Among 324 cases of aplastic anemia newly diagnosed from January 1973 to September 1976 by the members of the study group on the specific hematologic diseases supported from the Ministry of Health and Welfare of Japan, forty four cases were associated with the administration of chloramphenicol (CP). They consisted of about 15% of all cases of aplastic anemia and 30% of secondary cases. These CP associated cases showed the following characteristics; about 70% cases were female; length of the preclinical period or mortality rate were not correlated with the doses of CP administered; CP associated cases took more rapid courses than others and all fatal cases died within three months after the diagnosis of aplastic anemia; granulocytes counts were significantly lower than those of other cases. In addition, 4 cases were hematologically almost normal just before the CP administration and then became pancytopenic within 3 months. In these cases, induction of aplastic anemia by CP administration was strongly suspected. From these observations, it was concluded that the cases who developed aplastic anemia within 3 months of CP administration would be suspected of being induced by CP, and in those cases who were confirmed to be hematologically normal before the CP administration, this induction is strongly suspected. Only the latter cases would be rationally called as CP induced aplastic anemia.

抄録全体を表示

Mechanism of reversible deppression of hematopoiesis due to chloramphenicol was investigated in ICR male mice using spleen colony method.
(1) Hematopoietic suppression was characterized by marked decrease of reticulocyte count and erythrocyte ⁵⁹Fe incorporation. These findings were normalized following withdrawal of chloramphenicol treatment. A negative correlation was proved between red cell iron utilization and daily dose of chloramphenicol.
(2) Number of splenic colony from bone marrow cells treated by chloramphenicol in vivo was proved to be significantly increased following injection for 7 days and decreased to control value at least 2 weeks after cessation. Erythroid/Granuloid colony ratio appcared to be elevated at the same time.
(3) Number of CFU-s homed in the spleen of chloramphenicol treated recipient mice decreased as time passed after injection, accompanying with cloudy swelling of the organ.
From these results, it is suggested that the differentiation of erythroid stem cell to erythroblast may be impaired by chloramphenicol in the reversible suppression of erythropoiesis.

抄録全体を表示

The pathogenesis of aplastic anemia has not been clarified, but stem cell failure has been considered as the basis of development of the disease.
Chloramphenicol (CP) has been suggested to be one of causative agents for aplastic anemia.
We have studied the in vivo effect of CP on hemopoietic stem cells in normal mice. Numbers of in vitro colony-forming cells (CFU-C) and spleen colony-forming cells (CFU-S) were not significantly changed in femur or spleen of the mice injected with large dose of CP for long period, notwithstanding an inhibitory effect of CP on colony growth in vitro. Then, we investigated the effect of CP on CFU-C in W-anemic mice in which number of CFU-S is extremely reduced, and produced the various hemopoietic states to observe the effect of CP administration on the stem cell.
In in vivo experiments using W-anemic mice, CFU-C of the femur and spleen was not influenced by CP administrations.
A remarkable increase of CFU-C in the spleen was observed after endotoxin injections, in which CP worked as an inhibiting agent. Both CFU-C and CFU-S were reduced by CP administration in mice which received syngeneic bone marrow transplantation after lethal irradiation. A mode of action of CP on hemopoietic stem cells in vivo was discussed on the bases of these results.

抄録全体を表示

In order to clarify the mechanism of myelotoxicity of chloramphenicol (CP), the comparative studies were performed on CP induced colony growth inhibition of CFU-E, CFU-C and CFU-S in C57BL mice marrow cells in vitro and in vivo.
In vitro effect of CP: ⁵⁹Fe-incorporation into heme of reticulocytes was not affected by CP at 1000 μg/ml or less. Erythropoietin responsiveness of marrow cells was inhibited at 500 μg/ml. The colony growth of CFU-E and CFU-C was inhibited dose-dependently by CP, and 50% inhibition occurred at 17 μg/ml in CFU-E and 19 μg/ml in CFU-C respectively. The colony growth activity of marrow cells pretreated with CP was maintained better in CFU-S than CFU-E.
In vivo effect of CP: The colony growth of CFU-E, CFU-C and CFU-S in marrow cells from mice injected with CP (5 mg for 7 days) did not change, significantly compared to that of saline control mice as well as CFU-S in lethally irradiated recipient mice given the same dose of CP.
These results indicates that CP clearly exhibits a selective inhibition on the differentiation and proliferation of committed stem cell in vitro. However, the discrepancy of the action of CP in vitro and vivo raises an important problem. It might relate with the modifying host factors, but not relate the drug-metabolizing host ability because CFU-E colony growth inhibition was occurred by the addition of the serum from mice injected with CP.
These data of present work provide some evidence to the studies on the mechanism of myelotoxicity of CP.

