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FLORENCE NIGHTINGALE BIBLIOGRAPHY
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hypertension is close. In such cases, however, hypertension may persist after removal of the tumour,3 despite the return of the level of urinary pressor amines to normal. It seems most probable that hypercases
of essential
tension due to the secretions of the tumour may itself initiate another, and usually irreversible, hypertensive mechanism which may be identical with that in essential hypertension. These facts could not be explained by assuming that excessive noradrenaline secretion is the cause of essential hypertension. J. W. LITCHFIELD. London, W.1. AGAMMAGLOBULINÆMIA SIR,—Dr. Bowley and Mr. Dunsford, in their letter of Nov. 13, express their doubt as to the blood-group of the patient described in the paper by Dr. Grant and Dr. Wallace (Oct. 2). As Dr. Grant and Dr. Wallace were so kind as to allow me to perform the serological investigations and used part of my report to them in their paper, I feel that I should make a few comments on the letter by Dr. Bowley and Mr. Dunsford. To save space, the authors quoted only a very brief part of my report and omitted what, in the eyes of hsematoserologists, would appear to be important findings. Their main purpose, however, was to give a succinct description of a highly intriguing clinical picture and to draw the attention of clinicians and pathologists to this condition which is probably more frequent than had been recognised in the past. I was grieved to note that Dr. Bowley and Mr. Dunsford could have entertained the idea that so primitive precautions for the determination of a blood-group as they suggest might have been omitted in a blood-transfusion laboratory. Surely these are pitfalls well-known to any hæmatoserologist and it has been the practice for many years in my laboratory to use group-0 serum routinely in the investigation of all samples submitted here. This investigation was not, of course, omitted in the case reported by Dr. Grant and Dr. Wallace, and to put the minds of Dr. Bowley and Mr. Dunsford at rest, I would like to mention that the cells of this patient were repeatedly investigated with a number of oc, &bgr;, and at least five different &bgr;&agr; (group 0) sera. One of the latter contained a potent immune oc. The investigation was performed at 4°C and 18°C and no agglutination was seen with any antiserum used on the cells. Absorption experiments were also performed using the patient’s cells and group-0 and group-A cells as controls. They showed clearly that oc was not taken up by the patient’s cells as the titre of the antiserum was found to be the same as the one found after the serum had been " absorbed with group-0 cells and was unchanged. Dr. Bowley and Mr. Dunsford seem to want to have it both ways. They seem to assume that the patient’s group was really A4 (or Ax, whatever one likes to call these subgroups), and they gloss over the fact that if this was really the case, one would have expected the serum of the patient to contain an antibody acting on all group-A cells, as many writers, amongst them Mr. Dunsford, have found. In a lecture given in Holland Mr. Dunsford suggested : " The sera of the same type [A4] have always been found to agglutinate A1, A2 and B cells at 20°C but not to react with group 0 cells." Again, to put the writers’ minds at rest, I would like to say that exhaustive tests for the presence of an anti-A On only one were performed using Ai, A2’ and A3 cells. occasion did we find a very weak reaction with an Ai cell at room-temperature, the " agglutinates " consisting of two to three cells and being completely broken up by a very gentle rocking of the slide. As the absence of an anti-A was the remarkable finding after the group of the patient had been determined to our full satisfaction, of a
3. Hamilton, M., Litchfield, J. W., Brit. Heart J. 1953, 15, 241.
Peart, W. S., Sowry, G. S. C.
of investigations were performed the same result. The sentence "... it is surely surprising that the anti-B agglutinins are unaffected." makes strange reading. Surely, science has still many surprises in store for all of us and it is my conviction that it is the first duty of a scientist to record his findings truthfully, even if they should surprise some of his colleagues. I am sure that Dr. Bowley and Mr. Dunsford will be still more surprised to learn that two further cases of agammaglobulinæmia are at present under observation who show the same type of behaviour. They will shortly be published by Dr. W. T. Cooke, who has kindly agreed to my mentioning these cases in this letter. One case is group 0 (tested with group-0 sera !) and has oc and no &bgr; (another surprise !). The other case is group A but lacks the &bgr; agglutinin. It is perhaps worth mentioning that this latter case was discovered when a specimen was routinely investigated for its blood-group. These cases constitute real exceptions to Landsteiner’s rule. I too am surprised at their dogmatic statement that .. such persons ... do not produce A substance in their saliva." I was not able to find any literature supporting this statement but we have (unpublished observation) investigated a patient whose blood-group satisfies all the criteria for an A4 but whose saliva contains group-A substance.
course,
a
great number
giving always
’
W. WEINER.
Birmingham.
