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Biomedical subjects

A Saeki

Publications and source records attributed to A Saeki.

At least 19 recordsLinked to original sources
PubMed1996

Adverse influence of systemic vascular stiffening on cardiac dysfunction and adaptation to acute coronary occlusion.

BACKGROUND: [corrected] Age is an independent risk factor for increased mortality from ischemic heart disease. Arterial stiffening with widening of the pulse pressure may contribute to this risk by exacerbating cardiac dysfunction after total coronary artery occlusion. METHODS AND RESULTS: To test the above hypothesis, 14 open-chest dogs underwent surgery in which the intrathoracic aorta was bypassed with a stiff plastic tube. Directing ventricular outflow through the bypass widened the arterial pulse pressure from 41 to 115 mm Hg at similar mean pressure and flow. Hearts ejecting into the native aorta (NA) exhibited only modest dysfunction after two minutes of mid-left anterior descending coronary artery occlusion. However, the same occlusion applied during ejection into the bypass tube (BT) induced far more severe cardiodepression (ie, systolic pressure fell by -41+/-10 mm Hg for BT versus -15+/-3 mm Hg for NA, and end-systolic volume rose by 15+/-3 versus 6+/-2 mL), with a threefold greater decline in ejection fraction. This disparity was not due to higher baseline work loads because total pressure-volume area was similar in both cases. Furthermore, marked increases in basal work load and wall stress induced by angiotensin II infusion (in four additional studies) did not reproduce this behavior. Although peak systolic chamber stress was greater with the BT, this did not increase systolic dyskinesis as measured in the central ischemic zone. However, the total mass of myocardium that was rendered severely ischemic (ie, flow reduced by > or = 80%) was twice as large with BT ejection, likely expanding the region of dyskinesis. This disparity may relate to altered phasic coronary flow during BT ejection, which displays marked enhancement of systolic flow and renders the heart more vulnerable to diminished mean and systolic perfusion pressures. CONCLUSIONS: Cardiac ejection into a stiff systemic vasculature augments cardiac dysfunction and ischemia due to coronary occlusion by tightening the link between cardiac systolic performance and myocardial perfusion. This may contribute to the higher mortality risk from ischemic heart disease due to age.

Acute Disease↗
PubMed1996

Minimal role of nitric oxide in basal coronary flow regulation and cardiac energetics of blood-perfused isolated canine heart.

1. The role of nitric oxide (NO) in the regulation of basal coronary perfusion and ventricular chamber energetics was studied in isovolumetrically contracting isolated blood-perfused canine hearts. Hearts were cross-perfused by a donor animal prior to isolation, and chamber volume controlled by a servo-pump. Coronary sinus flow and arterial-coronary sinus oxygen difference were measured to determine energetic efficiency. 2. NO synthase (NOS) was competitively inhibited by NG-monomethyl-L-arginine (L-NMMA; 0.5 mg kg-1, intracoronary), resulting in a reduction of acetylcholine (50 micrograms min-1)-induced flow augmentation from 143 to 62% (P < 0.001). 3. NOS inhibition had no significant effect on basal coronary flow. Coronary pressure-flow relationships were determined at a constant cardiac workload by varying mean perfusion pressure between 20 and 150 mmHg. Neither the shape of the relationship, nor the low-pressure value at which flow regulation was substantially diminished were altered by NOS inhibition. 4. Myocardial efficiency was assessed by the relationship between myocardial oxygen consumption and total pressure-volume area (PVA), with cavity volume altered to generate varying PVAs. This relative load-independent measure of energetic efficiency was minimally altered by NOS inhibition. 5. These results contrast with isolated crystalloid-perfused heart experiments and suggest that in hearts with highly controlled ventricular loading and whole-blood perfusion, effects of basal NO production on coronary perfusion and left ventricular energetics are minimal.

Acetylcholine↗
PubMed1996

Effects of milrinone and sulmazole on left ventricular mechanoenergetics in canine hearts.

