MELANOSIS COLI
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53 MELANOSIS COLI delayed-as in pernicious anaemia; (8) we have exceptionally seen pernicious anaemia in a girl of 19 ; three of our cases of achrestic anaemia were over 60 ; (9) the patients may not have survived long enough to show nervous complications, which are notable only in a proportion of true pernicious anaemia patients ; (10) none of our cases had any haemorrhage, in fact when discussing the differential diagnosis we state that the presence of hemorrhage suggested aplastic anaemia. Dr. Zanaty in a letter in your issue of Dec. 18th has explained what he means by " macroblast." Apparently he feels that since the distinction between " macroblast " and " megaloblast " is difficult in histo- logical sections of bone-marrow, the " megaloblasts " in the bone-marrow of our cases of achrestic anaemia might have been " macroblasts." We agree that it is much easier to distinguish primitive cells of the normoblast series (macroblasts) from primitive megalo- blasts in smears of sternal puncture material than in histological sections, but the histological picture of the femoral bone-marrow (which we examined in our cases) is highly characteristic in pernicious anaemia and, in our experience, quite easily dis- tinguished from that of pseudo-aplastic anaemia; this difference is quite irrespective of terminologies and we refer Dr. Zanaty to the descriptions of Turnbull.3 3 The histological structure of the bone- marrow in our cases of achrestic anaemia resembled that of pernicious anaemia and not that of the commoner pseudo-aplastic anaemia; hence our suggestions about its aetiology. The occurrence of typical megaloblastic hyper- plasia-as judged by sternal puncture material-in cases of megalocytic anaemia resistant to liver therapy has been reported by Dameshek and Valentine 4 (1937) ; we have noted such a case ourselves and correlated it with typical histological changes in the femoral marrow exactly like our reported cases of achrestic anaemia. It will be seen that Dr. Zanaty’s cases differ in many respects from our cases of achrestic anaemia ; on the other hand, they fit very well the published descriptions of pseudo-aplastic anaemia, and we have little doubt that he has correctly diagnosed them as such. Since they are not examples of achrestic anaemia, we feel that his criticisms of our suggestions as to the aetiology of this anaemia are not valid. We are, Sir, yours faithfully, JOHN F. WILKINSON, M. C. G. ISRAËLS. Department of Clinical Investigations and Research, Royal Infirmary, Manchester, Dec. 20th, 1937. MELANOSIS COLI To the Editor of THE LANCET SIR,-I was pleasantly surprised to receive a reprint from Sir Arthur Hurst of an article in Guy’s Hospital Reports on melanosis coli 5 in which he states that " the chief causative factor is not constipation, nor conversion of a constituent of anthracene laxative into melanin, but the artificial diarrhoea produced by aperients of any kind taken on account of constipa- tion." In 1933, in collaboration with J. H. Willard and Joseph Bank,6 I reported 41 cases of melanosis coli diagnosed by sigmoidoscopy. Since Hurst quotes this article at length and minimises the significance of the anthracenes in their aetiological relationship to 3 Turnbull, H., in Vaughan’s The Anæmias, 2nd ed. Oxford, 1936. 4 Dameshek, W., and Valentine, E. H., Arch. Path. 1937, 23, 159. 5 Hurst, A. F., Guy’s Hosp. Rep. 1937, 87, 332. 6 Bockus, H. L., Willard, J. H., and Bank, J., J. Amer. med. Ass. 1933, 101, 1; Lancet, 1933, 2, 877. melanosis coli, I feel that some comment should be made on his argument. We found that in every patient from whom a detailed laxative history could be obtained (35 cases), one of the anthracene com- pounds had been used over long periods. It was stated at that time that the anthracene laxatives contain resinous substances and " in the form usually dispensed contain some pigment matter which seems intimately related to the active principle. It seems highly probable that the anthracene laxatives either contain pigment or elaborate a pigment within the colon, which is phagocytised by the deep mucosal cells, causing melanosis coli. Whether melanosis coli can develop in individuals who have not taken any of the anthracene laxatives it is impossible to state. The use of some of the laxatives in the anthracene group dates back to antiquity." Hurst writes that " the diarrhoea results in excessive putrefaction of protein throughout the colon," and concurs in the opinion expressed by Pick that the melanin results from aromatic protein decomposition products of the contents of the colon under the influence of an oxidative