cells in bone marrow, hypercalcemia, bone lesions, and a homogenous (mono¬ clonal) protein in serum and urine with decreased concentrations of normal serum
renal
immunoglobulins.
failure,
one
He also had
of the most
common
complications of multiple myeloma. The occurrence of multiple myeloma in young persons is important not only for diagnostic purposes (ie, the possi¬ bility of myeloma should be considered regardless of age) but also for staging of myeloma. It was considered that the growing rate of myeloma cells is slow and that at least 20 years of preclinical growth period is common for multiple myeloma.1 The extreme rarity of mye¬ lomas in young people would support a slow growth rate4; however, this inter¬ pretation has been challenged.5 The finding of multiple myeloma in young persons might shed some light on the role of environmental factors in this disease. ROMESH Kohli, MD Adrian Vladutiu, MD The Buffalo General Hospital Buffalo, NY
1. Clough V, Delamore IW, Whittaker JA: Multiple myeloma in a young woman. Ann Intern Med 86:117-118,
1977. 2. Maeda K, Abesamis CM, Kuhn LM, et al: Multiple myeloma in childhood: Report of a case with breast tumors as a presenting manifestation. Am J Clin Path 60:552-558, 1973. 3. Hewell GM, Alexanian R: Multiple myeloma in young persons. Ann Intern Med 84:441-443, 1976. 4. Hobbs JR: Monitoring myelomatosis. Arch Intern Med 135:125-130, 1975. 5. Salmon SE, Durie BGM: Cellular kinetics in multiple myeloma: A new approach to staging and treatment. Arch
this hospital, and he had given negative answers to all questions asked, including the question, "Have you ever
had hepatitis (jaundice), kidney or liver disease, or close contact with hepatitis within the last six months?" However, his medical records showed that he had been a patient in the hospital in September 1974 and that he had had hepatitis three years prior to that. This donor has moved to Indiana and cannot be reached. Questioning of the donor's mother revealed that both he and his mother were aware that he had had hepatitis. His mother expressed extreme chagrin that he had persisted in donating blood, unbeknown to her, despite the fact that he knew be had had hepatitis, that he knew that he might transmit the illness to a recipient, and that she had repeatedly cautioned him against donating blood. Thus, this person apparently mani¬ fests some great need to donate blood and feels obliged to do so even with the knowledge that he has had hepatitis and that he is not allowed to donate blood with that medical history. Inso¬ far as this blood bank is strictly volun¬ teer, monetary considerations do not enter into the donor's motivations to give blood; hence, we believe this constitutes a new variety of the Munchausen syndrome. Lynn Bauer, RN, investigated this unusual case for us.
Intern Med 135:131-138, 1975.
Munchausen Bank
Variety
Syndrome:
Lewis G. Lefer, MD R. Peter Rosier, MD Fort Myers, Fla
Blood
To the Editor.\p=m-\The following case report shows a bizarre sequence of events that should alert blood bank personnel and blood bank directors to what we believe constitutes a new variety of the Munchausen syndrome with grave medicolegal implications. On April 23, 1977, a male patient was admitted to the hospital with a diagnosis of upper gastrointestinal bleeding. He was jaundiced at the time of admission and had abnormal liver function tests and HBsAg positive serum. The patient was hospitalized previously on Jan 4, 1977, for upper gastrointestinal bleeding, for which he had received three units of blood. Investigation of blood bank records showed that all three of the donors were HBsAg negative. Two of the donors had donated blood several times with no sequelae; both returned to the hospital blood bank for a repeated HBsAg test, which was negative. The third donor was a first-time donor at
Biological Antithrombin
III
Levels
To the Editor.\p=m-\The MEDICAL NEWS article "Automated Test Measures
Functional Antithrombin, Coagulation Enzymes" (report of Jayed Fareed, PhD, and Harry L. Mesmore, MD) confirms my observations1 and those of others2,3 that there is poor correlation between immunological (total) and functional antithrombin III levels in disease states. Fareed and Mesmore point out that at Loyola University Stritch School of Medicine antithrombin III assay by chromogenic sub-
(still an investigational procedure) is being used to identify three groups of patients: hereditary thromstrates
bophiliacs, patients with hypercoagulable states, and patients who may be resistant to heparin therapy. Clearly, a
fourth area where this test may be indicated is in women ingesting oral contraceptives; 13 of 14 international studies have provided data showing that women with an increased predisposition to thromboembolic phenomena while ingesting oral contraceptives
Downloaded From: http://jama.jamanetwork.com/ by a New York University User on 06/15/2015