BACKGROUND: The effect of cardiotonic drugs with calcium-sensitizing effect (Ca2+ sensitizers) on cardiac mechanoenergetics is not fully understood. Accordingly, the effects of milrinone (a phosphodiesterase inhibitor) and sulmazole (a calcium sensitizer with a phosphodiesterase-inhibiting effect) on left ventricular mechanics and energetics were studied. METHODS AND RESULTS: In excised, cross-circulated canine hearts, myocardial oxygen consumption (Vo2), left ventricular contractility index (Emax), and systolic pressure-volume area (a measure of ventricular total mechanical energy) were measured before and during administration of either drug. Milrinone significantly increased Emax by 108.7 +/- 45.9% (mean +/- SD), from 6.3 +/- 3.5 to 13.1 +/- 6.8 mmHg.mL-1.100 g (P < .05), and sulmazole, by 73.6 +/- 54.2%, from 6.3 +/- 2.6 to 10.3 +/- 2.9 mmHg.mL-1.100 g (P < .05). Milrinone significantly abbreviated the contraction duration (Tmax) from 171 +/- 19 ms to 153 +/- 20 ms (P < .05), whereas sulmazole did not (164 +/- 36 ms to 161 +/- 31 ms, not significant), suggesting that the inotropic mechanisms of these two drugs differed. However, both drugs significantly increased the Vo2 intercept of the Vo2/pressure-volume area relation (milrinone: 0.027 +/- 0.004 to 0.036 +/- 0.003 mL O2/beat/100 g, P < .05; sulmazole: 0.025 +/- 0.005 to 0.032 +/- 0.006 mL O2/beat/100 g, P < .05) without significantly changing the slope (reciprocal of contractile efficiency). This parallel upward shift of the Vo2/pressure-volume area relation was similar to that observed with epinephrine and ouabain in our previous studies. CONCLUSIONS: These results suggest that the two positive inotropic drugs exhibit similar mechanoenergetic effects in the normal canine heart despite the different mechanisms of action.

Animals↗
PubMed1996

Mechanoenergetics of negative inotropism of ventricular wall vibration in dog heart.

Mechanical vibration depresses cardiac contractility. We studied the mechanoenergetic effects of this negative inotropism in the left ventricle (LV) of an isolated, cross-circulated dog heart preparation. We took full advantage of the mechanoenergetic relationship among the LV end-systolic elastance (Emax, contractility index), systolic pressure-volume area (PVA), and myocardial oxygen consumption (VO2). PVA is a measure of the total mechanical energy that cardiac contraction generates. PVA correlates closely with VO2. The VO2 intercept of the VO2-PVA relation reflects the VO2 component for excitation-contraction (E-C) coupling plus basal metabolism (PVA-independent VO2). VO2 above the PVA-independent VO2 reflects the VO2 component for mechanical contraction (PVA-dependent VO2). When we applied 70-Hz vibration of 2-mm amplitude to a LV wall region, it instantly decreased Emax and PVA by 20%, followed by a 10% decrease in VO2 at a fixed volume. However, the vibration neither lowered the VO2-PVA relation obtained at different LV volumes, unlike ordinary negative inotropism, nor changed its slope (1.88 +/- 0.23 vs. 1.86 +/- 0.23 x 10(-5) ml O2.mmHg-1.ml-1). The virtually zero delta PVA-independent VO2/delta Emax with vibration indicates a much smaller O2 cost of Emax than that seen with calcium and propranolol inotropism. These mechanoenergetics support the hypothesis that mechanical vibration primarily suppresses cardiac contractility without suppressing E-C coupling.

Animals↗
PubMed1996

Pulse pressure-related changes in coronary flow in vivo are modulated by nitric oxide and adenosine.

Acute increases in arterial pulsatile load imposed on the left ventricle can increase coronary flow without commensurate changes in myocardial oxygen consumption. One explanation is that augmenting pulsatile perfusion at the same mean pressure itself stimulates flow by releasing endothelium-mediated vasorelaxant factors such as NO. The present study tested this hypothesis and determined whether NO and adenosine modulate this response. In open-chest anesthetized dogs, the distal left anterior descending coronary artery (LAD) was whole-blood-perfused by a novel servopump system to control mean and pulsatile perfusion pressure within the isolated vascular bed. Central aortic pressure was measured, stored to computer memory, and then digitally modified (varying the pulse pressure [PP]) to generate a real-time servocommand that was still synchronous with ventricular contraction. Left heart workload was unchanged. LAD flow was measured before and after increasing the PP (to 60 to 100 mm Hg) from baselines of either 0 or 40 mm Hg. With normal basal coronary vascular tone, raising the PP increased flow (+9 +/- 2% at a PP of 100 mm Hg). This response was markedly amplified (+39 +/- 8%) when basal tone was first partially reduced by adenosine. Competitive inhibition of NO synthase by N omega-monomethyl-L-arginine reduced acetylcholine and PP-dependent flow responses by 50%. Thus, enhanced pulsatile perfusion increases in vivo coronary flow in part by triggering NO release. The marked augmentation of the PP response with reduced basal coronary tone from adenosine suggests that this mechanism may play a role in improving myocardial perfusion during exercise.

