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Reappearance of beriberi heart disease in Japan
Reappearance of Beriberi Heart Disease in Japan A Study of 23 Cases
CHUICHI AKIRA
KAWAI.
M.D.
WAKABAYASHI,
M.D. TADASHI MATSUMURA, M.D.* YOSHIKI YUI, M.D. Kyoto, lopan
From the Third Division, Department of Internal Medicine, Faculty of Medicine, Kyoto University. This study was supported, in part, by Grant for Cardiomyopathy from the Ministry of Health and Welfare and Grant 357308, 1978, from the Ministry of Education, Japan. Part of this study was presented at the Symposium on “Secondary Myocardial Disease” of the 44th Scientific Session of the Japanese Circulation Society, Tokyo, 1979. Requests for reprints should be addressed to Dr. Chuichi Kawai, 3rd Division, Department of Internal Medicine, Kyoto University Hospital, 53 Kawaracho Shogoin. Sakyoku, Kyoto 606, Japan. Manuscript accepted March 31,198O. * Present address: Department of Cardiology, Tenri Hospital, 200 Mishimacho, Tenri City, Japan.
Twenty-three Japanese patients with beriberi heart disease, 17 of them teenagers, were studied. The recent tendency for teenagers to take excessive sweet carbonated soft drinks, instant noodles and powermill-polished rice readily induces relative thiamine deficiency. A sudden increase in thiamine requirements due to strenuous exercise can result in overt beriberi heart disease. Alcohol had nothing to do with the development of the disease. Characteristic features commonly seen in teenage patients include peripheral edema, low peripheral vascular resistance, increased venous pressure, enlarged heart, T wave abnormalities, hyperkinetic circulatory state and increased circulating blood volume. Thiamine deficiency was confirmed by a decrease in blood thiamine concentration, a decrease in erythrocyte transketolase activity and an increase in thiamine pyrophosphate (TPP) effect. Improvement was rapidly achieved with thiamine administration, balanced nutrition and rest, especially in the teenage patients. Increased circulating blood volume was useful in differentiating beriberi heart disease from hyperthyroidism. Beriberi heart disease was once widespread in Japan; 26,797 patients died of shoshin [sudden collapse] beriberi in 1923 [I]. Since its etiology was found to be thiamine deficiency by Shimazono [2,3], the incidence of beriberi heart disease decreased gradually until it disappeared almost completely [4]. However, during the past four years, beriberi heart disease has been reported, mainly in adolescents, throughout Japan [5-71. Thiamine deficiency has also been noted in patients receiving prolonged treatment with potent diuretics [8]. Thus, beriberi heart disease has reappeared in modern cardiology. The clinical features and predisposing factors are analyzed in 23 patients seen by us during the past four years. MATERIAL
AND METHODS
Of the 23 patients [aged 15 to 52 years, average 21 years], 17 were under the age of 20; 19 were male and four female. Thiamine was determined by the thiochrome method of Fujiwara and Matsui [9]. Erytbrocyte transketolase (ETK) activity was determined in a series of three tubes: one for zero time control, the second fdr the original activity and the third for the thiamine pyrophosphate (TPP) effect, i.e., the percentage stimulation of enzyme activity above the original activity produced by adding TPP to the sample before assay. The TPP effect reflects the proportion of apoenzyme not saturated with thiamine [lo]. Twelve normal volunteers, aged 19 to 53 years (average age 30 years], provided control values for the blood thiamine level, ETK activity and TPP effect.
September 1966
The American Journal of Medicine
Volume 69
383
REAPPEARANCE
TABLE I
OF BERIBERI
HEART
DISEASE
IN JAPAN-KAWAI
ET AL.
?Jood Thlamlne Concentration, Erythrocyte Transketolase (ETK) Actlvlty and Thlamlne Pyrophosphate (TPP) Effect in Patients with Beriberi Heart Disease Under and Over the Age of 20 and in Normal Controls
Subjec&Studled Patients with ber@ri heart disease Under 20 Over 20 Normal groirp
No.