抄録全体を表示

First, we studied 35 published cases of “chloramphenicol-hepatitis-aplastic anemia syndrome.”
In clinical features, those cases resembled to aplastic anemia attributed to chloramphenicol rather than “hepatitis aplastic anemia syndrome”, so we thought that causes of both hepatitis and aplastic anemia were probably related to chloramphenicol.
Second, we studied the influence of liver disorders and chloramphenicol on the hemopoietic stem cell compartment.
The results were summalized as follows;
1) Chloramphenicol added to culture medium showed concentration related inhibition of in vitro colony formation in man and mice.
2) Chloramphenicol given to donor mice reduced CFUc but not CFUs.
3) Chloramphenicol given to recipient mice did not affect the number of splenic colonies, but produced ultrastructural changes of erythroblasts in colonies.
4) CFUc of patients with acute hepatitis and liver cirrhosis were fewer than normal individuals, but CFUc and CFUs in mice with hepatic injury by CCl₄ were not affected.
5) Liver injury by CCl₄ did not affect the splenic colony formation in recipient mice.
6) Chloramphenicol given to mice with liver injury by CCl₄ reduced CFUc of donor and splenic colony numbers in recipient.

抄録全体を表示

The thrombolytic effect of urokinase (UK) was evaluated in vivo and in vitro. PTT, silicone PTT, prothrombin time and fibrinogen were determined by ordinary methods. Plasmin, plasminogen, plasminogen activator were assayed using the euglobulin fraction and plasminogen free fibrin plate. Fibrinolytic split products were estimated using SCT and STT (30'). Plasmin inhibitor was measured by the fibrin clot lysis time method. Platelet aggregation studies were performed using an aggregometer (Bryston Co.). Platelet aggregation rate, T1/2, and R were estimated. R has been reported to be associated with Factor XII activity, and a low R indicates hypercoagulability.
Results and conclusion.
1) The effects of UK on the coagulofibrinolytic system and platelet function in rabbits were examined and the following results were obtained.
a) A hypercoagulable state (shortening of silicone PTT and PTT) and a hyperaggregable state of the platelet (small R) were observed following administration of small one shot doses of UK (1×10³, 10×10³U).
b) A hyperfibrinolytic effect (elevation of activator, decrease of plasminogen and increase of FDP) was observed when large one shot doses (100×10³, 200×10³U) of UK were administered.
2) The effect of UK on clot lysis in vitro was evaluated and the following results were obtained.
a) Newly formed clot was dissolved more easily by UK than old clot but 4 hours after clot formation, the thrombolytic effect of UK was not changed.
b) Plasminogen-free clot, prepared using lysin-sepharose affinity chromatography, was not dissolved by UK in plasminogen-free medium but was dissolved in medium containing plasminogen.
c) The effect of UK on clot lysis by activation of intrinsic clot plasminogen was inhibited by the inhibitor in the medium.
d) Clot lysis was observed when a clot was incubated for one hour in medium containing 100 U/ml of UK, but not in that 10-50 U/ml of UK. However, clot lysis was also observed when a clot was incubated for 24 hours in medium containing only 10 U/ml of UK. This means that a clot dissolves when incubated for a long time in medium containing even small doses of UK.
3) The effect of UK on clot lysis in vivo was evaluated. A clot was placed in a chamber connected in a carotid-jugular extracorporeal shunt of a rabbit. Weights of the clot and mural actual thrombus were determined to evaluate the effect of UK after its infusion.
a) The clot did not dissolve and mural thrombus increased when 10-100×10³ U of UK was administered by one shot. This means that the initial infusion gave rise to a paradoxical coagulant effect mediated by activation of some coagulant factors and a low-grade process of plasminogen activation.
b) The clot dissolved to a small degree when more than 100×10³ U of UK with heparin was administered for one hour.
c) Clot lysis, however, was observed clearly when 100×10³ U of UK was infused for 24 hours with heparin. This suggested that for clot lysis by UK, the blood level of UK and heparin must be kept constant.

