Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 95

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

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In obstructive jaundice Vaquez and Ribierre have also shown that the resistance of the red corpuscles is as a rule distinctly increased, an observation which we have been able to confirm.

Pathological Anatomy .-- Several individuals presenting the syndrome of hemolytic jaundice have come to necropsy (Vaquez, Giroux and Aubertin ; Oettinger; Gandy and Brulé; Widal and Joltrain; Roque and Chalier; Micheli; Möller; Wil- son; Tileston and Griffin). The cases of Vaquez, Giroux and Aubertin, Gandy and Brulé, Wilson, and Tileston and Griffin, were apparently of congenital origin; the others, probably acquired. In all cases, however, the essential features appear to have been general evidences of an hæmolytic process as

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JOHNS HOPKINS HOSPITAL BULLETIN.

manifested by a siderosis of liver, spleen and kidneys. The autopsy in the case of Vaquez and Giroux is of especial interest as it occurred in a congenital case in which death followed splenectomy, so that complications with other terminal pro- cesses were ruled out. The lesions which have been confirmed in the later cases, were as follows:

A marked congestion of the spleen especially confined to the pulp, the engorgement of which was in rather striking con- trast to the relative emptiness of the sinuses. There were few macrophages in the splenic pulp, more in the sinuses. The endothelial cells were stuffed with iron containing pigment.

The liver showed no evidence of biliary obstruction, no angio-cholitis. Many of the liver cells, especially in the centro-lobular zones, were, however, stuffed with large gran- ules of ochre pigment.

There was moderate siderosis of the cells of the convoluted tubules of the kidney, and marked hyperplasia of the marrow.

These observations have been confirmed, in great part, in all cases which have come to necropsy, affording thus abundant evidence of the hemolytic character of the process. The siderosis of the kidney, which is usually present, has, however, been very moderate in some instances, and was apparently absent in Gandy and Brule's case of congenital haemolytic jaundice, where death occurred in the course of a pneumonia as well as in Micheli's instance of the acquired form of the disease. In no instance was there evidence of biliary obstruc- tion.

Pathogenesis .- The pathogenesis of this remarkable syn- drome is by no means clear. The evidence of a chronic hæmolytic process is not so very different, indeed, from that which one sees in various other conditions, such especially as Addisonian or bothriocephalus anæmia, conditions in which chronic jaundice is not uncommon. The clinical picture in some of the acquired forms of the disease with crises of ag- gravation of the malady, may almost resemble paroxysmal hæmoglobinuria. Here, as Donath and Landsteiner have shown, there is in the serum a true auto-hæmolysin. But in paroxysmal hæmoglobinuria there is no evidence of a dimin- ished resistance of the red blood corpuscles .* In Addisonian anæmia, as has already been said, the resistance of the red blood corpuscles is usually increased.

On the other hand there is no evidence of a specific hæmo- lysin in these instances of jaundice associated with corpuscular fragility, so that one has been tempted to separate an hæmo- lysinic jaundice, such as the jaundice with pernicious anæmia or that seen with paroxysmal hæmoglobinuria, from the jaun- dice associated with corpuscular fragility, to which the name hemolytic has come to be applied-a deplorable complication of terms.

This is, however, not to say that the primary causal element

* It is true that Meyer and Emmerich believe that they have been able to demonstrate a diminished resistance of the red cor- puscles in paroxysmal hæmoglobinuria against changes of tem- perature, dilute acids and saponin. Meyer and Emmerich: Ueber paroxysmale Hæmoglobinurie. Deutsches Arch. f. klin. Med., Leipsig, 1909, XCVI, 287-327.

in some of the instances of so-called acquired haemolytic jes dice may not be the presence of toxic haemolytic substarts : the organism. Indeed, there is some reason to believe that t- may be the case. Troisier, for instance, in his recent s. advances various arguments in support of the hypothesis ts the fragility of the red corpuscles in these cases of hans'- jaundice is dependent upon the fact that they have dra: become sensitized by union with an hæmolytic amboceptcz.

However this may be, we are in the presence of a remake. clinical syndrome-acholuric, pleiochromic, jaundice, atx corpuscular fragility, granulation of the red corpuscles : vital staining, post-mortem evidences of blood destructive the form of siderosis of the liver, spleen and kidneys, atse. of evidence of the presence of hemolytic substances in t. serum.

