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Vasopressin and Cardiac Performance
References 1 Holmes CL, Patel BM, Russell JA, et al. Physiology of vasopressin relevant to the management of septic shock. Chest 2001; 120:989 –1002 2 Malay MB, Ashton RC Jr, Landry DW, et al. Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma 1999; 47:699 –703 3 Tsuneyoshi I, Yamada H, Kakihana Y, et al. Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock. Crit Care Med 2001; 29:487– 493 4 Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997; 95:1122–1125 To the Editor: We thank Dr. Jackson and Dr. Shorr for their thorough discussion, in response to our recent review1 of the effects of vasopressin on cardiac performance. We also conducted a retrospective review in our institution of 50 patients who had received vasopressin for hemodynamic support in septic shock.2 In the subset of patients with a pulmonary artery catheter in place, we found a mean decrease in cardiac index of 11% at 4 h of treatment with vasopressin infusion. This effect appeared to be dose related; doses ⬎ 0.03 U/min were significantly associated with a decrease in the cardiac index (p ⫽ 0.0026). We agree that the potential for a decrease in cardiac index should be anticipated at higher than physiologic doses of vasopressin. We also agree that the use of vasopressin in septic shock should await the results of a randomized controlled trial that assesses both mortality and hemodynamic outcomes. Cheryl L. Holmes, MD Keith R. Walley, MD James A. Russell, MD St. Paul’s Hospital Vancouver, BC, Canada Correspondence to: Cheryl L. Holmes, MD, St. Paul’s Hospital, McDonald Research Wing, Room 292, 1081 Burrard St, Vancouver, BC V62 1Y6, Canada
order to make a decision on whether or not to conduct the blood transfusion, it is important that anemia-induced hemoglobin loads to kidneys and other organs are correctly evaluated. Haptoglobin, which is produced mainly in the liver, combines with hemoglobin produced as a result of hemolysis. This haptoglobin-hemoglobin complex is then taken into the liver and metabolized there. However, the amount of haptoglobin produced is often not enough to keep up with excessive hemolysis. As a result, a state of ahaptoglobinemia is induced, as in this clinical case. Moreover, when excessive hemoglobin amounts continue to be released, the haptoglobin elimination mechanism cannot keep up and, eventually, another metabolic route begins functioning. In other words, hemes are removed from excessive hemoglobin to become methemes and combined with albumin to form methemalbumin, which is metabolized in the liver. In view of this metabolic flow, detecting haptoglobin/metheme is exceedingly useful in detecting the level of hemoglobin load in anemia patients. The detection of both haptoglobin and methemalbumin fractions in the serum from patients was conducted using 5% polyacrylamide gel electrophoresis and o-dianisidine staining method (Figure 1). The metheme concentration is directly proportional to the staining level of methemalbumin.2 This method allows simultaneous evaluation of both haptoglobin and metheme. Disappearance of haptoglobin and increase of metheme indicates extremely serious anemia. Detection of haptoglobin and methemalbumin contributes useful information for continued hemolysis follow-up. Toshio Okazaki, PhD Tatsuo Nagai, MD Kitasato University Graduate School of Medical Sciences Mitsuyuki Suzuki Kitasato University School of Allied Health Sciences Kanagawa Prefecture, Japan Correspondence to: Toshio Okazaki, PhD, Department of Clinical Hematology, Kitasato University of Allied Health Sciences, 1-15-1 Kitasato, Sagamihara-shi, Kanagawa Prefecture 228-8555, Japan; e-mail: [email protected]
References 1 Holmes CL, Patel BM, Russell JA, et al. Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120:989 –1002 2 Holmes CL, Walley KR, Chittock DR, et al. The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series. Intensive Care Med 2001; 27:1416 – 1421
References 1 Kuo P-H, Yang P-C, Kuo S-S, et al. Severe immune hemolytic anemia in disseminated tuberculosis with response to antituberculosis therapy. Chest 2001; 119:1961–1963 2 Nagai T, Okazaki T, Yanagisawa Y. Quantitative analysis of methemalbumin by polyacrylamide gel electrophoresis. Clin Lab 1997; 43:765–768 To the Editor:
Usefulness of Methemoglobin/ Haptoglobin Analysis in the Follow-up of Severe Immune Hemolytic Anemia To the Editor: I was surprised and impressed by the dramatic improvement observed in a Coombs-positive hemolytic anemia patient reported by Kuo et al (June 2001).1 This outstanding result seems to have resulted from the fact that haptoglobin functioned properly, thanks to the healthy liver, which minimized damage to the kidneys and other organs caused by the onset of anemia. However, we may not always achieve such successful results. In 1724