抄録全体を表示

Concerning dose of urokinase, much amount of it has been administered in U.S.A. and European countries (8, 9, 10, 11). The authors investigated on the effects of urokinase on coagulation, fibrinolysis and platelets by in vitro and in vivo studies.
(1) Urokinase showed fibrinolysis rather than fibrinogenolysis, and made PTT shorter in its clotting time from activation of Factor XII, and damaged platelet function in in vitro and in vivo studies. The rabbits who were infused 6,000 to 60,000 CTA units of urokinase showed many microthrombi in lungs and kidneys.
(2) Heparin showed the promoting effect on fibrinolytic activity of urokinase in in vitro studies, and when urokinase was infused into the rabbits with heparin no microthrombi were observed in the lungs and kidneys.
(3) In clinical case, when urokinase was administered alone, PTT was shortened, platelet retention rate was decreased, but elevated fibrinolysis was observed for 6 to 8 hours at 12,000 units of it. For prevention of the coagulation system from hyper-coagulable state, 12,000 CTA units of urokinase was administered with 5,000 units of heparin three times per day for five days, and then anti-coagulant therapy using coumarine was applied continually. If the clinical signs were not improved, urokinase was again administered with this anti-coagulant therapy.

抄録全体を表示

The conventional assay methods of coagulation are encountering the difficulties in the detection of the hypercoagulable state including thrombosis, because the most of these methods were developed for the detection of the hypocoagulable state.
It has been argued that the qualitative change in fibrinogen occurred in the process of hypercoagulability. The fibrin molecules, produced by the small amount of thrombin, form the complexes with fibrinogen, FDP and other plasma protein instead to form solid fibrin polymers. These complexes are called as soluble fibrin monomer complexes (SFMC), and the presence of these high molecular complexes of fibrinogen derivatives in plasma would suggest the hypercoagulable state. The detection method of SFMC was described in this paper.
One ml of each plasma specimen was chromatographed on Biogel A-5m column (15×300mm), and the elution profile of fibrinogen antigen was obtained using TRCHII or SCT. After the analysis of 91 cases of normal, thrombotic, DIC and other cases, the elution profiles were classified into three typical patterns: normal, thrombotic and DIC (Fig. 1). The elution volumes at which the fibrinogen antigen begun to flow out of the column was arbitrarily designated as the initiation volume (V₁). It was concluded that from the other experiments in vivo and in vitro that the decrease of Vi of test plasma suggested the presence of the small amount of SFMC and this index was found to well reflect the hypercoagulable state of thrombosis and DIC (Fig. 2).
At the thrombolysis in vivo, the fibrinogen remains relatively resistant to fibrinolysis in the circulating blood. This beneficial mechanism was simulated in vitro and it was found that three factors are essential for the differentiating fibrinolysis: the substrate is fibrin, the activation of plasminogen is performed in situ and the sufficient amount of plasma inhibitors is present.
Sixty thousands units of UK were infused into three cases of cerebral thrombosis respectively (Fig. 4). Platelet count, PT, PTT, fibrinogen concentration nor FDP were not changed all through the experiments and only the temporal shortening of euglobulin lysis time was observed. It was supposed that the repeated infusion of UK at several hours are necessary for the sufficient thrombolytic therapy.
Vi's of these cases were increased after the infusion of UK which suggested the disappearance of SFMC from the circulating blood and indicated the effectiveness of thromblytic therapy. But 24 hours later the Vi's were again returned to the preinfusion value, and the thrombolytic therapy with UK seemed not necessarily improve the hypercoagulable state itself.
In the course of thrombolytic therapy of a case of atrial fibrillation, the abrupt discontinuation of UK was followed by the thromboembolic attacks of left renal artery and internal carotid artery in spite of the combined anticoagulant therapy with Warfarin (Fig. 7). Vi of this case remained at the decreased level of throbosis and finally the value turned to the pattern of DIC. It was stongly recommended that the anticoagulants or the agents suppressing platelet function are combined with the thrombolytic therapy. for the prevention of this kind of rebound.