BloodThiamine WlfW
13 8 5 12
2.29’ f 1.06 2.22 f 1.16 2.40 f 0.95 6.96 f 1.26
ETKActivity ~~/mlfhr) 361’ 363 359 868
& f: f +
156 141 197 308
TPP Effect (%I 56.2+ 54.8 58.4 3.0
f f f +
39.1 41.0 40.4 4.7
NOTE: All values f standard deviation. Patients with beriberi heart disease versus normal group: * p
Hemodynamic studies were carried out in 13 patients by an analog simulation method of the radiocardiogram [ll]; 130 subjects (mean age: 31.1f 13.9years) without apparent heart disease were used as controls. &dent’s t-test was used for statistical analysis [12] and expressed as the mean f standard deviation (SD]. RESUkS incidence and Predisposing Factors. In 20 of the 23 patients (87 percent) symptoms developed between June and tiovember. Eight were engaged in strenuous athletics, and one, a 17 year old high school boy, fell sick after heavy physical labor in the hot summer. A history of alcohol intake, unlike Occidental beriberi, was obtained in only one patient, a 52 year old man. Nearly all the patients had a dietary history of excessive intake of carbohydrates, such as powermillpolished rice without thiamine supplementation, sweet carbonated soft drinks and instant noodles, which lack thiamine. A multicenter cooperative study sponsored by the Minist~ of Health and Welfare of Japan revealed that high school students with beriberi had a diet high in catbohydrates, 541 g/day, and low in animal protein, 21 g/day (the carbohydrate and animal protein intake per capita per day in. Japan in 1976was 332 g and 38.1 g, respectively]. The daily intake of thiamine in beriberi patients was 0.28 to 0.98 mg [4]. Symptoms kd Signs. In all 23 patients peripheral edema developed, usually the initial sign, or ‘*wet beriberi.” Easy fatigability, general malaise, palpitation and dyspnea were also common. Numbness of the lower extremities with gait disturbance was noted in only one case. The knee jerk was diminished in six and abolished in two. Peripheral neuritis, “dty beriberi,” was infrequent. The pulse rate was usually high but rarely exceeded lZO/min. The neck veins were engorged, and the venous pressure was abpve 200 mm Hz0 in many cases but returned rapidly to normal as edema disappeared. In the younger patients !otier diastolic pressure, therefore increased pulse pressure, was characteristic, but not in the older patients. There was galltip rhythm at the apex and nonspecific mid-sysjolic murmurs between the left sternal border and the apex. The second pulmonic sound was usually accentuate+ Seasonal
384
September 1980 The American Journal of Medicine
The heart size was normal or slightly enlarged. Cardiac enlargement at the onset of beriberi heart disease was sometimes so mild that it was only recognized when compared with another chest film taken a week or two later. Nearly half of our patients had an apparently normal-sized heart with a cardiothoracic ratio less than 50 percent; even in them, the heart size diminished definitely after treatment. Sinus tachycardia and flattening Electrocardiogram. or inversion of the T waves were the main changes. The T wave changes were minimal but definite in 19 of the 23 cases when before and after treatment electrocardiograms were compared. Eight patients were under and Hemodynamic Studies. five over 20 years of age. Characteristic changes were increased cardiac index, stroke index, heart rate, blood turn-over rate, circulating blood volume and decreased peripheral vascular resistance, more prominent in the younger group, especially in five patients under 20 years of age who were examined during the acute stage of the disease. Markedly increased cardiac index, stroke index andcirculating blood volume, and markedly decreased peripheral vascular resistance in these patients were significantly different from those in patients over 20 years of age (p
Comparison of Hemodynamic Changes Between Patients with Beriberi Heart Disease and Hyperthyroidism. Hemodynamic changes in beriberi heart
disease in the acute stage were compared with those in six patients with hyperthyroidism. Increase in cardiac index (beriberi heart disease, 7.93 f 0.83 liters/min/m? hyperthyroidism, 7.00 f 1.06 liters/min/m2) and decrease in peripheral vascular resistance (beriberi heart disease, 454.6 f 48.7 dynes-set-cm-5; hyperthyroidism, 667 f 202 dynesasec-cm+) were obvious in both groups [normal: cardiac index: 4.21 f 0.71 liters/min/mz, peripheral vascular resistance: 1,142 f 245 dynes-see cm-s). The increase in heart rate was more pronounced, so the increase in stroke index was less marked in hyperthyroidism. A marked increase in circulating blood volume with normal distribution in the body was char-
Volume 89
REAPPEARANCE
OF BERIBERI
HEART
DISEASE
IN JAPAN-KAWAI
Ll
H-R
l/min/m2
bea:s/min
3OL
dyne
P
gec.cm-
Figure 1. Changes of hemodynamic parameters before and after treatment in patients under and above 20 years of age. Cl = cardiac index, SI = stroke index, HR = heart rate, PVR = peripheral vascular resistance, F/V = blood turnover rate, CBV = circulatory blood volume.
