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GASTRIC ACIDITY AND ITS SIGNIFICANCE
390 from it. A strong wind was blowing and at one time it seemed as if the fire might spread to involve the whole building ; but the efforts of the brigade were soon successful in confining it to the storeroom and the anatomy lecture theatre. Here the fire blazed furiously, the dry wood of the benches igniting readily, and before long flames were seen to be coming through the roof. In about an hour and a half, however, the fire was under control and subdued. It was feared at first that Prof. T. Walmsley’s room
laboratory in the tower would have been destroyed, but we understand that, apart from damage to the roof, there has been no other serious loss. Directly beneath the fire was the museum which contained a large and valuable collection of anatomical and pathological specimens. Though part of the the fire was damaged by breaking through in ceiling one place, it did not collapse and the contents of the museum were only slightly damaged. The building is now closed and in the hands of the salvage authorities.
and the
"
CORRESPONDENCE Advances in Allergy," London, 1931), and it is generally claimed that the acidity is lowered ; we (Dharmendra and Napier: Indian Med. Gaz., 1935, lxx., 301), however, found it increased; but admittedly our cases were not true allergic asthma nor was the analysis done at the time of an attack. I am, Sir, yours faithfully, L. EVERARD NAPIER, M.R.C.P. Lond.,
GASTRIC ACIDITY AND ITS SIGNIFICANCE
To the Editor
of THE
LANCET SIR,-Prof. Apperly’s paper in your issue of Jan. 4th will have been read by many with interest, as it is both stimulating and provocative. By the time this reaches you I feel sure you that will have received letters from others who can refute from experience some of the assumptions that Prof. Apperly makes from indirect evidence. You may, however, feel that my experience, in another country, is also worth
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-
Professor of Tropical Medicine. School of Tropical Medicine, Calcutta, Jan. 31st.
FAMILIAL CIRRHOSIS AND TELANGIECTASIA
recording.
To the Editor of THE LANCET There must be a mass of evidence on record to contradict the statement that "When the former SiR,—Iwas much interested in Dr. Parkes Weber’s [the red cell content of the blood] falls to about half paper on the familial tendency to development of or two-thirds normal (on the average) free acid discirrhosis and more especially in his reference You yourself have appears from the stomach." to the relationship between cirrhosis and telangiectasia made a mild protest against this statement in an of the Osler type. As Dr. Weber points out there annotation in the same issue. I will quote only have been many valuable papers on this disease, from a series of my cases that I am at the moment particularly by H. I. Goldstein, but it is remarkable analysing ; in a series of fractional gastric analyses on how few members of the profession are familiar with 33 Assam tea-garden coolies whose blood haemoglobin the condition. In a letter to THE LANCET (1933, content ranged from 17 to 45 per cent., mean 32 per i., 116) Goldstein said that there are "probably cent. (100 per cent.==13’75 grammes per 100 c.cm.), recorded to date about 110 or 120 families and about in 27 the maximum gastric acidity (free) was from 700 persons suffering from Rendu-Osler-Weber’s 25 to 90 c.cm. of N/10 hydrochloric acid per 100 c.cm., disease (heredofamilial epistaxis with or without in 2 it was 20 c.cm., in 3 there was free acid but less familial haemorrhagic telangiectasia) in the entire than 20 c.cm., and in 1 case only was there achloravailable medical literature of the world." When not In this last case at one considers that Osler’s original paper was written (histamine given). hydria the beginning of treatment the haemoglobin was 29 per in 1901 (and a family showing epistaxis was described cent. (4 g.), but it improved to 80 per cent. (11 g.) by Babbington in 1865) and, further, that cases have when a trace of free acid appeared in one sample been reported from all over the world, these figures are undoubtedly very small