- Email: [email protected]
URINE SPECIFIC GRAVITY TEST STRIPS
1340 demonstrate a late response only. Lee and associates failed to appreciate this important point-namely, that our group of isolated late responders gave negative skin prick test responses to the relevant allergen, possessed only allergen-specific IgG4 antibodies in their sera, and were only identified as a result of screening the sera of a large group of atopic subjects.2 These differences in approach to the selection of patients could possibly explain why patients 7, 10, 11, and 12 in the study of Lee et al. gave dual reactions in the apparent absence of circulating IgG4 antibody. Alternatively, this could be due to the adoption of a different criterion for the presence or absence of allergen-specific antibodies of this IgG subclass in the patients’ sera. We compared our RAST results with the mean value obtained from analysis of the sera of thirty normal (non-allergic) individuals, considering any test serum value which was 2SD above this mean to be raised significantly. Lee et al. related their test serum RAST binding value to that of a positive ’references serum, apparently assigned an arbitrary value of 100 U/ml of IgG4 antibody which was directed against an irrelevant allergen (milk). The basis on which this particular serum was selected as reference for sera containing IgG4 antibodies of other specificities, and the reason for considering a test value greater than 20% in relation to this as significantly raised, is not stated. Hence, it is possible that one laboratory is being more stringent than the other in deciding what RAST value corresponds to a raised serum IgG4 level. For instance, if one takes the limit of positivity of the RAST values of Lee et al. as 5 U/ml, their 4-13 inclusive are not immunological findings on inconsistent with our findings. Lee et al. claimed that we used only one control but we clearly stated that we did control provocation tests on two of us (one of whom, T. A., was allergic to a non-test allergen) and on an intrinsic asthma patient. We also indicated that the patients were challenged with full-strength control solution, thus acting as their own controls. We made no mention of medication at the time of challenge since we assumed that it would be taken for granted that we would not have done provocation testing without stopping all drugs for at least 24 h before challenge. Lee and associates did not indicate whether any of their grasspollen-sensitive patients had previously undergone hyposensitisation. We avoided including any such patients in our study because there is some evidence that IgG4 antibodies to grass pollens produced as a result of such treatment may not behave in the same way as those found in the circulation of non-hyposensitised
patients ,2
hayfever patients. We suggest that there is scope for further bronchial provocation testing and other clinical studies (preferably by other laboratories, too), before IgG4 antibodies are dismissed as being "unlikely to play an important role in allergic disease". Rheumatology and Allergy Research Unit, Department of Immunology, Medical School, University of Birmingham, Birmingham B15 2TJ
C. M. GWYNN T. ALMOSAWI D. R. STANWORTH
URINE SPECIFIC GRAVITY TEST STRIPS
SIR,-I would like to comment on the letter from Dr Robson and colleagues (Nov. 20, p. 1164). We too have evaluated the new reagent strip ’N-Multistix SG’.3 We tried to draw attention to the fact that evaluation of simple ward tests of this sort should recognise that the clinician is searching for a broad classification for his patient and that he is unlikely to (and should not) place the same emphasis on this as he might place on a physiological measurement of urine osmolality. To compare the two techniques by a correlation coefficient is an oversimplification. We have taken particular interest in patients whose results do not correlate when two or more of the traditional methods of assessing concentration are contrasted with the new Ames test strip. 2. Gwynn CM, Almosawi T, Stanworth DR. Clinical associations with specific IgG4 antibodies. Clin Allergy 1982; 12: 459-64. 3. Frew AJ, McEwan J, Bell G, Heath M,
and
serum
allergen-
Knapp MS. Estimation of urine specific gravity osmolality using a simple reagent strip. Br Med J 1982; 285: 1168.