-age< D---.u
4.
2.
3. S-
1.
3. G-
heart disease. In hyperthyroidism, circulating blood volume was increased only slightly; thus, increase in the flow to volume (F:V) ratio was more pronounced in hyperthyroidism than in beriberi heart disease. ETK and TPP Effect (Table I).
The blood thiamine level and the ETK activity were lower, and the TPP effect significantly higher than normal (p
In most of the patients in the present series beriberi heart disease developed in the summer, presumably because subjects with relative thiamine deficiency have
September
20 4*0
b
before
,
after
2. 5’
2.1o-
mfam+ SD (normal
control)
a sudden increase in thiamine requirements due to strenuous physical exertion during the hot summer. The recent tendency of Japanese teenagers to take excessive carbohydrates such as polished rice, instant noodles, which lack thiamine, and sweet carbonated drinks readily leads to relative thiamine deficiency. Alcohol intake was not a factor in our series. Patients under the age of 20 years demonstrated characteristic features of beriberi heart disease, whereas a hyperkinetic circulatory state was less prominent in older patients, although the grade of thiamine deficiency was essentially equal, In chronic thiamine deficiency, microscopic examination of the myocardium of patients as well as of experimental animals demonstrates severe hydropic degeneration, extensive fibrosis and necrosis, loss of striations and interstitial and perivascular edema [13-161. With these degenerative changes of the myocardium it is assumed that a hyperkinetic circulatory
acteristic of beriberi
Level,
2oyo age 2
aftc.r
O-
2.
0.
before
1/ml
m
1.
Blood Thiamine
ET AL.
1980
The American Journal of Medicine
Volume
89
385
REAPPEARANCE OF BERIBERI HEART DISEASE IN JAPAN-KAWAI
state or high cardiac output cannot be maintained for long. In fact, beriberi heart disease with a hyperkinetic cardiac state, has never been produced in experimental animals with chronic thiamine deficiency [17], Although the thiamine requirement should decrease with age, atypical clinical signs and symptoms with little hyperkinetic circulation in older patients may represent an intermediate process to the advanced stage of beriberi heart disease due to long-standing thiamine deficiency. The response to thiamine administration was prompt in the younger patients but generally poor in the older patients. In the younger patients, a favorable therapeutic effect was obtained with rest alone.
ET AL
It deserves mention that a marked increase in circulating blood volume is an important feature in the differentiation of beriberi heart disease from hyperthyroidism, both of which represent hyperkinetic circulatory states. The increase in circulating blood volume is related to the common occurrence of peripheral edema in beriberi heart disease. AC~~~EDGMENT We are indebted to Dr. Yoshinori Itokawa, Professor of Hygiene, Kyoto University, for thiamine measurements, and to Dr. Alice S. Gary for pertinent advice on the manuscript.
REFERENCES 1.
2. 3.
4. 5. 6. 7. 8. 9.
386
Inoue K, Katsura E: Etiology and pathology of beriberi. In: Shimazono N, Katsura E, eds. Review of Japanese literature on beriberi and thiamine. Vitamin B Research Committee of Japan, Tokyo: Igaku Shoin, 1975; 1. Shimazono J: Kakke (beriberi) (in Japanese). Jap J Med 1919: 7: 237.
