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the statement that displacement of the stomach resonance -,was pathognomonic of tumours in the latter situation.- 1

Mr. PEARCE GOULD, in reply, remarked that the case just 1referred to was somewhat unusual. All tumours of the small iomentum must push down the stomach, and the resonanceof that organ would not only be obscured but wouldre-appear below. ’

MEDICAL SOCIETY OF LONDON.

The Chemistry of Gout. IA MEETING of this society was held on March 26th, Dr.

F. T. ROBERTS, the President, being in the chair.Dr. A. P. LUFF read a paper on the Gelatinous form of

Sodium Biurate and its bearing on the Treatment of Gout.It was, he said, now a universally admitted fact thatthe deposition of sodium biurate was intimately related tothe gouty paroxysm. He strongly shared the view of thelate Sir William Roberts that uric acid when first introducedinto the blood existed solely as sodium quadriurate. It was,however, a very unstable body and soon changed into sodiumbiurate, which at first assumed the gelatinous modification;and this if not eliminated in the urine was slowly or rapidly(according to circumstances) changed into the almost in-soluble crystalline form, which by its deposition in thetissues caused the gouty paroxysm. If this change fromgelatinous to crystalline form could he delayed thegouty attack could be delayed or postponed. He hadfor some time been studying the effects exerted byvarious drugs on the conversion of the biurate into thecrystalline form. He had shown on previous occasions thatthe conversion was accelerated when the alkalinity of theblood was increased by means of sodium bicarbonate, whereasthe conversion was delayed and diminished when potassiumbicarbonate was used. He had now carried out a

similar series of experiments the results of which showed:(1) that sodium salts considerably accelerated the conversionof the gelatinous biurate into the crystalline variety and thattheir employment in the treatment of gout was apparentlynot desirable; (2) that potassium salts delayed the con-version of the gelatinous biurate into the crystalline formand also that when the conversion was once started it wasslowed by the presence of these salts; (3) that lithium salts,although they did not delay the initial conversion of thegelatinous biurate, yet when the conversion was once startedit was slowed by the presence of these salts and especiallyby the lithium carbonate ; (4) that piperazine did not delaythe initial conversion of the gelatinous biurate and butslightly slowed the conversion when once started ; and

(5) that lysidine, although it delayed the conversion of thegelatinous biurate into the crystalline form, yet when theconversion was once started it had practically no effect inslowing it. From the results of these experiments it appearedthat for the special purpose referred to in the treat.ment of gout the potassium salts were the most useful,that the lithium salts ranked next, and that piperazintand lysidine were not nearly so useful. These result;were entirely in accord with his clinical experience. HEdid not for one moment wish to contend that the beneficial action of the salts of the alkali metals in th.treatment of gout was to be solely gauged either by thei:solvent action on deposits of sodium biurate or by thei:inhibitory action on the conversion of the gelatinous biurateinto the crystalline form. Undoubtedly many of them weriextremely useful in the gouty state by their stimulatingeffect upon metabolism, by their remedial action upon thgastric and hepatic functions, by their diuretic action, an(

by diminishing the acidity of the urine. He feared that thpurport of a paper published by him in THE LANCET o

June llth, 1898, had been somewhat misunderstood i:this respect. He did not, however, question-still less deny-the utility of many of those drugs in the therapeutics c

gout, but he wished to point out that the oft-repeated statEment that most of these drugs were useful for their greasolvent action on gouty deposits was a loose and erroneonstatement which it would be wiser in future to avoicAnother important point demonstrated by his recent experments was that the higher the alkalinity of the blood froithe presence of sodium bicarbonate the more rapid and tbmore complete was the conversion of the soluble gelatinorbiurate into the comparatively insoluble and crystalline form!This point was of great interest, since he believed that tl