if they truly represent only (11 hours) in the fractional gastric analysis. Though I have always accepted the view that the incidence of this disease. From personal anaemia, per se, may lead to hypochlorhydria or even experience I have thought for some time that the achlorhydria, recent experience adds very little figures must be fictitiously low. During the past support to this view ; I will cite two cases actually six years I have personally observed 10 families in my wards at the moment: one is a case of hypersuffering from this disease, including in their number chlorhydria (maximum 75 c.cm. N/10 HCl) with 56 affected persons; all these people live in the 2’75 g. of haemoglobin (20 per cent.), and the other West Riding of Yorkshire and as far as I have been a case of hypochlorhydric microcytic anaemia in able to trace them the families are unrelated and have which, though the haemoglobin increased from 2’47 not been previously recorded. The wealth of clinical to 16’00 g. in three months, the maximum hydromaterial in Leeds is certainly remarkable, but it is chloric acid concentration only increased from 12 very unlikely that about 10 per cent. of all the cases to 14 c.cm. of familial telangiectasia in the world are living in ’None of our experience in this country suggests the West Riding. A considerable number of my that gastric acidity is diminished in a hot climate. cases have shown that the profession as a whole is The normal gastric acidity is higher than that usually unfamiliar with the condition and though several recorded in England and North America (Napiei of the patients have been transferred to me by Dr. J. T. and Gupta: Indian Jour. Med. Res., 1935, xxiii., 455), Ingram, others have come as cases of anaemia of There are of course other factors to be considered unknown origin, epistaxis, and even headache. but all Indians do not live on the traditional highlyr The association of telangiectasia with hepatic spiced diet, nor is the evidence conclusive that at cirrhosis is of great interest and I agree with Dr. Weber highly spiced diet leads to permanent hyperchlor that the telangiectasia is probably a congenitalhydria ; it may lead to gastritis, the final result o:f developmental dysplasia of the small blood-vessels, and that the cirrhosis may be the result of associated which is hypochlorhydria or even achlorhydria. in 3 theri the asthma, Regarding gastric acidity developmental dysbiotrophy of the liver. At the same time there can be no doubt that cirrhosis is are many references in the literature (e.g., Hurst : not an essential feature of this disease at any of its Brit. Med. Jour., 1930, i., 1138 ; and Bray: " Recen t
hepatic
.
.
.
,
-
laboratory in the tower would have been destroyed, but we understand that, apart from damage to the roof, there has been no other serious loss. Directly beneath the fire was the museum which contained a large and valuable collection of anatomical and pathological specimens. Though part of the the fire was damaged by breaking through in ceiling one place, it did not collapse and the contents of the museum were only slightly damaged. The building is now closed and in the hands of the salvage authorities.
and the
"
CORRESPONDENCE Advances in Allergy," London, 1931), and it is generally claimed that the acidity is lowered ; we (Dharmendra and Napier: Indian Med. Gaz., 1935, lxx., 301), however, found it increased; but admittedly our cases were not true allergic asthma nor was the analysis done at the time of an attack. I am, Sir, yours faithfully, L. EVERARD NAPIER, M.R.C.P. Lond.,
GASTRIC ACIDITY AND ITS SIGNIFICANCE
To the Editor
of THE
LANCET SIR,-Prof. Apperly’s paper in your issue of Jan. 4th will have been read by many with interest, as it is both stimulating and provocative. By the time this reaches you I feel sure you that will have received letters from others who can refute from experience some of the assumptions that Prof. Apperly makes from indirect evidence. You may, however, feel that my experience, in another country, is also worth
---
-.
-
-
Professor of Tropical Medicine. School of Tropical Medicine, Calcutta, Jan. 31st.
FAMILIAL CIRRHOSIS AND TELANGIECTASIA
recording.