Shimazono J: Beriberi. In: Stepp W, Gyorgy P, eds. Avitaminosen und verwandte krankheitszustande. Berlin: Julius Splingor, 1927; 539. Abe T, Hashizume N, Igata A, et al.: Studies on pathogenesis in beriberi heart disease and beriberi neuropathy (in Japanese). Nutrition Diet 1977; 30: 523. Kawai C, Wakabayashi A, Hirose K, et al.: A beriberi heartlike syndrome: metabolic heart disease or non-specific myocarditis [abstract)? Jap Circ J 1976; 40: 514. Kusukawa R, Kinoshita M, Shimono Y, et al.: The clinical findings of seven cases with high output failure resembling beriberi syndrome (abstract), Jap Circ J 1976; 40: 515. Seriu Y, Uehata H. Bito K, et al.: Five young patients with beriberi heart disease (abstract). Jap Circ J1976: 40: 515. Yui Y, Fujiwara H, Mitsui H, et al.: Furosemide-induced thiamine deficiency (abstract). Jap Circ J 1978; 42: 744. Fujiwara M, Matsui K: Determination of thiamine by the thiochrome reaction; application of cyanogen bromide in
September 1980
The American Journal of Medicine
place of potassium ferricyanide. Anal Chem 1953; 25: 810. 10. Brin M, Tai M, Ostashever AS, et al.: The effect of thiamine deficiencv on the activitv of ervthrocvte hemolvsate transketoiasa. J Nutr 1960; $1: 273. * _ 11. Kuwahara M. Hirakawa A, Kinoshita M. et al.: Analvsis of radiocardiogram by analog computer simulation: Int J Biomed Eng 1972; 1: 13. 12. Remington RD. Schork MA: Statistics with application to the biological and health sciences. Englewood Cliffs, NJ: Prentice-Hall, 1967; 192. 13. Wolf PL, Levin MB Shoshin beriberi. N Engl JMed 1960;262: 1302. 14. Toreson LWE: Diffuse isolated myocarditis associated with dietary deficiency. Arch Intern Med 1944; 73: 375. 15. Yoshitoshi Y, Shibata N, Yamashita S: Expe~mental studies on the beriberi heart. I. Cardiac lesions in thiamine deficient rats. Jap Heart J 1961; 2: 42. 16. Follis RH Jr. Miller MH, Wintrobe MM, et al.: Development of myocardial necrosis and absence of nerve degeneration in thiamine deficiency in pigs. Am J Path01 1943; 19: 341. 17. Hirota Y, Kane RL, Abelmann WH: Cardiovascular effects of exercise in hamsters with experimental thiamine deficiency. Jap Circ J 1979: 43: 99.
Volume 69
CHUICHI AKIRA
KAWAI.
M.D.
WAKABAYASHI,
M.D. TADASHI MATSUMURA, M.D.* YOSHIKI YUI, M.D. Kyoto, lopan
From the Third Division, Department of Internal Medicine, Faculty of Medicine, Kyoto University. This study was supported, in part, by Grant for Cardiomyopathy from the Ministry of Health and Welfare and Grant 357308, 1978, from the Ministry of Education, Japan. Part of this study was presented at the Symposium on “Secondary Myocardial Disease” of the 44th Scientific Session of the Japanese Circulation Society, Tokyo, 1979. Requests for reprints should be addressed to Dr. Chuichi Kawai, 3rd Division, Department of Internal Medicine, Kyoto University Hospital, 53 Kawaracho Shogoin. Sakyoku, Kyoto 606, Japan. Manuscript accepted March 31,198O. * Present address: Department of Cardiology, Tenri Hospital, 200 Mishimacho, Tenri City, Japan.