have decreased antithrombin III levels after ingesting the agents.4 One caution is that chromogenic substrates are still investigational and expensive but are also fraught with what appear to be important problems, as pointed out in several recent reports. The British National Institute of Biological Standards and Controls have done the first comparative study of synthetic substrates vs normal substrates for the assay of thrombin.5 This study showed that the S-2160, S2238, and chromozyme-TH chromo¬ genic substrates are of little use when measuring biological activity of throm¬ bin (and thus antithrombin III, which relies on chromogenic substrate detec¬ tion of residual thrombin). In addition, another recent report suggests that chromogenic substrates cannot be used in native plasma but only in plasma apparently void of albumin, as albumin interferes with chromogenic substrate assays." In addition, it should be pointed out that functional assays for antithrombin III approved by the Food and Drug Administration are available in this country and in Europe.T'8 Rodger L. Bick, MD Bay Area Hematology Oncology Medical
Group,
Inc
Santa Monica, Calif 1. Bick RL: Immunological and functional AT-III levels in disease states. Am J Clin Pathol, to be published. 2. Losito R, Beaudry P, Valderrama JC, et al: Antithrombin III and factor VIII in patients with neoplasms. Am J Clin Pathol 68:258-262, 1977. 3. Tiger-Nilsson AC: Antithrombin in infancy and childhood. Paediatr Scand 64:624-628, 1975. 4. Bick RL: Hypercoagulability and thrombosis, in
Current Concepts of Hemostasis and Thrombosis, workshop manual No. 548. Chicago, American Society of Clinical Pathologists, 1977. 5. Gaggney PJ, Lord K, Brasher M, et al: Problems in the assay of thrombin using synthetic peptides as substrates. Thromb Res 10:549-556, 1977. 6. Musumeci V, Lanolfi R, Bizza B: Amidolytic assay of thrombin bound to
2-macroglobulin
in
plasma. Hemostasis
6:98-109, 1973.
7. Von Kaulla E, von Kaulla KN: Antithrombin III and disease. Am J Clin Pathol 48:69-81, 1967. 8. Bick RL, Kovacs I, Fekere LF: A new two-stage functional assay for antithrombin III (heparin cofactor): Clinical and laboratory evaluation. Thromb Res 8:745-756, 1976.
Football Injuries. \p=m-\Inthe Nov 7 issue of The Journal (238:2049-2051, 1977), the second sentence of the second paragraph of the BRIEF REPORT 'Burning Hands' in Football Spinal Cord Injuries" should read as follows: "In a survey of high school and college athletic programs conducted during 1973 to 1974, he documented 476 spinal cord inju"
ries\p=m-\onepermanent injury for every 28,000 football participants." Of the 476 total
spinal
cord
injuries,
(54%) occurred secondary
participation.
46
to football
renal
immunoglobulins.
failure,
one
He also had
of the most
common
complications of multiple myeloma. The occurrence of multiple myeloma in young persons is important not only for diagnostic purposes (ie, the possi¬ bility of myeloma should be considered regardless of age) but also for staging of myeloma. It was considered that the growing rate of myeloma cells is slow and that at least 20 years of preclinical growth period is common for multiple myeloma.1 The extreme rarity of mye¬ lomas in young people would support a slow growth rate4; however, this inter¬ pretation has been challenged.5 The finding of multiple myeloma in young persons might shed some light on the role of environmental factors in this disease. ROMESH Kohli, MD Adrian Vladutiu, MD The Buffalo General Hospital Buffalo, NY
1. Clough V, Delamore IW, Whittaker JA: Multiple myeloma in a young woman. Ann Intern Med 86:117-118,
1977. 2. Maeda K, Abesamis CM, Kuhn LM, et al: Multiple myeloma in childhood: Report of a case with breast tumors as a presenting manifestation. Am J Clin Path 60:552-558, 1973. 3. Hewell GM, Alexanian R: Multiple myeloma in young persons. Ann Intern Med 84:441-443, 1976. 4. Hobbs JR: Monitoring myelomatosis. Arch Intern Med 135:125-130, 1975. 5. Salmon SE, Durie BGM: Cellular kinetics in multiple myeloma: A new approach to staging and treatment. Arch
this hospital, and he had given negative answers to all questions asked, including the question, "Have you ever
had hepatitis (jaundice), kidney or liver disease, or close contact with hepatitis within the last six months?" However, his medical records showed that he had been a patient in the hospital in September 1974 and that he had had hepatitis three years prior to that. This donor has moved to Indiana and cannot be reached. Questioning of the donor's mother revealed that both he and his mother were aware that he had had hepatitis. His mother expressed extreme chagrin that he had persisted in donating blood, unbeknown to her, despite the fact that he knew be had had hepatitis, that he knew that he might transmit the illness to a recipient, and that she had repeatedly cautioned him against donating blood. Thus, this person apparently mani¬ fests some great need to donate blood and feels obliged to do so even with the knowledge that he has had hepatitis and that he is not allowed to donate blood with that medical history. Inso¬ far as this blood bank is strictly volun¬ teer, monetary considerations do not enter into the donor's motivations to give blood; hence, we believe this constitutes a new variety of the Munchausen syndrome. Lynn Bauer, RN, investigated this unusual case for us.