Adenosine↗
PubMed1996

[Diagnosis of pulmonary aspergillosis in cases with cavity as sequela of tuberculosis].

Non-invasive pulmonary aspergillosis is frequently seen in cases with cavity as sequela of tuberculosis. Diagnosis of non-invasive pulmonary aspergillosis is not easy except for cases whose chest X-ray findings show a typical fungus ball. How to diagnose pulmonary aspergillosis was studied in 21 patients who showed changes in the radiological findings of cavity as sequela of tuberculosis. We made sputum culture of Aspergillus, measurement of precipitin antibody titer to Aspergillus fumigatus and measurement of PASTOREX ASPERGILLUS in serum and sputum on the 21 patients (group A). PASTOREX ASPERGILLUS in sputum was evaluated in three grades: 1+ approximately 3+. We diagnosed 14 patients as pulmonary aspergillosis (PA group) among the 21 patients taking into account the chest X-ray findings and the results of the above-stated investigations. The types of chest X-ray findings of these 14 patients were fungus ball type (FB) in 2 patients, productive aspergilloma on the inner wall of a cavity (PAIC) in 8, mixed type with FB and PAIC in 2 and non-specific change in 2. However, there were 3 patients with the chest X-ray findings suggestive of PAIC in 7 patients (non-PA group) who were not diagnosed as pulmonary aspergillosis. Sputum culture were positive in 11 patients of PA group (79%) and negative in all patients of non-PA group. Precipitin antibody were positive in 8 patients of PA group (67%) and negative in all patients of non-PA group. PASTOREX ASPERGILLUS in serum were negative in all 21 patients. PASTOREX ASPERGILLUS in sputum were 3+ (+3) in all 14 patients of PA group and in 2 patients of non-PA group and 2+ (+2) in 2 patients of non-PA group. 12 patients of PA group were treated by antifungal agents and 11 patients responded well to the treatment. We also made sputum culture of Aspergillus and measurement of PASTOREX ASPERGILLUS in sputum on 14 patients (group B) who had respiratory diseases with stable cavities and 17 patients (group C) who had respiratory diseases without a cavity. In group B, sputum culture were positive in 1 patient and PASTOREX ASPERGILLUS in sputum were 3+ (+3) in 2 patients, 2+ (+2) in 1 and 1+ (+) in 2. In group C, sputum culture were negative in all patients and PASTOREX ASPERGILLUS in sputum were 3+ (+3) in 1 patient, 2+ (+2) in 3 and 1+ (+) in 2. Measurement of PASTOREX in sputum was a useful tool to diagnose non-invasive aspergillosis in addition to sputum culture and measurement of precipitin antibody titer. The sensitivity of PASTOREX in sputum was high but its specificity was low, however, its specificity could be raised by applying semi-quantitative analysis of PASTOREX in sputum.

Adult↗
PubMed1996

[Hyperuricemia and insulin resistance].

Hyperuricemia is often associated with obesity, hypertension and dyslipidemia, and is thought to be a risk factor for cardiovascular disease, thereby making resemblance to the insulin resistance syndrome. Our data showed a low, but significant correlation between serum uric acid concentration and the degree of insulin resistance (GIR) estimated by euglycemic hyperinsulinemic clamp method in 67 subjects with combined normal glucose tolerance and IGT(r = -0.278, p < 0.05). Plasma HDL-C and TG levels were also correlated with uric acid levels. One hundred sixty NIDDM patients who had undergone the clamp study were stratified into 5 groups according to the serum uric acid level. In the top quintile (UA : 7.8 +/- 0.8 mg/dl), BMI, male prevalence, plasma TG, HDL-C, fasting IRI, and total IRI response(0 + 60 + 120 min) during meal tolerance test were significantly higher, while age and GIR value tended to be lower without significance compared with those in the bottom quintile (UA : 3.4 +/- 0.5 mg/dl). These results, which are in agreement with the previous studies, support the notion that elevated serum uric acid is a feature of insulin resistance syndrome.

Cardiovascular Diseases↗
PubMed1995

Prevalence of macro- and microvascular diseases in non-insulin-dependent diabetic and borderline glucose-intolerant subjects with insulin resistance syndrome.