alkalinity of the blood of gouty patients was always higherthan the normal alkalinity of blood. This view was opposedto the prevailing one that gout was associated with an "aciddyscrasia." This latter opinion, however, so far as he couldascertain, was a pure assumption and had apparently neverbeen based upon any actual determinations of the alkalinityof the blood of gouty individuals. It received its first shockfive years ago when Klemperer showed by actual determina-tions of the blood of gouty subjects that the alkalinitywas not below that of healthy blood. He had since madea number of determinations of the alkalinity of the bloodof healthy and gouty individuals with the result that thealkalinity was higher than the average alkalinity of theblood of healthy individuals. The alkalinity of the bloodof healthy adults varied from 0’161 to 0’185 per cent. ofsodium carbonate, with an average of 0-167 per cent. Thealkalinity of the blood of gouty patients varied from 0’193to 0 251 per cent., with an average of 0’217 per cent., whichwas nearly one-third higher than that of normal blood.Since this increased alkalinity of the blood was due to ahigher proportion of sodium carbonate or bicarbonate, andsince these substances accelerated the conversion of the

gelatinous biurate into the crystalline variety, and thereforethe precipitation of the latter, it was intelligible why suchblood was prone to hasten and to augment the formation ofgouty deposits. The inference was, therefore, that thisincreased alkalinity determined the gouty paroxysm.

Dr. WILLIAM BAIN (Harrogate) read a paper on the Actionof Various Drugs and Diets on the Excretion of Nitrogen inGout. The object of his series of observations was todetermine if possible the variations in nitrogenous elimina-tion occurring in a case of gout under ordinary conditionsand to note the effect of different diets and certain drugs onsuch variations. For this purpose urea, uric acid, thealloxur bases, and ammonia were estimated in the urea toserve as a measure of the total nitrogenous changes ; theuric acid and alloxur bases to serve as a possiblesign of modified production of these bodies ; and theammonia as an indication of the general amount ofinorganic acid dealt with during the day’s metabolism.With regard to the origin of uric acid there were

two alleged sources: (1) it might be a derivative of thealloxur bases combined within the molecule of the nucleo-proteid of cells or similar substances in the food ; and (2) itmight be produced by synthetic processes in the liver orelsewhere from simple nitrogenous compounds, such as-

ammonia. The patient, a well-built man, aged 65 years, wasadmitted into the Leeds General Infirmary in November,1899, under the care of Dr. A. G. Barrs (to whom Dr. Bain wasindebted for the opportunity of investigating the case). The

family and previous histories were unimportant. The patienthad been suffering from severe and constantly-recurringattacks of gout for five years and there were very obvious goutychanges in the hands, feet, and other joints. He had no painin them excepting during the inflammatory attacks. The

large amount of deposit in a short time was specially remark-able. The abstemious habits of the patient and theabsence of gout in the family history were also note-

worthy. After describing the methods employed in esti-, mating the various substances Dr. Bain exhibited his results, in the form of a table. After sodium salicylate there was: only a slight increase in the uric acid. Under guaiacum. uric acid was markedly increased. It was thought that this

drug probably acted on the uric acid stored in the body rather; than by increased production. Iodide of potassium caused an: increase in the urea and uric acid. Vegetable diet increased; the uric acid. Dr. Bain also made reference to the experi-

ments of Minkowski which added much interest to hist estimation of the alloxur bases. This observer had adminis-

tered adenin to four dogs in doses varying from a quarter toE two grains several times a day. After two grains vomitingi ensued and the other symptoms noted were violent action ofthe heart, a heaving pulse, with an increase in blood-pressure.f The urine contained leucocytes, albumin, casts, and epithe-- lial cells. Three of the animals were killed about the fourtht day and the other one died. Post mortem crystals ofs biurate were found deposited in the renal tubules.. It was an interesting fact that this train of sym-- ptoms with deposition of biurate could be experi-11 mentally induced by one of the alloxur bases, and it

e suggested that one or more of them might be a factor in thes evolution of gout. Uric acid, on the other hand, had not!. been shown by experiment to produce any such symptoms.e With advancing knowledge it was possible that uric acid

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might be relegated to a secondary position in the causationof gout. It was to be regretted that this line of researchhad not been extended and it was unfortunate that pureadenin was almost impossible to obtain. Apart from xanthinthe amount of alloxur bases appearing in the urine was soexceedingly small that their separate estimation was a

matter of great difficulty. Dr. Bain suggested the possi-bility that the retention of adenin within the system mightdetermine the deposition of biurate in the tissues.