Several questions naturally suggest themselves.

1. Where does the hæmolysis take place?

2. Where does the bilirubin circulating in the blood find' origin ?

3. What is the primary cause of this condition?

1. As to the manner and seat of the hæmolysis there tv: been varying opinions. Some (Minkowski, Chauffard, Vagy -! fancy that, gathered in the pulp of the spleen which, as : been seen, is always markedly engorged, the abnormally fra ;.: corpuscles are there destroyed. Others (Widal and his pup' are inclined to believe that the destruction occurs in the genes. circulation, the débris accumulating as it always does in t spleen, and accounting thus for the symptoms and manifests tions on the part of that organ. One observation, as pointe: out by Castaigne, is strongly in favor of the circulatory orit of the hæmolysis, namely, the siderosis of the kidneys, whi : is often demonstrable. Otherwise no important evidence cz be adduced in support of one or the other of these views which in the end, are essentially the same, excepting in so far as the. bear upon the second question.

2. The Cause of the Jaundice .- Most observers have be lieved the jaundice to be immediately hepatic in origin d: to the over-production of bile by a liver overstocked, $0 1: speak, with the products of blood destruction. The old idea that this was, in a sense, after all, an obstructive jaundi: owing to the inspissation of the bile and the engorgement c: the intra-hepatic bile passages, or to a diffuse intrahepati: cholangitis, must, however, be abandoned as a result of the clinical and pathological observations of some of these cases. If the hepatic origin of the jaundice be accepted, we must f. back upon the assumption of Minkowski, that the overworksi hepatic cell gives off a part of the excess of bile which i: produces into the capillaries, as well as into the bile passages.

Widal and his pupils, however, advance another hypothesis. which is in many ways inviting. Pointing out the rapidit with which jaundice follows experimental blood destruction in animals, they call attention to the lack of evidence of any inspissation of the bile, referring especially to one of thei: patients on whom a cholecystostomy was performed for sus- pected stone. The gall bladder and ducts were empty, and the bile which was discharged from the fistula in large quanti-

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emgly fluid. On the hand they observe that Langhans and Quincke have nstrated bilirubin in the seat of old hemorrhagic foci, Sabrazès and Muratet have observed the presence of in in cerebro-spinal fluid after cerebral hæmorrhage, hat Froin has shown that hæmoglobin may be changed iliary pigment in hemorrhagic exudates in the meninges 1 the pleura, observations which have been confirmed by in and Troisier, Widal and Joltrain and others. The in which various observers have demonstrated in the they believe to be due to a direct transformation from globin through bilirubin such as has been shown to occur morrhagic exudates (Troisier : Thèse). They point to ict that in cases presenting the syndrome of which we een speaking, despite the long-continued jaundice, there evidence of the ordinary symptoms of biliary retention, oms which they believe to be due to the action of biliary namely, pruritus, bradycardia and emaciation. Bile acids never been found in blood or urine. Nor do the red scles show the increased size and heightened resistance potonic salt solutions which Rist and Ribadeau-Dumas e to indicate an acquired tolerance for intoxication by holate of sodium. Everything, they think, points to the ice of a purely pigmentary cholæmia which, theoretically, easily arise in the blood itself. This is a conceivable ductive hypothesis. The objections based upon the ab- of hæmoglobin in the circulation, which have been against this idea are answered by Widal by the assump- of a destruction of the corpuscles so gradual that the ity of hæmoglobin is too small to be recognizable. It t be said, however, that the symptoms of ordinary biliary cation are never present, rare though they be, for itching en observed in one or two instances. On the other hand gument that the absence of these symptoms is evidence purely pigmentary character of the jaundice is based : false assumption, for King and Stewart have shown ; is, in fact, upon the bile pigment, that bradycardia s.