ferment produced by the connective tissue cells of the mucosa. I do not see how it is possible to deny this mechanism for melanin deposits in the bowel, but he has added nothing to prove it. His claim that any aperient capable of causing diarrhoea may result in melanosis is based upon 2 case reports. The first patient had taken senna pods (an anthracene laxative) for sixteen years. No mention was made of the type of aperient used in the second case ; apparently the essayist was unable to determine the laxative or laxatives employed. Obviously one cannot set aside a clinical experience in 35 patients with melanosis coli, who had used one of the anthracenes, on any such evidence. We analysed a separate group of 300 patients with constipation without evidence of melanosis. Only 12-3 per cent. of this group had used one of the anthracenes. Most of the patients had been taking non-anthracene laxatives for years, sufficient to cause a soft evacuation, yet melanosis did not occur. Possibly the statistics of some observers giving a rather high incidence of melanosis coli, proximal to colonic carcinoma have been somewhat responsible for Hurst’s views. Macroscopic evidence of melanosis coli in cancer of the colon has been exceedingly rare in our experience. Even though one admits its frequent occurrence in bowel cancer, there is nothing in the literature to indicate that the melanosis in these cases may not have resulted from the use of one of the popular anthracene laxatives. Sir Arthur Hurst has not presented sufficient proof to cause one to abandon the part played by the anthracenes in the production of melanosis coli. It is my feeling that diarrhoea in association with ordinary putrefactive changes is probably not the cause of this condition. I am, Sir, yours faithfully, H. L. BOCKUS. WANTED SPECIMENS OF NORMAL SEMEN To the Editor of THE LANCET SiB,—The obtaining of material for research is a perennial difficulty. At the present moment I happen to be associated with Mr. B. P. Wiesner, Ph.D., on an investigation of changes in the semen occurring in various types of male infertility. Our chief difficulty at the outset is to obtain sufficient speci- mens of semen, to serve as " controls," from those who have produced families. I would like to bring particularly to the notice of the staffs of hospitals for
Transcript of MELANOSIS COLI
53MELANOSIS COLI
delayed-as in pernicious anaemia; (8) we haveexceptionally seen pernicious anaemia in a girl of
19 ; three of our cases of achrestic anaemia were over60 ; (9) the patients may not have survived longenough to show nervous complications, which are
notable only in a proportion of true perniciousanaemia patients ; (10) none of our cases had anyhaemorrhage, in fact when discussing the differentialdiagnosis we state that the presence of hemorrhagesuggested aplastic anaemia.Dr. Zanaty in a letter in your issue of Dec. 18th
has explained what he means by " macroblast."
Apparently he feels that since the distinction between" macroblast " and " megaloblast " is difficult in histo-logical sections of bone-marrow, the " megaloblasts "in the bone-marrow of our cases of achrestic anaemiamight have been " macroblasts." We agree that itis much easier to distinguish primitive cells of thenormoblast series (macroblasts) from primitive megalo-blasts in smears of sternal puncture material than inhistological sections, but the histological picture ofthe femoral bone-marrow (which we examined inour cases) is highly characteristic in perniciousanaemia and, in our experience, quite easily dis-
tinguished from that of pseudo-aplastic anaemia;this difference is quite irrespective of terminologiesand we refer Dr. Zanaty to the descriptions ofTurnbull.3 3 The histological structure of the bone-marrow in our cases of achrestic anaemia resembledthat of pernicious anaemia and not that of thecommoner pseudo-aplastic anaemia; hence our
suggestions about its aetiology.The occurrence of typical megaloblastic hyper-
plasia-as judged by sternal puncture material-incases of megalocytic anaemia resistant to liver therapyhas been reported by Dameshek and Valentine 4(1937) ; we have noted such a case ourselves andcorrelated it with typical histological changes inthe femoral marrow exactly like our reported cases ofachrestic anaemia.
It will be seen that Dr. Zanaty’s cases differ in
many respects from our cases of achrestic anaemia ;on the other hand, they fit very well the publisheddescriptions of pseudo-aplastic anaemia, and we havelittle doubt that he has correctly diagnosed them assuch. Since they are not examples of achresticanaemia, we feel that his criticisms of our suggestionsas to the aetiology of this anaemia are not valid.