Dr. A. E. SANSOM confessed that he was still in a mazeof doubt as to the pathology of gout, though experimentsseemed to be elucidating some of the problems. There wasno doubt that the deposit of urates was the cause of a goutyattack ; but why should it, he asked, be afterwards got ridof in some cases but not in others ? 7 The absence of pain,too, in some cases was inexplicable. It seemed to himdoubtful whether those violent and destructive paroxysms ofacute gout sometimes observed could be explained whollyand solely by sodium biurate. Surely there must be some-thing that was associated with it which prevented metabolism.The subject of treatment also was beset with difficulty. Ifsodium salts promoted and potash salts delayed depositionwhy was it that they got such good results from the twotogether ? Piperazin in his experience did seem to do goodin some cases. Laboratory experiments were very useful,but they were still a long way off the truth.The PRESIDENT congratulated Dr. Luff on his welcome

and interesting researuhes. He had never thought verymuch of piperazin or lysidin in the treatment of gom and hehad mostly come back to the potash salts or a combinationof potash and soda. Dr. Bain’s case was an interesting oneand he remembered to have met with a case resembling this inthe extreme gouty development without anything to accountfor it, for the patient was both a teetotaler and a vegetarian.

Dr. A. P. LUFF, in reply, thought that the disappearanceof the deposit in some cases and not in others dependedupon the alkalinity of the blood. If this was high then theblood could not remove the deposits. The presence or

absence of pain in different cases depended, he believed, uponthe rapidity of deposition. It was the suddenness of thedeposition which caused the pain. Referring to the necrosisof certain tissues he doubted whether such a processoccurred in cases of true gout. He had never seen necrosisof cartilages in true gout, and he thought it possible thatthe alleged cases were rheumatoid arthritis on which acutegoat had supervened. Dr. Bain’s case bad been very care-fully investigated. He would like to know what were therelative lengths of time for the administration of thedifferent substances. He thought that in so many experi-ments in one patient the gouty state must have beenin different phases at different times. The fact that gua1acllmeliminated uric acid was quite, in keeping with his ex-

perience and that of Sir Alfred Garrod.’ Given in the formof resin it was certainly a prophylactic.

Dr. BAIN, in reply, mentioned the doses and duration ofthe administration of the different drugs. There was aninterval of three days between each, but the patient beganby being put on a fixed diet for nine days. He thought thequestion of pain would depend upon the structures that wereinvolved. As to the necrotic changes he quite agreed withDr. Luff. Dr. Chalmers Watson had found in chronic gouta myelocyte which was not to be found in normal blood, butDr. Bain had not found tbis in one case which he hadexamined. He quite agreed with Dr. Sansom that theremust be something besides the biurate to produce gout andhe had suggested that it might be adenin. The markedeffect which this had had upon the blood-pressure and theoccurrence of uric acid in the kidneys of Minkowski’s dogswere arguments in favour of this view.

CLINICAL SOCIETY OF LONDON.

A Case of Dermoid Cyst within the Spinal Canal.-Reductionof the Deformity of Spinal Caries by -Jfan?tal ect4 fication.A MEETING of this society was held on March 23rd, Sir

R. DOUGLAS PowELL, Bart., President, being in the chair.Dr. W. HALE WHITE and Mr. A. D. FRIPP communicated

a paper on a case of Dermoid Tamoar growing within theSpinal Canal in which an attempt was made to remove thegrowth. The patient was a man, aged 26 years, who had beensuffering from a very chronic form of Hodgkin’s disease.He was first seen by Dr. Hale White and Mr. Fripp withMr. A. F. Wilson at the end of March, 1899. In themiddle of January, 1899, the patient began to comp’ain