at the moment impossible to form a definite opinion his question. While all recognize the hæmolysis as the cause of the jaundice, the majority of observers still › a point of view similar to that of Vaquez and Auber- ich has been well summarized by Chalier. According the condition represents "a lesion of the blood of n cause terminating in destruction of the red blood les, in secondary splenic hyperplasia with the forma- an excess of iron-containing pigment and an over- ion of bile by the liver as a result of the superabun- { pigment to transform, and, consecutively jaundice." own words (Vaquez and Aubertin), " .... if the cause of hæmolytic jaundice is in an alteration of the immediate cause is without doubt an increased func- ¿tivity of the liver cell: there may exist, indeed, a wver-activity of the liver just as there exists a glyco- er-activity of the liver, and hemolytic icterus would an icterus through hepatic over-activity (' ictère par

hyper-hépatie ')." Their idea as to the manner in which the bile pigment enters the blood is doubtless similar to that ex- pressed by Leuret, " With the blood pigment modified by the spleen the hepatic cell proceeds to produce an excess of bili- rubin to a degree such that in certain cases it overflows and secretes bile at both poles : whence hepatogenous icterus "-es- sentially the idea of Minkowski. The question must be re- garded as still open, and there is much that would attract one to the hæmatogenous hypothesis of Widal, the argument in favor of this point of view being set forth strongly in the thesis of Troisier.

3. As to the third question, the primary cause of the cor- puscular fragility, a positive answer cannot be given.

In congenital hæmolytic jaundice it has generally been assumed that the fragility of the red blood corpuscles is an inherited defect. The red cell, it might be fancied, has here failed to acquire those powers of resistance which are ordi- narily gained in the first days of extra-uterine life, retaining permanently its original fragility. In the acquired forms of the disease the question is, however, by no means so simple. Widal, Abrami and Brulé, by intra-peritoneal injections of toluylendiamin, have produced in animals a jaundice with clinical and pathological phenomena similar to those observed in hæmolytic jaundice in the human being. . According to the dose, the process was more acute and severe, or slower and more gradual and persisting for a long period after the last injection of the poison. No hemolytic properties could be found in the serum. On the other hand the red blood cor- puscles showed a markedly diminished resistance to hypotonic saline solutions as well as a granulation on vital staining, while evidences of increased marrow activity were striking. The urine in some of these cases, however, contained bile pigment. Obstructive jaundice in animals results neither in anæmia, granular corpuscles, nor increased fragility. Indeed, the re- sistance of the red blood corpuscles is always normal or in- creased. Here, then, is a similar phenomenon produced pri- marily by a soluble toxic substance, and while in many in- stances in the human being, no such cause is apparent, in other cases, such as those occurring in malaria, syphilis and uncinariasis, the primary action of some circulating toxic substance would appear to be certain. It may be, as suggested by Widal, that the marrow, constantly called upon, ends by producing corpuscles less resistant than the normal. But under such circumstances we must fancy that some poisons have acted primarily on blood or marrow. What these may be we know not. The fever associated with paroxysmal aggrava- tions in some cases of acquired hemolytic jaundice is suggest- ive of an infection.

It is possible, then, that the corpuscular fragility as well as the granular corpuscles, the main stigmata of the syndrome, may sometimes be secondary to the action of some circulating toxic substance or substances.

Treatment .- Various essays have been made in the treat- ment of both congenital and acquired haemolytic jaundice. Widal and his pupils have shown clearly that the persistent administration of iron is the one method from which good

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results may be obtained. In the severe acquired forms rest in bed and the other adjuvants suitable for the treatment of any grave anæmia should be adopted. In congenital hæmo- lytic jaundice recovery is unknown, but a temporary improve- ment in the anemia may be obtained by persistent treatment with iron. In acquired haemolytic jaundice long continued treatment may result in apparent, perhaps, indeed, in com- plete recovery (Widal, Abrami and Brulé). This is a very important fact when one reflects upon the futility of treat- ment with iron in Addisonian anæmia, a malady which may so closely resemble this syndrome. *

* * *

The studies, then, of the last several years have brought out a fairly definite clinical syndrome, that of acholuric jaundice associated with splenomegaly and fragility of the red blood corpuscles. In its purest form this group of symptoms is manifested in a sharply defined disease picture, congenital, often familial splenomegalic jaundice. It is probable that many of Gilbert's cases of chronic simple jaundice with sple- nomegaly as well as of Hayem's infectious splenomegalic jaun- dice are examples of the disease.

A similar condition is, however, not infrequently met with in adult life. In these so-called acquired cases the symptoms are usually considerably more acute and severe than in the congenital malady.

The syndrome has, moreover, been found in a variety of other instances of non-obstructive jaundice associated with various infections or poisons.

What the essential primary element in these cases may be is not at present clear.