We are, Sir, yours faithfully,JOHN F. WILKINSON,M. C. G. ISRAËLS.
Department of Clinical Investigations and Research,Royal Infirmary, Manchester, Dec. 20th, 1937.
MELANOSIS COLI
To the Editor of THE LANCETSIR,-I was pleasantly surprised to receive a
reprint from Sir Arthur Hurst of an article in Guy’sHospital Reports on melanosis coli 5 in which he statesthat " the chief causative factor is not constipation,nor conversion of a constituent of anthracene laxativeinto melanin, but the artificial diarrhoea produced byaperients of any kind taken on account of constipa-tion." In 1933, in collaboration with J. H. Willardand Joseph Bank,6 I reported 41 cases of melanosiscoli diagnosed by sigmoidoscopy. Since Hurst quotesthis article at length and minimises the significanceof the anthracenes in their aetiological relationship to
3 Turnbull, H., in Vaughan’s The Anæmias, 2nd ed. Oxford,1936.4 Dameshek, W., and Valentine, E. H., Arch. Path. 1937,
23, 159.5 Hurst, A. F., Guy’s Hosp. Rep. 1937, 87, 332.
6 Bockus, H. L., Willard, J. H., and Bank, J., J. Amer. med.Ass. 1933, 101, 1; Lancet, 1933, 2, 877.
melanosis coli, I feel that some comment should bemade on his argument. We found that in everypatient from whom a detailed laxative history couldbe obtained (35 cases), one of the anthracene com-pounds had been used over long periods. It wasstated at that time that the anthracene laxativescontain resinous substances and " in the form usuallydispensed contain some pigment matter which seemsintimately related to the active principle. It seems
highly probable that the anthracene laxatives eithercontain pigment or elaborate a pigment within thecolon, which is phagocytised by the deep mucosalcells, causing melanosis coli. Whether melanosiscoli can develop in individuals who have not takenany of the anthracene laxatives it is impossible tostate. The use of some of the laxatives in theanthracene group dates back to antiquity."
Hurst writes that " the diarrhoea results in excessiveputrefaction of protein throughout the colon," andconcurs in the opinion expressed by Pick that themelanin results from aromatic protein decompositionproducts of the contents of the colon under theinfluence of an oxidative ferment produced by theconnective tissue cells of the mucosa. I do not seehow it is possible to deny this mechanism for melanindeposits in the bowel, but he has added nothing toprove it. His claim that any aperient capable ofcausing diarrhoea may result in melanosis is based
upon 2 case reports. The first patient had takensenna pods (an anthracene laxative) for sixteen
years. No mention was made of the type of aperientused in the second case ; apparently the essayistwas unable to determine the laxative or laxatives
employed. Obviously one cannot set aside a clinicalexperience in 35 patients with melanosis coli, whohad used one of the anthracenes, on any suchevidence. We analysed a separate group of 300
patients with constipation without evidence ofmelanosis. Only 12-3 per cent. of this group hadused one of the anthracenes. Most of the patientshad been taking non-anthracene laxatives for years,sufficient to cause a soft evacuation, yet melanosisdid not occur.
Possibly the statistics of some observers givinga rather high incidence of melanosis coli, proximalto colonic carcinoma have been somewhat responsiblefor Hurst’s views. Macroscopic evidence of melanosiscoli in cancer of the colon has been exceedingly rarein our experience. Even though one admits its
frequent occurrence in bowel cancer, there is nothingin the literature to indicate that the melanosis inthese cases may not have resulted from the useof one of the popular anthracene laxatives.
Sir Arthur Hurst has not presented sufficientproof to cause one to abandon the part played by theanthracenes in the production of melanosis coli.It is my feeling that diarrhoea in association withordinary putrefactive changes is probably not thecause of this condition.
I am, Sir, yours faithfully,H. L. BOCKUS.
WANTED SPECIMENS OF NORMAL SEMEN
To the Editor of THE LANCETSiB,—The obtaining of material for research is
a perennial difficulty. At the present moment I
happen to be associated with Mr. B. P. Wiesner, Ph.D.,on an investigation of changes in the semen occurringin various types of male infertility. Our chief
difficulty at the outset is to obtain sufficient speci-mens of semen, to serve as
" controls," from thosewho have produced families. I would like to bringparticularly to the notice of the staffs of hospitals for