Twenty-three Japanese patients with beriberi heart disease, 17 of them teenagers, were studied. The recent tendency for teenagers to take excessive sweet carbonated soft drinks, instant noodles and powermill-polished rice readily induces relative thiamine deficiency. A sudden increase in thiamine requirements due to strenuous exercise can result in overt beriberi heart disease. Alcohol had nothing to do with the development of the disease. Characteristic features commonly seen in teenage patients include peripheral edema, low peripheral vascular resistance, increased venous pressure, enlarged heart, T wave abnormalities, hyperkinetic circulatory state and increased circulating blood volume. Thiamine deficiency was confirmed by a decrease in blood thiamine concentration, a decrease in erythrocyte transketolase activity and an increase in thiamine pyrophosphate (TPP) effect. Improvement was rapidly achieved with thiamine administration, balanced nutrition and rest, especially in the teenage patients. Increased circulating blood volume was useful in differentiating beriberi heart disease from hyperthyroidism. Beriberi heart disease was once widespread in Japan; 26,797 patients died of shoshin [sudden collapse] beriberi in 1923 [I]. Since its etiology was found to be thiamine deficiency by Shimazono [2,3], the incidence of beriberi heart disease decreased gradually until it disappeared almost completely [4]. However, during the past four years, beriberi heart disease has been reported, mainly in adolescents, throughout Japan [5-71. Thiamine deficiency has also been noted in patients receiving prolonged treatment with potent diuretics [8]. Thus, beriberi heart disease has reappeared in modern cardiology. The clinical features and predisposing factors are analyzed in 23 patients seen by us during the past four years. MATERIAL
AND METHODS
Of the 23 patients [aged 15 to 52 years, average 21 years], 17 were under the age of 20; 19 were male and four female. Thiamine was determined by the thiochrome method of Fujiwara and Matsui [9]. Erytbrocyte transketolase (ETK) activity was determined in a series of three tubes: one for zero time control, the second fdr the original activity and the third for the thiamine pyrophosphate (TPP) effect, i.e., the percentage stimulation of enzyme activity above the original activity produced by adding TPP to the sample before assay. The TPP effect reflects the proportion of apoenzyme not saturated with thiamine [lo]. Twelve normal volunteers, aged 19 to 53 years (average age 30 years], provided control values for the blood thiamine level, ETK activity and TPP effect.
September 1966
The American Journal of Medicine
Volume 69
383
REAPPEARANCE
TABLE I
OF BERIBERI
HEART
DISEASE
IN JAPAN-KAWAI
ET AL.
?Jood Thlamlne Concentration, Erythrocyte Transketolase (ETK) Actlvlty and Thlamlne Pyrophosphate (TPP) Effect in Patients with Beriberi Heart Disease Under and Over the Age of 20 and in Normal Controls
Subjec&Studled Patients with ber@ri heart disease Under 20 Over 20 Normal groirp
No.
BloodThiamine WlfW
13 8 5 12
2.29’ f 1.06 2.22 f 1.16 2.40 f 0.95 6.96 f 1.26
ETKActivity ~~/mlfhr) 361’ 363 359 868
& f: f +
156 141 197 308
TPP Effect (%I 56.2+ 54.8 58.4 3.0
f f f +
39.1 41.0 40.4 4.7
NOTE: All values f standard deviation. Patients with beriberi heart disease versus normal group: * p
Hemodynamic studies were carried out in 13 patients by an analog simulation method of the radiocardiogram [ll]; 130 subjects (mean age: 31.1f 13.9years) without apparent heart disease were used as controls. &dent’s t-test was used for statistical analysis [12] and expressed as the mean f standard deviation (SD]. RESUkS incidence and Predisposing Factors. In 20 of the 23 patients (87 percent) symptoms developed between June and tiovember. Eight were engaged in strenuous athletics, and one, a 17 year old high school boy, fell sick after heavy physical labor in the hot summer. A history of alcohol intake, unlike Occidental beriberi, was obtained in only one patient, a 52 year old man. Nearly all the patients had a dietary history of excessive intake of carbohydrates, such as powermillpolished rice without thiamine supplementation, sweet carbonated soft drinks and instant noodles, which lack thiamine. A multicenter cooperative study sponsored by the Minist~ of Health and Welfare of Japan revealed that high school students with beriberi had a diet high in catbohydrates, 541 g/day, and low in animal protein, 21 g/day (the carbohydrate and animal protein intake per capita per day in. Japan in 1976was 332 g and 38.1 g, respectively]. The daily intake of thiamine in beriberi patients was 0.28 to 0.98 mg [4]. Symptoms kd Signs. In all 23 patients peripheral edema developed, usually the initial sign, or ‘*wet beriberi.” Easy fatigability, general malaise, palpitation and dyspnea were also common. Numbness of the lower extremities with gait disturbance was noted in only one case. The knee jerk was diminished in six and abolished in two. Peripheral neuritis, “dty beriberi,” was infrequent. The pulse rate was usually high but rarely exceeded lZO/min. The neck veins were engorged, and the venous pressure was abpve 200 mm Hz0 in many cases but returned rapidly to normal as edema disappeared. In the younger patients !otier diastolic pressure, therefore increased pulse pressure, was characteristic, but not in the older patients. There was galltip rhythm at the apex and nonspecific mid-sysjolic murmurs between the left sternal border and the apex. The second pulmonic sound was usually accentuate+ Seasonal