Most important for the moment is the recognition of those apparently idiopathic examples of acquired hæmolytic jaun- dice simulating pernicious anæmia, cholelithiasis, the so-called splenic anæmias, or, indeed, icterus gravis-most important because of the fact that the recognition and persistent treat- ment of some of these cases with iron may bring about a great improvement, and, perhaps, a permanent recovery.

The recognition of this syndrome has opened up again, and in an interesting manner, the question as to the possibility of a purely hæmatogenous jaundice.

The methods of studying the corpuscular resistance neces- sary for the diagnosis of such cases are, of course, too delicate for use by the busy practitioner, but they may be carried out easily in any well-equipped laboratory. One may hope that a re-investigation of some of the many instances of non-obstruc- tive jaundice by means of these methods of study may help to shed further light upon an interesting field of medicine.

ABRAMI, P. LITERATURE.

Nouveau cas d'Ictère hemolytique congenital et familial. Bull. et mém. Soc. med. d. hop. de Par., 1908, 3. s., xxvi, 329-335.

ARKWRIGHT, J. A.

Family group of cases of enlarged liver and spleen with jaundice. Edinb. M. J., 1903, n. s., xiil, 52-54. ARMAND-DELILLE et FEUILLIE.

Anémie splenomegalique avec fragilité globulaire. Bull. et mém. Soc. med. d. hop. de Far., 1909, 3. s., xxvil, 266-271. BARLOW, SIR T., and SHAW, B.

Inheritance of recurrent attacks of jaundice and of abdominal crises with hepato-splenomegaly. Trans. Clin. Soc., Lond., 1902, xxxv, 155- 163 ; also Med. Press and Circular, 1902, Ixxiil, 564.

BARTON, W. M.

Acquired hemolytic ictero-anemia ; Widals' syndrome. Am. J. M & 1910, cxl, 239-246. BASILE, G.

Gli itteri emolitici e l'infezione sifilitica. Il Policlinico, 1909, ITl .: prat., 1291. (Summary of the article of Gaucher and Giroux.) BÉNECH, E., et SABRAZÈS, J.

Ictère hemolytique chronique avec splenomegalle. Gaz. hebd di: med. de Bordeaux, 1909, xxx, 469-472.

BENJAMIN, E., and SLUKA, E.

Über eine chronische mit Ikterus einhergehende Erkrankung des Bitte Berl. klin. Wehnschr., 1907, xliv, 1065-1069.

. BERNARD, L.

A propos de l'origine syphilitique des Ictères splenomegaliques. B et mém. Soc. méd. d. hop. de Par., 1908, 3. s., XIV, 158. BERNARD, L., et TROISIER, J.

Sur un cas d'intoxication saturnine avec méningite, anémie et kthx Bull. et mém. Soc. med. d. hop. de Par., 1908, xxv, 3. B., 753-762 BETTMAN.

Uber eine besondere Form chronischen Ikterus. Muenchen !! Wchnschr., 1900, xlvii, 791.

BIGART.

Les ictères hemolytiques. J. de med. Int., Par., 1909, rill, 24-21.

BRULÉ, M.

Les ictères hemolytiques acquis. Thèse de Paris, 1909, nº 88 (vti full table of references).

BUÉ, V.

Les ictères du nouveau-né. Gaz. d. mal. infant. (etc.), Par, 1% x, 185-190. BURGERHOF.

Congénitale familiaire icterus. Geneesk. Bl. u. Klin. en Lab. T. è prakt. Haarlem, 1907-8, xiii, 241-266.

CADE.

Une famille d'ictériques ; cholemie familiale et ictères hemolyticis

Bull. et mém. Soc. med. d. hôp. de Par., 1908, 3. s., xxv, 421-429. CADE and CHALIER.

Ictère hemolytique et cholémie familiale. Lyon med., 1908, cxl, 930-95℃ CAMPANI, A., e FERRARI, G.

Sopra un caso d'ittero cronico infantile. Clin. Med., ital., 1908, Il. 394-407. CAPORALI, L.

I. Anemia splenica infantile. II. Ittero cronico congenito. Med. itel. Napoli, 1906, ili, 373-375. CASTAIGNE, J.

Le foie et le fer. Leurs rapports a l'etat pathologique. Presse Det. Par., 1906, xiv, 771; 785.