colleagues I would encourage the use of this strip, cautiously at this stage. We plan to publish our analysis of patients in whom there has been a discrepancy between a Unlike Robson and
new
conventional measurement of concentration and the N-multistix SG result. If others keep a careful note of patients in whom there is such a discrepancy the correct role for this new method may emerge. Until then I suggest that an assesment of urine concentration by this method is much better than no measurement of urine concentration at all in a case where such information helps clinical decision making. Tests should not be used in isolation to make major decisions, and caution is always necessary when a new method is introduced. I suspect that most of the concern expressed by Robson and colleagues is based on the implied correlation between specific gravity and the result of the new test. The manufacturer’s literature shows that something very different from the weight of dissolved solids is being measured: the test is a guide to what the specific gravity may be, not a measure of it. There are situations where specific gravity is not a good measure of urine concentration, and I agree that urine osmolality must be measured when a very important clinical decision has to be made. 10 1 Lambley Lane, Burton Joyce, MARTIN S. KNAPP Nottingham NG 14 5BL PROPRANOLOL AND ARTERIAL AMMONIA IN LIVER CIRRHOSIS
SIR,-We read with interest the article on the effect of propranolol arterial ammonia concentrations in liver cirrhosis by Dr van Buuren and colleagues (Oct. 30, p. 951). Four of their six patients with cirrhosis had raised basal arterial ammonia levels. In two of these, ammonia levels rose after 3 days’ treatment with propranolol and then started to fall after 6 days of treatment; the level in one other patient rose during propranolol treatment to reach a peak 3 days after the drug was stopped; the fourth patient’s arterial blood ammonia did not change. They further illustrate two cirrhotic patients with normal basal arterial ammonia levels in whom the concentration rose with propranolol therapy and three other patients with fatty infiltration whose ammonia levels appeared to fall with therapy. These are small numbers on which to attempt to analyse the altered pharmacodynamic effects of propranolol on arterial ammonia levels, and the results are difficult to interpret. It is unjustified to assert that the rise in ammonia levels of similar proportions in the patients with normal basal levels "argues against" the proposal that saturation of an overloaded uptake mechanism by reduced hepatic blood flow could account for the change. Ammonia levels do not accurately follow the degree of hepatic damage and can be affected by many factors other than solely hepatic function (diet, intestinal bleeding, bacterial floral). Normal basal levels therefore do not imply that an uptake system is not operating at a saturated level. Two of the three patients with fatty infiltration had significant hypoalbuminaemia, which suggests at least a moderate degree of abnormal hepatocellular function, yet these patients had no rise in the arterial ammonia levels during beta blockade. The cirrhotic patients used in this study represent patients with severe liver disease (four had persistent ascites despite diuretic therapy, three had serum albumin levels less than 30 g/1, and one had a serum bilirubin of 298 j1molll). Patient 3, without ascites or oesophageal varices, showed no significant change in arterial ammonia levels with propranolol therapy. This patient, the only cirrhotic patient in whom the arterial ammonia did not rise, was also the only patient to be taking an antibiotic known to affect the intestinal bacteria flora involved in the synthesis of ammonia.1 The average age of the patients with fatty infiltration was only 44, compared with the average for the cirrhotic group, which was 65. Hence, comparisons between these two groups must be made with on
care.
Department of Medicine, Ninewells Hospital and Medical School, Dundee DDI 9SY
P. C. HAYES A. N. SHEPHERD
1. Sherlock S. Disease of the liver and biliary system, 6th ed. Oxford: Blackwell Scientific
Publications, 1981 chap. 8.
patients ,2
hayfever patients. We suggest that there is scope for further bronchial provocation testing and other clinical studies (preferably by other laboratories, too), before IgG4 antibodies are dismissed as being "unlikely to play an important role in allergic disease". Rheumatology and Allergy Research Unit, Department of Immunology, Medical School, University of Birmingham, Birmingham B15 2TJ
C. M. GWYNN T. ALMOSAWI D. R. STANWORTH
URINE SPECIFIC GRAVITY TEST STRIPS
SIR,-I would like to comment on the letter from Dr Robson and colleagues (Nov. 20, p. 1164). We too have evaluated the new reagent strip ’N-Multistix SG’.3 We tried to draw attention to the fact that evaluation of simple ward tests of this sort should recognise that the clinician is searching for a broad classification for his patient and that he is unlikely to (and should not) place the same emphasis on this as he might place on a physiological measurement of urine osmolality. To compare the two techniques by a correlation coefficient is an oversimplification. We have taken particular interest in patients whose results do not correlate when two or more of the traditional methods of assessing concentration are contrasted with the new Ames test strip. 2. Gwynn CM, Almosawi T, Stanworth DR. Clinical associations with specific IgG4 antibodies. Clin Allergy 1982; 12: 459-64. 3. Frew AJ, McEwan J, Bell G, Heath M,
and
serum
allergen-
Knapp MS. Estimation of urine specific gravity osmolality using a simple reagent strip. Br Med J 1982; 285: 1168.
