726 muscular injection. This drug, which is not a C17-alkylsubstituted androgen, did not produce any rise in s.G.o.T. and produced only one slightly abnormal S.G.P.T. reading. At the end of ten weeks no change in the lipid levels could be detected.
These data suggest that, in gross hypertriglyceridxmia, methandienone causes a considerable reduction in chylomicrons and very low density lipoproteins and thus in serum-triglyceride levels. In those cases in which a gross hypercholesterolxmia is also present, a significant reduction in this lipid may be found. Apparently, however, when the initial cholesterol levels are not grossly abnormal, a rise in the serum-cholesterol may accompany even a profound fall in triglycerides. M. C. STONE. Leigh, Lanes. A SIDE-EFFECT OF ORAL CONTRACEPTIVES
of oral contraceptives has become but increasing number of cases small widespread, of vasomotor rhinitis have been appearing, the timing of which corresponds exactly to the " 20 days ". This condition seems to be more severe with the oestrogen type than the progesterone. I should be interested to know if this is a rare sideeffect or if only a few of those afflicted bother to seek advice.
SIR,-Since the
use
a
more
E.N.T.
Department,
St. Bartholomew’s Hospital, London, E.C.1.
L. N. DOWIE.
CHOICE OF BLOOD FOR ACID-BASE STUDIES
SIR,-Dr. Searcy and his colleagues (Dec. 7) are blood will provide valuable information
correct: venous
acid-base status. Their confirmation of is most welcome because there is still reports previous reluctance great among physicians to accept the results of venous pH determinations. about
the
In the past
seven
years I have
routinely
measured
blood pH and Pc02 in over 6000 suspected case of acid-base disturbance.Arterial or arterialised capillary blood is required at times, but properly collected venous blood is the only practical sample for routine use. The assumed unreliability of venous blood is a medical myth, In 1917, Parsons2 calculated a venous-arterial pH difference venous
of only -0°02 units for his own blood, and Van Slykefound a venous-arterial pH difference of only -0-03 units in 3 resting dogs. Petersstudied 14 patients in severe congestive failure, stating, It is fair to add that the patients selected for this study were chosen because it seemed likely that they would present maximum venous-arterial differences." The differences found were: -0-02 (4 cases), -0-03 (1 case), -0-04 (4 cases), --0-05 (3 cases), -0-06 (1 case), and -0’08 (1 case) pH units. In Japan, 5 resting normals had venous-arterial differences of -0-025 to -0-040.5 In America, 50 resting medical students had a mean venous-arterial pH difference of -0 053 between the jugular vein and the brachial artery, but only 0-02 to - 0-03 between an arm vein and the artery; suggesting greater metabolic activity in the brain.During acidosis, the jugular venous-arterial pH differences in 14 diabetics ranged from -0°00 to -0°08, and after recovery the range narrowed to - 0.02 to -0°06.’ 60 emphysematous subjects had venousarterial Pc02 differences of +to +11 mm. Hg.* 15 normals at rest had a mean venous-arterial pH difference of -004, but during exercise the mean difference rose to —0.06.9 16 independent measurements of venous-arterial pH difference were made in 2 resting subjects and the differences found were small and constant.1o Brooks and Wynn 11 described a method for obtaining venous blood for pH and Pc02 studies in respiratory failure and anaesthesia. They showed that warm arms at rest had clinically insignificant venous-arterial pH and PC02 differences, If the arm was cold (skin temperature below 35°C) they used an electric warming blanket. Finally, I have studied 36 subjects at rest and found a venous-arterial pH difference of -0-00 to —0.03. 12 "
-
HUMAN INSULIN ANTIBODIES DETECTED BY IMMUNOFLUORESCENT TECHNIQUE
SiR,-Dr. Pav
al.l report that, using the complement consumption technique they found insulin antibodies in the serum of 34% of 154 diabetics. A positive reaction was seen in 33% of those who had never received insulin. By immunofluorescent technique we have studied2 17 sera from diabetic subjects and 2 from normal people. Of the former, 14 had been treated with insulin before the test and 3 had never received insulin. et
Gamma-globulins from
diabetic labelled
patients,
with fluorescein, were
challenged
with a section of normal human pancreas removed one hour after death. 8 of the 14 sera from patients who had previously received insulin, and 1 of the 3 who had never been treated with
insulin, were positive. Using bovine and pork pancreas, human pancreas sampled
twenty-four hours after death, and
normal pancreas (Langerhans coloured by gamma-globulin labelled with fluorescin from a diabetic patient never treated with insulin (x520: reduced by a quarter).
Human
island)
other orsans such as kidney and thyroid, we always obtained a negative reaction. The 2 sera from normal people studied in the same way were negative. All reactions were sensitised by complement. Department of Morbid Anatomy, University of Bologna, Italy. Department of Medical Pathology, University of Bologna, Italy.
A. M. MANCINI G. COSTANZI. G. A. ZAMPA.
1. Páv, J., Ježková, Škraha, F. Lancet, 1963, ii, 221 2. Bonomini, V., Costanzi, G., Mancini, A. M., Zampa, G. A. Boll. Soc. ital. Biol. sper. 1963, 39, 193.
All reported studies reveal a small but constant venousarterial pH and Pco2 difference in resting subjects. Therefore, unreliable results are not caused by any inherent defect in venous blood, but rather by improper techniques for blood collection. The subject must be at rest and supine at least fifteen minutes. He should be kept warm with bedcovers or blankets. No " hand pumping" is permitted at any time. If the vein can be entered without a tourniquet, this should be done. However, if a tourniquet is used, it must be used properly. Place the tourniquet on tightly, don’t permit fist clenching, and draw the first 10 ml. of venous blood for 1. Gambino, S. R. Amer. J. clin. Path. 1959, 32, 301. 2. Parsons, T. R. J. Physiol. 1917, 51, 440. 3. Van Slyke, D. D., Cullen, G. E. J. biol. Chem. 1917, 30, 289. 4. Peters, J. P., Bulger, H. A., Eisenman, A. J. ibid. 1926, 67, 165. 5. Yoshimura, H. J. Biochem., Tokyo, 1936, 23, 335. 6. Gibbs, E. L., Lennox, W. G., Nims, L. F., Gibbs, F. A. J. biol. Chem. 1942, 144, 325. 7. Kety, S. S., Polis, B. D., Nadler, C. S., Schmidt, C. F. J. clin. Invest. 1948, 27, 500. 8. Hackney, J. D., Sears, C. H., Collier, C. R. J. appl. Physiol. 1958,12, 430 9. Mitchell, J. H., Sproule, B. J., Chapman, C. B. J. clin. Invest. 1958. 37, 1693. 10. Robin, E. D., Whaley, R. D., Crump, C. H., Travis, D. M. ibid. p.991. 11. Brooks, D., Wynn, V. Lancet, 1959, i, 227. 12. Gambino, S. R. Amer. J. clin. Path. 1959, 32, 298.