Les ictères hemolytiques avec siderose pigmentaire du fole. Bull 11 mém. Soc. med. d. hop. de Par., 1907, 3. s., xxiv, 1211-1216. Chronique. J. med. franc., 1910, 1v, 95.

Les ictères hemolytiques. J. med. franc., 1910, iv, 101-109.

CATHALA et DAUNAY.

Les hématies granuleuses, la résistance globulaire à la naissance et pendant les premiers jours. Compt. rend. Soc. de biol., Par., 1905 Ixiv, 801-803.

Recherches sur le sang et l'ictère simple du nouveau-né. Obstétrica Par., 1908, n. s., 1, 561-604.

CHALIER, J.

Les ictères hemolytiques. 8°, Lyon, 1909. These. (With an admirekk table of references to the literature.)

CHAUFFARD, A.

Maladies du fole, in Traite de med. (Charcot, Bouchard, Brissaudi. Par., 1892, ifi.

Ictère chronique dyspeptique avec cholurie minime et Intermittente Choluries sans ictère. Bull. et mem. Soc. med. d. hop. de Par., 1991 3. s., xvill, 444-449.

Pathogenle de l'ictère congénital de l'adulte. Semaine med., Par., 190%. xxvii, 25.

CHAUFFARD et RENDU.

La résistance globulaire normale chez l'adulte. Presse med., Par., 1901, xv, 345.

CHAUFFARD et FIESSINGER, N. Ictère congénital hémolytique avec lésions globulaires. Bull. et mém

Soc. méd. d. hôp. de Par., 1907, 3. s., xxiv, 1169-1184. Recherches experimentales sur les rapports entre l'hemolyse et les hématies granuleuses. Bull. et mém. Soc. med. d. hop. de Par., 3. 5. xxiv, 1367-1373.

Nouvelles recherches sur la genèse des hematies granuleuses. Compt rend. Soc. de blol., Par., 1907, 1xill, 672.

CHAUFFARD, A.

Les Ictères hemolytiques. Semaine med., Par., 1908, xxviii, 49-52; also Rev. gen. de clin. et de therap., Par., 1908, xxll, 84. Ikterus hæmolyticus. Allg. Wien. med. Ztg., 1908, lili, 462.

CHAUFFARD, A., et TROISIER, J.

Deux cas d'ictère hemolytique. Bull. et mém. Soc. med. d. hop. de Par., 1908, 3. s., xxv, 411-420. Contribution à l'étude des hemolysines dans leur rapport avec les anémies graves. Bull. et mém. Soc. méd. d. hop. de Par., 1908, 3. 8. xxvi, 94-105.

Des rapports de certaines anemies splenomegaliques avec l'ictère hémolytique congénital. Bull. et mém. Soc. méd. d. hop. de Par., 1909, 3. s., xxvii, 293.

CLAISSE et SOCQUET.

Insuffisance mitrale traumatique.

Asystolie. Gangrène des membres. Ictère hemolytique.

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JOHNS HOPKINS HOSPITAL BULLETIN.

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PRAHA HALBERLAE.

Über chronischen Ikterus. Berl. klin. Wehnschr., 1906, xlili, 1471-1474. OCKING, W. T.

A case of persistent jaundice of fifty years' standing. Quarterly Med. J., Sheffield, 1903, xi, 104.

ONNER, L. A., and ROPER, J. C.

The relations existing between bilirubinemia, urobilinuria, and uro- bilinemia. Tr. Ass. Am. Phys., Phila., 1908, xxiii, 222-245. JARRÉ, H.

Sur un cas d'anémie ankylostomiasique avec fragilitié globulaire et ictère hemolytique. Bull. Soc. path. exot. Par., 1909, 11, 97-101. 'HNI et ALEXIEFF.

De la résistance des globules deplasmatisées dans l'anémie. Compt. rend. Soc. de blol. Par., 1908, lxiv, 1101.

TIENNE, G.

Sur un cas probable d'ictère hemolytique. Rev. med. de l'est., Nancy, 1909, xll, 548-551.

ERRATA, A.

Über die klinische und morphologische Bedeutung der vitalfarbbaren Substanz und die basophile PunctIrung der Erythrocyten. Fol. hæma- tolog., Leipz., 1910, ix, I Th., 253-277.

EUILLIÉ, E.