colleagues I would encourage the use of this strip, cautiously at this stage. We plan to publish our analysis of patients in whom there has been a discrepancy between a Unlike Robson and
new
conventional measurement of concentration and the N-multistix SG result. If others keep a careful note of patients in whom there is such a discrepancy the correct role for this new method may emerge. Until then I suggest that an assesment of urine concentration by this method is much better than no measurement of urine concentration at all in a case where such information helps clinical decision making. Tests should not be used in isolation to make major decisions, and caution is always necessary when a new method is introduced. I suspect that most of the concern expressed by Robson and colleagues is based on the implied correlation between specific gravity and the result of the new test. The manufacturer’s literature shows that something very different from the weight of dissolved solids is being measured: the test is a guide to what the specific gravity may be, not a measure of it. There are situations where specific gravity is not a good measure of urine concentration, and I agree that urine osmolality must be measured when a very important clinical decision has to be made. 10 1 Lambley Lane, Burton Joyce, MARTIN S. KNAPP Nottingham NG 14 5BL PROPRANOLOL AND ARTERIAL AMMONIA IN LIVER CIRRHOSIS
SIR,-We read with interest the article on the effect of propranolol arterial ammonia concentrations in liver cirrhosis by Dr van Buuren and colleagues (Oct. 30, p. 951). Four of their six patients with cirrhosis had raised basal arterial ammonia levels. In two of these, ammonia levels rose after 3 days’ treatment with propranolol and then started to fall after 6 days of treatment; the level in one other patient rose during propranolol treatment to reach a peak 3 days after the drug was stopped; the fourth patient’s arterial blood ammonia did not change. They further illustrate two cirrhotic patients with normal basal arterial ammonia levels in whom the concentration rose with propranolol therapy and three other patients with fatty infiltration whose ammonia levels appeared to fall with therapy. These are small numbers on which to attempt to analyse the altered pharmacodynamic effects of propranolol on arterial ammonia levels, and the results are difficult to interpret. It is unjustified to assert that the rise in ammonia levels of similar proportions in the patients with normal basal levels "argues against" the proposal that saturation of an overloaded uptake mechanism by reduced hepatic blood flow could account for the change. Ammonia levels do not accurately follow the degree of hepatic damage and can be affected by many factors other than solely hepatic function (diet, intestinal bleeding, bacterial floral). Normal basal levels therefore do not imply that an uptake system is not operating at a saturated level. Two of the three patients with fatty infiltration had significant hypoalbuminaemia, which suggests at least a moderate degree of abnormal hepatocellular function, yet these patients had no rise in the arterial ammonia levels during beta blockade. The cirrhotic patients used in this study represent patients with severe liver disease (four had persistent ascites despite diuretic therapy, three had serum albumin levels less than 30 g/1, and one had a serum bilirubin of 298 j1molll). Patient 3, without ascites or oesophageal varices, showed no significant change in arterial ammonia levels with propranolol therapy. This patient, the only cirrhotic patient in whom the arterial ammonia did not rise, was also the only patient to be taking an antibiotic known to affect the intestinal bacteria flora involved in the synthesis of ammonia.1 The average age of the patients with fatty infiltration was only 44, compared with the average for the cirrhotic group, which was 65. Hence, comparisons between these two groups must be made with on
care.
Department of Medicine, Ninewells Hospital and Medical School, Dundee DDI 9SY
P. C. HAYES A. N. SHEPHERD
1. Sherlock S. Disease of the liver and biliary system, 6th ed. Oxford: Blackwell Scientific
Publications, 1981 chap. 8.