Intern Med 135:131-138, 1975.
Munchausen Bank
Variety
Syndrome:
Lewis G. Lefer, MD R. Peter Rosier, MD Fort Myers, Fla
Blood
To the Editor.\p=m-\The following case report shows a bizarre sequence of events that should alert blood bank personnel and blood bank directors to what we believe constitutes a new variety of the Munchausen syndrome with grave medicolegal implications. On April 23, 1977, a male patient was admitted to the hospital with a diagnosis of upper gastrointestinal bleeding. He was jaundiced at the time of admission and had abnormal liver function tests and HBsAg positive serum. The patient was hospitalized previously on Jan 4, 1977, for upper gastrointestinal bleeding, for which he had received three units of blood. Investigation of blood bank records showed that all three of the donors were HBsAg negative. Two of the donors had donated blood several times with no sequelae; both returned to the hospital blood bank for a repeated HBsAg test, which was negative. The third donor was a first-time donor at
Biological Antithrombin
III
Levels
To the Editor.\p=m-\The MEDICAL NEWS article "Automated Test Measures
Functional Antithrombin, Coagulation Enzymes" (report of Jayed Fareed, PhD, and Harry L. Mesmore, MD) confirms my observations1 and those of others2,3 that there is poor correlation between immunological (total) and functional antithrombin III levels in disease states. Fareed and Mesmore point out that at Loyola University Stritch School of Medicine antithrombin III assay by chromogenic sub-
(still an investigational procedure) is being used to identify three groups of patients: hereditary thromstrates
bophiliacs, patients with hypercoagulable states, and patients who may be resistant to heparin therapy. Clearly, a
fourth area where this test may be indicated is in women ingesting oral contraceptives; 13 of 14 international studies have provided data showing that women with an increased predisposition to thromboembolic phenomena while ingesting oral contraceptives
Downloaded From: http://jama.jamanetwork.com/ by a New York University User on 06/15/2015
have decreased antithrombin III levels after ingesting the agents.4 One caution is that chromogenic substrates are still investigational and expensive but are also fraught with what appear to be important problems, as pointed out in several recent reports. The British National Institute of Biological Standards and Controls have done the first comparative study of synthetic substrates vs normal substrates for the assay of thrombin.5 This study showed that the S-2160, S2238, and chromozyme-TH chromo¬ genic substrates are of little use when measuring biological activity of throm¬ bin (and thus antithrombin III, which relies on chromogenic substrate detec¬ tion of residual thrombin). In addition, another recent report suggests that chromogenic substrates cannot be used in native plasma but only in plasma apparently void of albumin, as albumin interferes with chromogenic substrate assays." In addition, it should be pointed out that functional assays for antithrombin III approved by the Food and Drug Administration are available in this country and in Europe.T'8 Rodger L. Bick, MD Bay Area Hematology Oncology Medical
Group,
Inc
Santa Monica, Calif 1. Bick RL: Immunological and functional AT-III levels in disease states. Am J Clin Pathol, to be published. 2. Losito R, Beaudry P, Valderrama JC, et al: Antithrombin III and factor VIII in patients with neoplasms. Am J Clin Pathol 68:258-262, 1977. 3. Tiger-Nilsson AC: Antithrombin in infancy and childhood. Paediatr Scand 64:624-628, 1975. 4. Bick RL: Hypercoagulability and thrombosis, in
Current Concepts of Hemostasis and Thrombosis, workshop manual No. 548. Chicago, American Society of Clinical Pathologists, 1977. 5. Gaggney PJ, Lord K, Brasher M, et al: Problems in the assay of thrombin using synthetic peptides as substrates. Thromb Res 10:549-556, 1977. 6. Musumeci V, Lanolfi R, Bizza B: Amidolytic assay of thrombin bound to
2-macroglobulin
in
plasma. Hemostasis
6:98-109, 1973.
7. Von Kaulla E, von Kaulla KN: Antithrombin III and disease. Am J Clin Pathol 48:69-81, 1967. 8. Bick RL, Kovacs I, Fekere LF: A new two-stage functional assay for antithrombin III (heparin cofactor): Clinical and laboratory evaluation. Thromb Res 8:745-756, 1976.
Football Injuries. \p=m-\Inthe Nov 7 issue of The Journal (238:2049-2051, 1977), the second sentence of the second paragraph of the BRIEF REPORT 'Burning Hands' in Football Spinal Cord Injuries" should read as follows: "In a survey of high school and college athletic programs conducted during 1973 to 1974, he documented 476 spinal cord inju"
ries\p=m-\onepermanent injury for every 28,000 football participants." Of the 476 total
spinal
cord
injuries,
(54%) occurred secondary
participation.
46
to football