FLORENCE NIGHTINGALE BIBLIOGRAPHY
have been entrusted by the Florence Nightingale International Foundation with the com pilation of A bibliography of the published writings of Florence Nightingale, together with a calendar of all her extant manuscripts and letters. I should be grateful if owners or custodians of any manuscripts or letters of Miss Nightingale would communicate with me with a view to the inclusion of their material in the forthcoming book. If it is possible to send the actual documents, these will be examined and returned without delay. In view of the large number of letters to be dealt with it is not proposed to copy them, but to compile a location list with a brief indication of the subject of each letter.
SIR,—I
The Wellcome Historical Medical Library, 183, Euston Road, London, N.W.1.
W. J. BISHOP.
EFFECTS OF CORTISONE AND CORTICOTROPHIN ON THE ADRENAL CORTEX SIR,—The article by Dr. Stoner and Dr. Whiteley, in your issue of Nov. 13, prompts us to add three further cases of patients who died during treatment with steroid hormones and whose adrenals were examined at necropsy. had suffered from rheumatoid arthritis was treated with cortisone 25 mg. q.d.s. for ten months, and then corticotrophin gel 80 mg. was given daily for two months. She died from cardiac failure and pneumonia, the corticotrophin having’been stopped three days before death. Section of the adrenals revealed that the cortical cells, especially the cells of the zona fasciculata. showed lipoid infiltration to an unusual degree-i.e., they were in the resting phase. A woman, aged 61, who had suffered from rheumatoid arthritis for twenty years, had been treated with aqueous corticotrophin (20 mg. q.d.s.) for one month when she developed pneumonia and died. Section of the adrenals showed that the cortical cells were depleted of lipoid granules-i.e., thev were in an active phase. A man, aged 53, who had suffered from rheumatoid arthritis for thirteen years and had been treated with cortisone for two months, died following pneumonia. Section of th adrenals showed degenerative changes in the cells of all three zones of the cortex with loss of nuclear staining and sometime complete dissolution of the cell ;the whole cortex was reduce in width and, in one adrenal, hmmorrhage had occurred into the cortex and peri-adrenal tissues. A woman,
aged 64,
for three years.
She
-
hypertension is close. In such cases, however, hypertension may persist after removal of the tumour,3 despite the return of the level of urinary pressor amines to normal. It seems most probable that hypercases
of essential
tension due to the secretions of the tumour may itself initiate another, and usually irreversible, hypertensive mechanism which may be identical with that in essential hypertension. These facts could not be explained by assuming that excessive noradrenaline secretion is the cause of essential hypertension. J. W. LITCHFIELD. London, W.1. AGAMMAGLOBULINÆMIA SIR,—Dr. Bowley and Mr. Dunsford, in their letter of Nov. 13, express their doubt as to the blood-group of the patient described in the paper by Dr. Grant and Dr. Wallace (Oct. 2). As Dr. Grant and Dr. Wallace were so kind as to allow me to perform the serological investigations and used part of my report to them in their paper, I feel that I should make a few comments on the letter by Dr. Bowley and Mr. Dunsford. To save space, the authors quoted only a very brief part of my report and omitted what, in the eyes of hsematoserologists, would appear to be important findings. Their main purpose, however, was to give a succinct description of a highly intriguing clinical picture and to draw the attention of clinicians and pathologists to this condition which is probably more frequent than had been recognised in the past. I was grieved to note that Dr. Bowley and Mr. Dunsford could have entertained the idea that so primitive precautions for the determination of a blood-group as they suggest might have been omitted in a blood-transfusion laboratory. Surely these are pitfalls well-known to any hæmatoserologist and it has been the practice for many years in my laboratory to use group-0 serum routinely in the investigation of all samples submitted here. This investigation was not, of course, omitted in the case reported by Dr. Grant and Dr. Wallace, and to put the minds of Dr. Bowley and Mr. Dunsford at rest, I would like to mention that the cells of this patient were repeatedly investigated with a number of oc, &bgr;, and at least five different &bgr;&agr; (group 0) sera. One of the latter contained a potent immune oc. The investigation was performed at 4°C and 18°C and no agglutination was seen with any antiserum used on the cells. Absorption experiments were also performed using the patient’s cells and group-0 and group-A cells as controls. They showed clearly that oc was not taken up by the patient’s cells as the titre of the antiserum was found to be the same as the one found after the serum had been " absorbed with group-0 cells and was unchanged. Dr. Bowley and Mr. Dunsford seem to want to have it both ways. They seem to assume that the patient’s group was really A4 (or Ax, whatever one likes to call these subgroups), and they gloss over the fact that if this was really the case, one would have expected the serum of the patient to contain an antibody acting on all group-A cells, as many writers, amongst them Mr. Dunsford, have found. In a lecture given in Holland Mr. Dunsford suggested : " The sera of the same type [A4] have always been found to agglutinate A1, A2 and B cells at 20°C but not to react with group 0 cells." Again, to put the writers’ minds at rest, I would like to say that exhaustive tests for the presence of an anti-A On only one were performed using Ai, A2’ and A3 cells. occasion did we find a very weak reaction with an Ai cell at room-temperature, the " agglutinates " consisting of two to three cells and being completely broken up by a very gentle rocking of the slide. As the absence of an anti-A was the remarkable finding after the group of the patient had been determined to our full satisfaction, of a