of loss of power in the legs. By the end of March therewas complete paraplegia without muscular wasting. Thebreathing was almost entirely diaphragmatic, the righthand was much stronger than the left, and all forms ofsensation were lost up to the level of the nipples ; therewas no hypera39thetic zone ; there was severe pain shootingdown both intercosto-humeral nerves and round the chestalong the second intercostal nerves, the lower limbs wererigid, the knee-jerks and plantar reflexes were exaggerated,and there was great superficial tenderness over the second,third, and fourth dorsal spine. There was incontinence ofurine with cystitis and obstinate constipation and greatdistension of the abdomen. The pulse was 120 and thetemperature generally was about 101° F. There were nosigns pointing to caries and aneurysm. The diagnosis wasthat there was some collection of fluid or a new growthwithin the spinal canal irritating the second dorsal nerveand compressing the cord below it. There was no evidencethat this was syphilitic or that it was malignant. Anexploratory laminectomy was performed, the second, third,and fourth dorsal arches being removed. A grey tumoursituated upon the outer surface of the dura mater was

exposed, which reached out of sight both above and below.Pieces of the growth were snipped away. The patientquickly rallied from the operation and the wound healedby first intention. The tumour proved on microscopicalexamination to be a dermoid cyst. The patient was

seen again by Dr. Hale White and Mr. Fripp eightweeks later. The pulse and the temperature were normal.There was slight and occasional voluntary movementin the legs. The exaggeration of the knee-jerks was

less and the rigidity had disappeared. There was

almost complete return of all forms of sensation downto the groins, but no improvement in the lower extremities.The radiating pains had disappeared. The chest movedbetter. The cystitis and incontinence had disappeared andthe constipation and abdominal distension were less. Therewas a large bedsore on the sacrum and another on thebuttock. Considerable as had been the improvement it

appeared to Dr. Hale White and Mr. Fripp that as

much of the tumour had been left behind, and as the

pressure symptoms were far from completely relieved,the only chance of benefiting the patient lay in a

further attempt at complete removal. A second opera-tion was performed. A large mass of the tumour wasfound to have grown backwards through the gap in the

spinal canal made at the first operation. The first, fifth,and sixth dorsal laminae were removed, but still no limitcould be seen to the growth. The patient rallied wellbut sank again eight hours after the operation.-The PRE-SIDENT remarked that the case was of interest as bearingon the question how far interference was justifiable in casesof this kind.-In reply to the President, Dr. HALE WHITEsaid that the case was unique as regarded the nature, thoughnot as regarded the position, of the tumour. Cases ofdermoid cysts had been recorded in the middle line betweenthe skin and the spines, but not within the spinal canal.Mr. ROBERT JONES (Liverpool) and Mr. A. H. TUBBY com-

municated a paper on the Reduction of the Deformity ofSpinal Caries, based on 99 cases of angular deformity fromPott’s disease treated by Manual Rectification, including theresults of the 25 cases which had been brought before theClinical Society of London in November, 1897. In this firstseries of 25 cases the following results had been obtained:five patients had died, four had discontinued treatment, 15were alive, well, and able to walk, and one was still re-

cumbent and sickly. As to the causes of death, one diedfour days after the operation, but post mortem no abnormalitywas found beyond some enlarged mesenteric glands;one died from tabes mesenterica 15 months after the

operation ; one died from pulmonary tuberculosis 16 monthsafrer the last stretching, one from intestinal obstructiontwelve months after, and one from diphtheria. Billroth,Menzel, Ja,S6, and Mohr estimated the death-rate from Pott’sdisease to be 25 per cent., the death-rate of the seriesobserved by Mr. Jones and Mr. Tubby being only 12 percent. Four of the cases developed abscesses, of whichtwo healed and one patient became paraplegic eightmonths after the operation, but had since recovered. Five ofthe 25 patients recovered from paraplegia as the immediateresult of the operation, recurrence taking place in one case.In five cases the curvature was practically obliterated andremained so with a spinal support, and the curve was muchimproved in ten of the cases. In a parallel series of non-recdaed cases three patients had died from tubercle, four