This study was undertaken to ascertain whether patients with insulin resistance syndrome, a cluster of risk factors for coronary artery disease (CAD), are really a high risk population for macro- and microvascular diseases in Japanese NIDDM and borderline glucose-intolerant subjects. A diagnosis of insulin resistance syndrome was made if four of the six following criteria are satisfied: glucose disposal rate < 2.2 mg/kg/min, fasting plasma IRI > 15 microU/ml or peak plasma IRI > 100 microU/ml during meal tolerance test, plasma triglyceride > 150 mg/dl at fasting or > 200 mg/dl after meal, serum HDL-cholesterol < 40 mg/dl, blood pressure > 140 mm Hg systolic and > 90 mm Hg diastolic or treatment with antihypertensive agents, and body mass index (BMI) > 27 for men or > 25 for women. We compared the prevalence of CAD, cerebral vascular disease (CVD), peripheral vascular disease (PVD), retinopathy and nephropathy between the insulin resistance syndrome group (group A, n = 57) and the remaining group (group B, n = 164). Both groups did not differ with respect to age, duration of diabetes, BMI, fasting plasma glucose, HbA1c, composition of NIDDM and borderline glucose-intolerance (BGI) or treatment modality. The prevalence of CAD was significantly higher in group A compared with that in group B (31.6% vs. 14.0%, P < 0.002), but not for CVD (8.8% vs. 3.7%, respectively, P = 0.12) or PVD (1.8% vs. 2.4%, respectively, P = 0.76). The prevalence of late-stage retinopathy in group A was significantly higher than that in group B (12.3% vs. 2.4%, respectively, P < 0.005). Macroalbuminuria, but not microalbuminuria, was significantly higher in group A than that in group B (12.3% vs. 3.6%, P < 0.02). We conclude that the insulin resistance syndrome preferentially increases the development of CAD, and is also involved in the progression of microvascular diseases.

Adult↗
PubMed1995

The relationship between insulin resistance and insulin secretion in Japanese subjects with borderline glucose intolerance.

Insulin resistance and impaired insulin secretion can be involved in the development of non-insulin-dependent diabetes mellitus (NIDDM), but their relative importance or temporal relationship are poorly understood. To elucidate this issue, we studied 51 subjects with borderline glucose intolerance (BGI) and 18 normal glucose tolerant subjects (NGT) according to the Japan Diabetes Society criteria. The glucose infusion rate (GIR, mg/kg/min), an index of whole body insulin resistance (IR), was measured by the euglycemic (80 mg/dl) hyperinsulinemic clamp technique (insulin infusion rate 1.12 mU/kg/min). Insulinogenic index (delta IRI/delta BS at 30 min) and the insulin area under the curve during a 75-g oral glucose tolerance test (OGTT) were estimated. In the BGI subjects, the GIR values showed marked variation ranging from 2.24 to 10.44 mg/kg/min (5.54 +/- 0.31, mean +/- S.E.M.). The GIR values were lower in obese BGI subjects compared with non-obese BGI and NGT subjects, and the insulin area was markedly higher in BGI subjects with increased insulin resistance. There was a significant negative correlation between the GIR values and the insulin area or delta IRI/delta BS (30') ratio in the subjects with BGI either in the whole group or solely in the non-obese group. We conclude that the increased insulin secretion compensates for the peripheral insulin resistance of subjects with slightly deteriorated glucose tolerance, implying that insulin resistance plays an important role in the pathogenesis of NIDDM in some fraction of Japanese population.

Adolescent↗
PubMed1995

Metabolic regulation and microangiopathy in a cohort of Japanese IDDM-patients.

In Caucasian patients with insulin-dependent diabetes mellitus (IDDM) proliferative diabetic retinopathy (PDR) and persistent proteinuria (PP) are associated, and major risk factors for development of microangiopathy have been identified. The aim of the present study was to evaluate whether these risk factors are also relevant and whether an association exists between the microangiopathic complications in Japanese IDDM-patients. A clinic-based cohort of 324 Japanese IDDM-patients was followed (a mean follow-up of 7 years). Annual examination for development of PDR and PP was performed. Fifty-eight patients developed PDR and 24 developed PP. Development of PDR was associated to high HbA1c-levels, i.e., the 4th quartile (RR 7.9, P < 0.0001), background retinopathy at admission (RR 9.9, P < 0.0001), high age at diabetes onset (RR 2.9, P < 0.0001) and female gender (RR 1.7, P < 0.05). Development of PP was associated to high HbA1c-levels (RR 2.8, P < 0.001) and background background retinopathy at admission (RR 7.9, P < 0.0001). The risk of developing PP was 9 times higher in patients developing PDR than in patients not developing PDR (P < 0.0001). The effect of metabolic control in our cohort was similar to that found in the DCCT and SDIS studies. In conclusion, development of PP is closely associated with PDR, also in Japanese IDDM-patients. The effect of metabolic control is the same as in Caucasian patients. Development of malignant angiopathy in IDDM-patients is not confined to Caucasian IDDM-patients, and the incidence rates are comparable to those found in Caucasian IDDM.

