfailure, namely oral eomycin and no proteins in the did.The following day, he was mentally much better and the'purpura was fading. Blood urea fell to 23 mg./IOO m\.on 4 October and remained normal thereafter. Neomycinwas discontinued and he was given a normal diet.The blood agglutination titre for leptospirosis wasrepeated on 19 October and had risen to a titre of1: 200,000. Urine microscopy and guinea-pig inoculationwere negative.On 26 October the CSF agglutination titre was 1: 300.The patient continued to improve clinically and theserum bilirubin decreased, with slight fluctuations (TableI).101050 little is known of the aetiology of 5LE that it is worthdrawing attention to a possible initiating factor in a particularcase.The suggestion is not merely of theoretic interest, but haspractical therapeutic implications. Oral phenoxymethyl penicil-lin therapy is being continued as attempted prophylaxis againstrecurrences of streptococcal pharyngitis. It is hoped that thismay improve the prognosis in this particular case of SLE.We wish to thank the Medical Superintendent, SomersetHospital, for permission to publish this case report; Dr. R. L.Peters for referring the patient to medical outpatient depart-ment and for his clinical observations; the Chemical Pathologyand Bacteriology Laboratories, UCT: the Haematology Labo-ratory, Groote Schuur Hospital: and Dr. E. Dowdle for thestimulus of his consultation in the management of this patient.Grants from the Staff Research Fund and the uffieldSpecial InveSTigaTionsThe urine contained bilirubin but at no stage was proteinuriapresent. Hb. 9 G/lOO m!.: WBC 20,OOO/cu.mm.: neutrophils76°~, lymphocytes J6°~: ESR 90 mm. in the first hour(Westergren). Blood smear-red blood cells were hypochromic,white blood cells were norma!. Platelet count 144,OOO/cu.mm.Prothrombin index 95%.Serum bilirubin: total 24·0 mg. / 100 m!., conjugated bili-rubin ]7·8 mg. /100 m!. Serum albumin 3-4 G /100 m!., serumglobulin 4·1 G /100 m!. Alkaline phosphatase 7 units. Thymolturbidity 24·0 units. Zinc turbidity 12 units. Serum amylaseThi case is presented because reports of leptospirosisdiagnose:! in life are very rare in South Africa.'"CASE REPORTA 53-year-old Coloured male was admitted to SomersetHospital on 29 September 1965. His occupation until 1950(not since) was as a labourer in the docks, cleaning theboilers in the tug-boats. In 1950, he developed bilateralpulmonary tuberculosis and was in a tuberculosis hospitalfor I year, and received antituberculous therapy for aperiod of I year and 9 months. Six months after leavinghospital he developed a sudden right hemiparesis. Untilthis present illness, he was walking about at home and inthe immediate vicinity. He is of poor social background,with a history of excess alcohol consumption.Present IllnessThis commenced suddenly on 20 September 1965. Hebecame anorexic and a companion noticed that he had ayellow discoloration of his eyes for the past week. He didnot observe any dark urine or change in the colour of hisstools; however, he is a very poor witness. No therapywas administered either before or during his presentillness. There was no history of headaches.Examination on AdmissionHe was drowsy, deeply jaundiced, apyrexial, and hadgeneralized purpura.There were no other abnormalities apart from pallor,clubbing of the fingers, long-standing right spastic hemi-paresis, and diminished movement of the right side of thechest with crepitations. There was no hepatomegaly.

Streptococcal pharyngitis and systemic lupus erythematosus

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Streptococcal pharyngitis and systemic lupus erythematosus

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