384
September 1980 The American Journal of Medicine
The heart size was normal or slightly enlarged. Cardiac enlargement at the onset of beriberi heart disease was sometimes so mild that it was only recognized when compared with another chest film taken a week or two later. Nearly half of our patients had an apparently normal-sized heart with a cardiothoracic ratio less than 50 percent; even in them, the heart size diminished definitely after treatment. Sinus tachycardia and flattening Electrocardiogram. or inversion of the T waves were the main changes. The T wave changes were minimal but definite in 19 of the 23 cases when before and after treatment electrocardiograms were compared. Eight patients were under and Hemodynamic Studies. five over 20 years of age. Characteristic changes were increased cardiac index, stroke index, heart rate, blood turn-over rate, circulating blood volume and decreased peripheral vascular resistance, more prominent in the younger group, especially in five patients under 20 years of age who were examined during the acute stage of the disease. Markedly increased cardiac index, stroke index andcirculating blood volume, and markedly decreased peripheral vascular resistance in these patients were significantly different from those in patients over 20 years of age (p
Comparison of Hemodynamic Changes Between Patients with Beriberi Heart Disease and Hyperthyroidism. Hemodynamic changes in beriberi heart
disease in the acute stage were compared with those in six patients with hyperthyroidism. Increase in cardiac index (beriberi heart disease, 7.93 f 0.83 liters/min/m? hyperthyroidism, 7.00 f 1.06 liters/min/m2) and decrease in peripheral vascular resistance (beriberi heart disease, 454.6 f 48.7 dynes-set-cm-5; hyperthyroidism, 667 f 202 dynesasec-cm+) were obvious in both groups [normal: cardiac index: 4.21 f 0.71 liters/min/mz, peripheral vascular resistance: 1,142 f 245 dynes-see cm-s). The increase in heart rate was more pronounced, so the increase in stroke index was less marked in hyperthyroidism. A marked increase in circulating blood volume with normal distribution in the body was char-
Volume 89
REAPPEARANCE
OF BERIBERI
HEART
DISEASE
IN JAPAN-KAWAI
Ll
H-R
l/min/m2
bea:s/min
3OL
dyne
P
gec.cm-
Figure 1. Changes of hemodynamic parameters before and after treatment in patients under and above 20 years of age. Cl = cardiac index, SI = stroke index, HR = heart rate, PVR = peripheral vascular resistance, F/V = blood turnover rate, CBV = circulatory blood volume.
-age< D---.u
4.
2.
3. S-
1.
3. G-
heart disease. In hyperthyroidism, circulating blood volume was increased only slightly; thus, increase in the flow to volume (F:V) ratio was more pronounced in hyperthyroidism than in beriberi heart disease. ETK and TPP Effect (Table I).
The blood thiamine level and the ETK activity were lower, and the TPP effect significantly higher than normal (p
In most of the patients in the present series beriberi heart disease developed in the summer, presumably because subjects with relative thiamine deficiency have
September
20 4*0
b
before
,
after
2. 5’
2.1o-
mfam+ SD (normal
control)
a sudden increase in thiamine requirements due to strenuous physical exertion during the hot summer. The recent tendency of Japanese teenagers to take excessive carbohydrates such as polished rice, instant noodles, which lack thiamine, and sweet carbonated drinks readily leads to relative thiamine deficiency. Alcohol intake was not a factor in our series. Patients under the age of 20 years demonstrated characteristic features of beriberi heart disease, whereas a hyperkinetic circulatory state was less prominent in older patients, although the grade of thiamine deficiency was essentially equal, In chronic thiamine deficiency, microscopic examination of the myocardium of patients as well as of experimental animals demonstrates severe hydropic degeneration, extensive fibrosis and necrosis, loss of striations and interstitial and perivascular edema [13-161. With these degenerative changes of the myocardium it is assumed that a hyperkinetic circulatory
acteristic of beriberi
Level,
2oyo age 2
aftc.r
O-
2.
0.
before
1/ml
m
1.
Blood Thiamine
ET AL.