To the Editor of THE LANCET There must be a mass of evidence on record to contradict the statement that "When the former SiR,—Iwas much interested in Dr. Parkes Weber’s [the red cell content of the blood] falls to about half paper on the familial tendency to development of or two-thirds normal (on the average) free acid discirrhosis and more especially in his reference You yourself have appears from the stomach." to the relationship between cirrhosis and telangiectasia made a mild protest against this statement in an of the Osler type. As Dr. Weber points out there annotation in the same issue. I will quote only have been many valuable papers on this disease, from a series of my cases that I am at the moment particularly by H. I. Goldstein, but it is remarkable analysing ; in a series of fractional gastric analyses on how few members of the profession are familiar with 33 Assam tea-garden coolies whose blood haemoglobin the condition. In a letter to THE LANCET (1933, content ranged from 17 to 45 per cent., mean 32 per i., 116) Goldstein said that there are "probably cent. (100 per cent.==13’75 grammes per 100 c.cm.), recorded to date about 110 or 120 families and about in 27 the maximum gastric acidity (free) was from 700 persons suffering from Rendu-Osler-Weber’s 25 to 90 c.cm. of N/10 hydrochloric acid per 100 c.cm., disease (heredofamilial epistaxis with or without in 2 it was 20 c.cm., in 3 there was free acid but less familial haemorrhagic telangiectasia) in the entire than 20 c.cm., and in 1 case only was there achloravailable medical literature of the world." When not In this last case at one considers that Osler’s original paper was written (histamine given). hydria the beginning of treatment the haemoglobin was 29 per in 1901 (and a family showing epistaxis was described cent. (4 g.), but it improved to 80 per cent. (11 g.) by Babbington in 1865) and, further, that cases have when a trace of free acid appeared in one sample been reported from all over the world, these figures are undoubtedly very small if they truly represent only (11 hours) in the fractional gastric analysis. Though I have always accepted the view that the incidence of this disease. From personal anaemia, per se, may lead to hypochlorhydria or even experience I have thought for some time that the achlorhydria, recent experience adds very little figures must be fictitiously low. During the past support to this view ; I will cite two cases actually six years I have personally observed 10 families in my wards at the moment: one is a case of hypersuffering from this disease, including in their number chlorhydria (maximum 75 c.cm. N/10 HCl) with 56 affected persons; all these people live in the 2’75 g. of haemoglobin (20 per cent.), and the other West Riding of Yorkshire and as far as I have been a case of hypochlorhydric microcytic anaemia in able to trace them the families are unrelated and have which, though the haemoglobin increased from 2’47 not been previously recorded. The wealth of clinical to 16’00 g. in three months, the maximum hydromaterial in Leeds is certainly remarkable, but it is chloric acid concentration only increased from 12 very unlikely that about 10 per cent. of all the cases to 14 c.cm. of familial telangiectasia in the world are living in ’None of our experience in this country suggests the West Riding. A considerable number of my that gastric acidity is diminished in a hot climate. cases have shown that the profession as a whole is The normal gastric acidity is higher than that usually unfamiliar with the condition and though several recorded in England and North America (Napiei of the patients have been transferred to me by Dr. J. T. and Gupta: Indian Jour. Med. Res., 1935, xxiii., 455), Ingram, others have come as cases of anaemia of There are of course other factors to be considered unknown origin, epistaxis, and even headache. but all Indians do not live on the traditional highlyr The association of telangiectasia with hepatic spiced diet, nor is the evidence conclusive that at cirrhosis is of great interest and I agree with Dr. Weber highly spiced diet leads to permanent hyperchlor that the telangiectasia is probably a congenitalhydria ; it may lead to gastritis, the final result o:f developmental dysplasia of the small blood-vessels, and that the cirrhosis may be the result of associated which is hypochlorhydria or even achlorhydria. in 3 theri the asthma, Regarding gastric acidity developmental dysbiotrophy of the liver. At the same time there can be no doubt that cirrhosis is are many references in the literature (e.g., Hurst : not an essential feature of this disease at any of its Brit. Med. Jour., 1930, i., 1138 ; and Bray: " Recen t
hepatic
.
.
.
,
-