We thank Dr. Okazaki and his colleagues for their interest in our article (June 2001).1 The reasons that corticosteroids and blood transfusion were not administered to our patient include his young age and the relatively well-preserved liver function and hemodynamics. We agree with Dr. Okazaki that we may not always achieve such successful results by antituberculosis therapy alone. We think Dr. Okazaki also makes a good point that detecting haptoglobin/metheme is useful in the assessment of hemoglobin load in patients with hemolytic anemia. This laboratory procedure, however, is uncommon in current hematology practice. However, serial laboratory data of our patient showed that the serum level of lactate dehydrogenase, a common biochemistry index, was well correlated with the clinical course of hemolysis. In Communications to the Editor
order to make a decision on whether or not to conduct the blood transfusion, it is important that anemia-induced hemoglobin loads to kidneys and other organs are correctly evaluated. Haptoglobin, which is produced mainly in the liver, combines with hemoglobin produced as a result of hemolysis. This haptoglobin-hemoglobin complex is then taken into the liver and metabolized there. However, the amount of haptoglobin produced is often not enough to keep up with excessive hemolysis. As a result, a state of ahaptoglobinemia is induced, as in this clinical case. Moreover, when excessive hemoglobin amounts continue to be released, the haptoglobin elimination mechanism cannot keep up and, eventually, another metabolic route begins functioning. In other words, hemes are removed from excessive hemoglobin to become methemes and combined with albumin to form methemalbumin, which is metabolized in the liver. In view of this metabolic flow, detecting haptoglobin/metheme is exceedingly useful in detecting the level of hemoglobin load in anemia patients. The detection of both haptoglobin and methemalbumin fractions in the serum from patients was conducted using 5% polyacrylamide gel electrophoresis and o-dianisidine staining method (Figure 1). The metheme concentration is directly proportional to the staining level of methemalbumin.2 This method allows simultaneous evaluation of both haptoglobin and metheme. Disappearance of haptoglobin and increase of metheme indicates extremely serious anemia. Detection of haptoglobin and methemalbumin contributes useful information for continued hemolysis follow-up. Toshio Okazaki, PhD Tatsuo Nagai, MD Kitasato University Graduate School of Medical Sciences Mitsuyuki Suzuki Kitasato University School of Allied Health Sciences Kanagawa Prefecture, Japan Correspondence to: Toshio Okazaki, PhD, Department of Clinical Hematology, Kitasato University of Allied Health Sciences, 1-15-1 Kitasato, Sagamihara-shi, Kanagawa Prefecture 228-8555, Japan; e-mail: [email protected]
References 1 Holmes CL, Patel BM, Russell JA, et al. Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120:989 –1002 2 Holmes CL, Walley KR, Chittock DR, et al. The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series. Intensive Care Med 2001; 27:1416 – 1421
References 1 Kuo P-H, Yang P-C, Kuo S-S, et al. Severe immune hemolytic anemia in disseminated tuberculosis with response to antituberculosis therapy. Chest 2001; 119:1961–1963 2 Nagai T, Okazaki T, Yanagisawa Y. Quantitative analysis of methemalbumin by polyacrylamide gel electrophoresis. Clin Lab 1997; 43:765–768 To the Editor:
Usefulness of Methemoglobin/ Haptoglobin Analysis in the Follow-up of Severe Immune Hemolytic Anemia To the Editor: I was surprised and impressed by the dramatic improvement observed in a Coombs-positive hemolytic anemia patient reported by Kuo et al (June 2001).1 This outstanding result seems to have resulted from the fact that haptoglobin functioned properly, thanks to the healthy liver, which minimized damage to the kidneys and other organs caused by the onset of anemia. However, we may not always achieve such successful results. In 1724
We thank Dr. Okazaki and his colleagues for their interest in our article (June 2001).1 The reasons that corticosteroids and blood transfusion were not administered to our patient include his young age and the relatively well-preserved liver function and hemodynamics. We agree with Dr. Okazaki that we may not always achieve such successful results by antituberculosis therapy alone. We think Dr. Okazaki also makes a good point that detecting haptoglobin/metheme is useful in the assessment of hemoglobin load in patients with hemolytic anemia. This laboratory procedure, however, is uncommon in current hematology practice. However, serial laboratory data of our patient showed that the serum level of lactate dehydrogenase, a common biochemistry index, was well correlated with the clinical course of hemolysis. In Communications to the Editor