Hemolyse, flux leucocytaires et ictère. Compt. rend. Soc. de biol., Par., 1908, 1xv, 626-628.

ESSINGER, N., et ABRAMI, P.

Les hematies a granulations ; procedes de coloration, valeur sem- éiologique. Revue de med., Par., 1909, xxix, 1-40.

OIN, G.

L'hématolyse anormale. Compt. rend. Soc. de biol., Par., 1906, Ixviii, 10-12.

NDY et BRULÉ, P.

Ictère hemolytique congenital, autopsie. hop. de Par., 1909, 3. s., xxviii, 369-375.

Bull. et mém. Soc. med. d.

UCHER et GIROUX.

Note préliminaire sur l'ictère hemolytique de la syphilis secondaire. Ann. d. mal. ven., Par., 1909, iv, 481-482. UCHER, E., et JOLTRAIN.

Purpura chronique de l'angiosclerose. Urobiligenie hemolytique locale. Urobilinhémie et urobilinurie. J. de med. int., Par., 1909, xil, 275-277. IHARDT.

Die Pathogenese des Ikterus. Muench. med. Wchnschr., 1905, III, 889- 392.

BERT, LEREBOULLET et HERSCHER.

Les trois cholémies congénitales. Bull. et mem. Soc. med. d. hop. de Par., 1907, 3. s., xxiv, 1203. (With abundant references to the liter- iture.)

BERT et LEREBOULLET.

Ja cholemie simple familiale. Son importance en pathologie. J. med. ranç., Par., 1910, iv, 110.

GEROT et SALIN, H.

ctère hemolytique acquis general et purpura avec ictère hemolytique ›cal, au cours d'une infection indeterminee. Arch. d. mal. du cœur etc.), Par., 1910, 111, 720-729.

LAIN, G., et TROISIER, J.

hysiologie pathologique de l'hematome pleural traumatique. La ligénie hemolytique locale. Semaine med., Par., 1909, xxix, 133. ontribution a l'etude des icteres hemolytiques locaux. Rev. de med., ar., 1909, xxix, 459.

KINS, C. P., and DUDGEON, L. F.

ongenital family cholæmia. Quart. J. Med., Oxford, 1908-9, 11, 165-177. EM, G.

ir une variete particuliere d'ictère chronique, ictère infectieux chro- que splenomegalique. Presse med., Par., 1898, vi, 121-125.

mivelle contribution a l'etude de l'ictère infectieux chronique spleno- igalique. Bull. et mem. Soc. med. d. hop. de Par., 1908, 3. s., XXV, 2-138.

HISON, R.

mily jaundice. Clin. J. Lond., 1909, xxxiv, 241-244.

HISON, R., and PANTON, P. N.

contribution to the study of congenital family cholæmia. Quart. Med., Oxford, 1908-9, 11, 432-437.

ESCO, H., et SALIGNAT.

fragilité globulaire varie-t-elle suivant que l'on opere sur le sang brine. fluore ou exalte? Compt. rend. Soc. de biol., Par., 1907, i, 778.

, F. H.

ioluric Jaundice. Proc. Roy. Soc. Med., 1910, iii (Clinical Section), ·

et LEVY-VALENSI.

nouveau cas d'ictère hemolytique congenital. Bull. et mem. Soc. I. d. hop. de Par., 1909, 3. s., xxvi, 219. G.

ro. emolitico della tuberculosi e funzione emolitica del fegato. Riv. eta di sc. med., Venezia, 1909, 1, 3-19.

J. H., and STEWART, H. A.

ct of the injection of bile on the circulation. . J. Exper. Med., N. Y., ), x1, 673.

NHALS.

· congenitalen Icterus mit kronischen Milztumor. Deutsches Arch. in. Med., Leipz., 1904, Ixxxi, 596-612.

LANDOUZY, L.

Anémie et ictère hemolytiques tuberculeux. Bacillo-tuberculose hémo- lysante, anémie grave et subictère, par fragilité globulaire chez un phthisique pulmonaire. Presse med., Par., 1910, xviii, 761.

LE GENDRE, P.

Ictère urobilinique chronique (durant depuis douze ans) chez un jeune homme de dix huit ans. Bull. et mem. Soc. med. d. hop. de Par., 1897, 3. s., xxiv, 457-459.

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 95

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189