Adolescent↗
PubMed1995

Cardiac quick-release contraction mechanoenergetics analysis using a cardiac muscle cross-bridge model.

Huxley's sliding filament cross-bridge muscle model coupled with parallel and series elastic components was simulated to examine the conflicting reports on the amount of energy saved by quick release at the peak contraction time. Cross-bridge energy utilization was determined by considering the ATP hydrolysis for the cross-bridge cycling. The quick-release cases were simulated by letting the muscle fiber suddenly shorten to the resting fiber length at peak systole, and then the contraction was allowed to continue at the resting length. Simulation results demonstrated that, using realistic parameter values, typically approximately 15% of the muscle fiber energy is used after peak systole (and approximately 30% of the cross-bridge energy), but this is also a function of the muscle fiber properties characterized by cross-bridge association and dissociation rate constants. Increasing the kinetic rate constants, the series elasticity, the initial fiber length, or the time of peak intracellular calcium will increase the amount of energy left, which may explain some of the discrepancies in the literature. Cardiac muscle hypertrophy will increase the fraction of muscle fiber energy left after peak systole to approximately 30%. The strongest indicator of the percent energy left at peak systole was the time the fiber reached peak systole, and as the fiber reached peak systole faster, the amount of energy saved by quick release increased.

Animals↗
PubMed1995

Newly discovered familial juvenile gouty nephropathy in a Japanese family.

Our attention was initially called to 2 young Japanese sisters with gout and renal insufficiency, which led to an investigation of members of their family with similar conditions. One sister, a 26-year-old woman who had suffered from polyuria since infancy, suffered from gout and renal insufficiency. Her younger sister also had a history of polyuria, hyperuricemia, and moderately reduced renal function. Their urinary uric acid levels were reduced but purine enzyme activities in the erythrocytes were normal. A renal biopsy specimen from the younger sister showed severe interstitial fibrosis with tubular atrophy. An investigation of the family revealed an autosomal dominant transmission pattern. We believe these are new familial cases of juvenile gouty nephropathy found in a Japanese family.

Adult↗
PubMed1995

systolic flow augmentation in hearts ejecting into a model of stiff aging vasculature. Influence on myocardial perfusion-demand balance.

Age-related arterial stiffening and widening of the pulse pressure elevates ventricular systolic wall stress while it lowers diastolic coronary perfusion pressure. These changes are thought to adversely alter the balance between myocardial work load and blood supply. To test this hypothesis, the native compliant thoracic aorta was surgically bypassed by a stiff tube in reflex-blocked anesthetized dogs. Ventricular outflow was directed into either native aorta or the bypass; the latter resulting in an increase in arterial pulse pressure from 37.8 to 107.5 mm Hg (P < .001), with minimal change in mean pressure and flow. Cardiac work load was assessed by pressure-volume area (PVA), which combines external and internal left ventricular work and is linearly related to myocardial oxygen consumption (MVO2), and by MVO2 itself. Regional phasic and mean coronary flow were measured in the left anterior descending coronary artery, and global flow was assessed by radiolabeled microspheres. Myocardial supply-demand balance was assessed by comparing flow at matched PVA or MVO2, flow-PVA relations, and endocardial-to-epicardial flow ratios. When blood flow was directed into the stiff bypass tube, peak systolic pressure, wall stress, and PVA all rose nearly 50%, yet diastolic perfusion pressure fell by 20 mm Hg (all P < .01). Rather than being compromised, however, mean coronary flow rose by 34%, maintaining the same endocardial-to-epicardial flow ratio (approximately 1.1). Flow augmentation persisted when data were compared at matched work load (PVA or MVO2), and mean arterial pressure, as well as over a range of work loads (P < .001 from ANCOVA of flow-PVA relations). The increased flow resulted from enhanced systolic perfusion, which nearly equaled diastolic flow when ejection passed into the stiff bypass. These data counter the notion that cardiac coupling with a stiff arterial system (as with aging) necessarily compromises myocardial flow versus metabolic demand. However, the data highlight a greater role of systolic flow under such conditions and also raise the novel suggestion that enhanced pulsatility of the arterial pressure waveform may itself augment coronary perfusion.