1980
The American Journal of Medicine
Volume
89
385
REAPPEARANCE OF BERIBERI HEART DISEASE IN JAPAN-KAWAI
state or high cardiac output cannot be maintained for long. In fact, beriberi heart disease with a hyperkinetic cardiac state, has never been produced in experimental animals with chronic thiamine deficiency [17], Although the thiamine requirement should decrease with age, atypical clinical signs and symptoms with little hyperkinetic circulation in older patients may represent an intermediate process to the advanced stage of beriberi heart disease due to long-standing thiamine deficiency. The response to thiamine administration was prompt in the younger patients but generally poor in the older patients. In the younger patients, a favorable therapeutic effect was obtained with rest alone.
ET AL
It deserves mention that a marked increase in circulating blood volume is an important feature in the differentiation of beriberi heart disease from hyperthyroidism, both of which represent hyperkinetic circulatory states. The increase in circulating blood volume is related to the common occurrence of peripheral edema in beriberi heart disease. AC~~~EDGMENT We are indebted to Dr. Yoshinori Itokawa, Professor of Hygiene, Kyoto University, for thiamine measurements, and to Dr. Alice S. Gary for pertinent advice on the manuscript.
REFERENCES 1.
2. 3.
4. 5. 6. 7. 8. 9.
386
Inoue K, Katsura E: Etiology and pathology of beriberi. In: Shimazono N, Katsura E, eds. Review of Japanese literature on beriberi and thiamine. Vitamin B Research Committee of Japan, Tokyo: Igaku Shoin, 1975; 1. Shimazono J: Kakke (beriberi) (in Japanese). Jap J Med 1919: 7: 237.
Shimazono J: Beriberi. In: Stepp W, Gyorgy P, eds. Avitaminosen und verwandte krankheitszustande. Berlin: Julius Splingor, 1927; 539. Abe T, Hashizume N, Igata A, et al.: Studies on pathogenesis in beriberi heart disease and beriberi neuropathy (in Japanese). Nutrition Diet 1977; 30: 523. Kawai C, Wakabayashi A, Hirose K, et al.: A beriberi heartlike syndrome: metabolic heart disease or non-specific myocarditis [abstract)? Jap Circ J 1976; 40: 514. Kusukawa R, Kinoshita M, Shimono Y, et al.: The clinical findings of seven cases with high output failure resembling beriberi syndrome (abstract), Jap Circ J 1976; 40: 515. Seriu Y, Uehata H. Bito K, et al.: Five young patients with beriberi heart disease (abstract). Jap Circ J1976: 40: 515. Yui Y, Fujiwara H, Mitsui H, et al.: Furosemide-induced thiamine deficiency (abstract). Jap Circ J 1978; 42: 744. Fujiwara M, Matsui K: Determination of thiamine by the thiochrome reaction; application of cyanogen bromide in
September 1980
The American Journal of Medicine
place of potassium ferricyanide. Anal Chem 1953; 25: 810. 10. Brin M, Tai M, Ostashever AS, et al.: The effect of thiamine deficiencv on the activitv of ervthrocvte hemolvsate transketoiasa. J Nutr 1960; $1: 273. * _ 11. Kuwahara M. Hirakawa A, Kinoshita M. et al.: Analvsis of radiocardiogram by analog computer simulation: Int J Biomed Eng 1972; 1: 13. 12. Remington RD. Schork MA: Statistics with application to the biological and health sciences. Englewood Cliffs, NJ: Prentice-Hall, 1967; 192. 13. Wolf PL, Levin MB Shoshin beriberi. N Engl JMed 1960;262: 1302. 14. Toreson LWE: Diffuse isolated myocarditis associated with dietary deficiency. Arch Intern Med 1944; 73: 375. 15. Yoshitoshi Y, Shibata N, Yamashita S: Expe~mental studies on the beriberi heart. I. Cardiac lesions in thiamine deficient rats. Jap Heart J 1961; 2: 42. 16. Follis RH Jr. Miller MH, Wintrobe MM, et al.: Development of myocardial necrosis and absence of nerve degeneration in thiamine deficiency in pigs. Am J Path01 1943; 19: 341. 17. Hirota Y, Kane RL, Abelmann WH: Cardiovascular effects of exercise in hamsters with experimental thiamine deficiency. Jap Circ J 1979: 43: 99.
Volume 69