3. Hamilton, M., Litchfield, J. W., Brit. Heart J. 1953, 15, 241.
Peart, W. S., Sowry, G. S. C.
of investigations were performed the same result. The sentence "... it is surely surprising that the anti-B agglutinins are unaffected." makes strange reading. Surely, science has still many surprises in store for all of us and it is my conviction that it is the first duty of a scientist to record his findings truthfully, even if they should surprise some of his colleagues. I am sure that Dr. Bowley and Mr. Dunsford will be still more surprised to learn that two further cases of agammaglobulinæmia are at present under observation who show the same type of behaviour. They will shortly be published by Dr. W. T. Cooke, who has kindly agreed to my mentioning these cases in this letter. One case is group 0 (tested with group-0 sera !) and has oc and no &bgr; (another surprise !). The other case is group A but lacks the &bgr; agglutinin. It is perhaps worth mentioning that this latter case was discovered when a specimen was routinely investigated for its blood-group. These cases constitute real exceptions to Landsteiner’s rule. I too am surprised at their dogmatic statement that .. such persons ... do not produce A substance in their saliva." I was not able to find any literature supporting this statement but we have (unpublished observation) investigated a patient whose blood-group satisfies all the criteria for an A4 but whose saliva contains group-A substance.
course,
a
great number
giving always
’
W. WEINER.
Birmingham.
FLORENCE NIGHTINGALE BIBLIOGRAPHY
have been entrusted by the Florence Nightingale International Foundation with the com pilation of A bibliography of the published writings of Florence Nightingale, together with a calendar of all her extant manuscripts and letters. I should be grateful if owners or custodians of any manuscripts or letters of Miss Nightingale would communicate with me with a view to the inclusion of their material in the forthcoming book. If it is possible to send the actual documents, these will be examined and returned without delay. In view of the large number of letters to be dealt with it is not proposed to copy them, but to compile a location list with a brief indication of the subject of each letter.
SIR,—I
The Wellcome Historical Medical Library, 183, Euston Road, London, N.W.1.
W. J. BISHOP.
EFFECTS OF CORTISONE AND CORTICOTROPHIN ON THE ADRENAL CORTEX SIR,—The article by Dr. Stoner and Dr. Whiteley, in your issue of Nov. 13, prompts us to add three further cases of patients who died during treatment with steroid hormones and whose adrenals were examined at necropsy. had suffered from rheumatoid arthritis was treated with cortisone 25 mg. q.d.s. for ten months, and then corticotrophin gel 80 mg. was given daily for two months. She died from cardiac failure and pneumonia, the corticotrophin having’been stopped three days before death. Section of the adrenals revealed that the cortical cells, especially the cells of the zona fasciculata. showed lipoid infiltration to an unusual degree-i.e., they were in the resting phase. A woman, aged 61, who had suffered from rheumatoid arthritis for twenty years, had been treated with aqueous corticotrophin (20 mg. q.d.s.) for one month when she developed pneumonia and died. Section of the adrenals showed that the cortical cells were depleted of lipoid granules-i.e., thev were in an active phase. A man, aged 53, who had suffered from rheumatoid arthritis for thirteen years and had been treated with cortisone for two months, died following pneumonia. Section of th adrenals showed degenerative changes in the cells of all three zones of the cortex with loss of nuclear staining and sometime complete dissolution of the cell ;the whole cortex was reduce in width and, in one adrenal, hmmorrhage had occurred into the cortex and peri-adrenal tissues. A woman,
aged 64,
for three years.
She
-