Aging↗
PubMed1995

Insulin sensitivity and negative insulin feedback after pancreas transplantation in insulin-dependent diabetic patients.

The aims of this study were to determine the change in the rate of insulin-stimulated glucose disposal (insulin sensitivity) and the ability of insulin to inhibit its own secretion in four pancreas-kidney transplant recipients with insulin-dependent diabetes mellitus. Insulin sensitivity (glucose infusion rate, GIR) was measured by a euglycemic hyperinsulinemic clamp technique before and 2, 6 and 12 months after transplantation. The GIR values in the four recipients were normalized within 2 months and remained normal for 12 months after transplantation, despite long-term steroid therapy for immunosuppression. Physiological hyperinsulinemia (50-70 microU/ml) suppressed plasma C-peptide, but its nadirs were still higher than the basal levels in normal controls. Taking into account evidence of a minimal increase in the concentration of circulating insulin that inhibits insulin secretion in healthy subjects and evidence of increased insulin secretion in pancreas recipients, the authors speculate that defective feedback inhibition of insulin secretion could contribute, at least in part, to the disproportionate basal hyperinsulinemia in patients with a denervated, transplanted pancreas in the absence of insulin resistance.

Adult↗
PubMed1995

Association of sick sinus syndrome with hyperinsulinemia and insulin resistance in patients with non-insulin-dependent diabetes mellitus: report of four cases.

We report four non-insulin-dependent diabetic (NIDDM) patients accompanied by a unique combination of sick sinus syndrome (SSS) and hyperinsulinemia of unknown etiology. SSS of all four cases was due to sinus arrest in association with paroxysmal atrial fibrillation (Rubenstein-III). Of special interest is that one patient showed a high prevalence of SSS and NIDDM among her close relatives. Hyperinsulinemia of moderate degree was seen at fasting state or after carbohydrate ingestion in the absence of obesity. The resistance to the action of insulin on glucose metabolism which was evaluated in three patients by the euglycemic hyperinsulinemic clamp study was found to be comparable to the lowest quartile level for common NIDDM patients. Because insulin is a physiological regulator of cell-membrane Na+/K+-ATPase, we speculate that malfunction of the sinus node automaticity may be caused by chronic exposure to hyperinsulinemia secondary to insulin resistance in these NIDDM patients.

Aged↗
PubMed1995

[RAEB in T with monosomy 7 after treatment of severe aplastic anemia with long term G-CSF].

A 19-year-old male who suffered from severe aplastic anemia had been treated with granulocyte colony stimulating factor (G-CSF) from September 1991. Marked increase of hematopoietic cells in his bone marrow was observed, and maintenance administration of G-CSF was continued. 15 months later, myeloblasts with nuclear abnormality increased, and 22 months later, myeloblasts with chromosomal abnormality presenting 46, XY, -7, +21 exceeded 20%, and aplastic anemia seemed to be transformed into refractory anemia with excess of blasts in transformation (RAEB in T). The usefulness of G-CSF in the treatment of aplastic anemia is now established, but there are some reports questioning the effect of long-term administration, especially transformation to MDS with monosomy 7. Leukemic transformation from aplastic anemia is very complex, but in some cases, long term administration of G-CSF may affect the natural course and may lead to the earlier development of leukemia.

Adult↗
PubMed1995

[Acute myelomonocytic leukemia complicated with syndrome of inappropriate secretion of antidiuretic hormone, nephrotic syndrome, and hemophagocytic syndrome].

A 59-year-old man was admitted to our hospital because of fever in August 1991. Bone marrow showed normocellularity with 41.5% of CD13, 14, 33 positive blasts, and a diagnosis of AMMoL was made. Laboratory investigation revealed hyponatremia and elevated serum ADH level, indicating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Intensive chemotherapy successfully induced hematological complete remission and his serum sodium level became normal. In February 1992, he developed proteinuria and findings were consistent with nephrotic syndrome (NS). Renal biopsy specimen showed membranous proliferative glomerulonephritis and massive infiltration of macrophages, and his serum interleukin 6 level was elevated. Five months later, he suffered from pancytopenia and elevation of biliary enzymes with increase of hemophagocytic histiocytes in his bone marrow (hemophagocytic syndrome). He transiently responded to low dose chemotherapy but he died due to severe infection. It is interesting that association between macrophages and/or cytokines with these various complications was suggested in AMMoL.

Fatal Outcome↗