抄録全体を表示

In this symposium entitled “Treatment of the Thrombosis”, the authors presented and discussed about five topics concerning the pathophysiology and management of the cerebral thromboembolism based upon 40 clinical materials and the experimental “no-reflow state” in cerebral ischemia produced by elevating intracranial pressure in dogs.
1) PATHOPHYSIOLOGY AND TREATMENT OF “ACUTE AND FATAL CEREBRAL THROMBO-EMBOLISM”: Thrombosis of the internal carotid artery and it's territory had a wide clinical spectrum ranging from TIA to a rapid fatal apoplectic stroke and it is essential to delineate three distinct clinical groups; (1) recurrent attacks with reversible neurologic deficit (2) acute apoplectic progressing stroke and (3) slowly progressing neurological deficit. Of 40 cases, there were 6 apoplectic stoke, 1 slowly progressing type and 33 with recurrent attacks. The acute apoplectic type showed that of acute intracranial space-taking lesion both in clinical and pathological pictures with fatal midbrain hemorrhage due to transtentorial herniation (Fig. 1A, 2A). Of interesting to note, an autopsy case treated with emergency decompressive craniectomy and expired one month later with multiple peptic ulcerations revealed no evidence of brain stem damage (Fig. 1B, 2B). The emergency decompression preventing the herniation proved to be a treatment of choice in cases with the “apoplectic and progressing stroke” of cerebral thrombo-embolism.
2) SOME REMARKS FOR USE OF UROKINASE AND HEPARIN IN THE TREATMENT OF CEREBRAL THROMBOEMBOLISM: Seventeen cases were treated with Urokinase with or without Heparin and the following remarks were obtained. (1) Thrombolytic therapy, to be effective, must be instituted before organized (non-soluble) thrombus and before the cerebral infarction occure, i.e. before 72 hours after the onset. (2) Coexistence of heart valve deseases, intracranial aneurysm, moderate to severe diabetes mellitus and operative wound, especially tracheostomy wound may constitute contraindication. (3) Partial occlusion-mural thrombus may be more effectively solved than complete occlusion of the artery.
3) SUPERFICIAL TEMPORAL AND MIDDLE CEREBRAL (STA-MCA) ANASTOMOSIS (Fig. 3, 4, 5): This was done in 18 cases with occlusive lesion in the carotid arterial system and the follow-up (6 to 22 months) results were reported (Table 1). Indication and contraindication of the procedure were discussed: TIA and RIND with demonstrable lesions sufficient to explain the attacks are good indication, while the acute apoplectic type is contraindication. Although severe neurological deficit is said to be contraindicated, 8 of 12 cases with moderate to severe neurlogical deficits showed limited but favorable results in our series.
4) CAROTID-VERTEBRAL ANASTOMOSIS: This anastomosis offered an additional soure of blood to the cerebral circulation in patients with vertebral artery occlusion or stenosis and was done in three cases. With 5 to 11 months follow-up, beneficial results were obtained in two cases. (as to surgical technique, refer Brain & Nerve 22: 1125∼1138, 1970)

抄録全体を表示

Radiations, chemical agents, viruses and genetic predispositions are considered as possible leukemogenic factors. In this paper authors have demonstrated; 1) a considerablly high frequency of chromosome aberrations of lymphocytes and bone marrow cells in atomic bomb survivors, 2) an existence of chromosome-breaking factor, which damages chromosomes of the normal individuals in the cultures containing the plasma from heavilly exposed survivors, 3) an induction of chromosome aberrations by benzene in the rat bone marrow cells and in the cultures of human lymphocytes, 4) an enhancement of chromosome aberrations of 200 rad irradiation by the treatment of benzene (synergetic effect) and 5) non-parallel relation in Fanconi anemia, an inherited chromosome breakage syndrome, between chromosome aberrations and sister chromatid exchanges induced mitomycin C.
Related with these results, possible relations between leukemogenesis and chromosome aberrations induced by radiations, chemical agents and genetic defect (s) were discussed.

抄録全体を表示

Using various bandings, studies were performed on human leukemic cell chromosomes. Materials comprised 4 cases with malignant lymphoma (ML), 24 cases with acute leukemia (AL), and 23 cases with chronic myelogenous leukemia (CML).
In cases with ML, there were remarkable changes of chromosome structure in addition to chromosome number, suggesting the occurrence of frequent intrachromosomal rearrangements. In 3 out of 24 cases with AL, C/G- or 8/21-translocation. in one case C (?8) trisomy, and also in one case 1/13 tandem translocation were identified. Reciprocal translocation between chromosomes 9 and 22 was identified in all cases with CML. The break point of the chromosome 22 was either band q11 (21 cases) or probably q12 (2 cases), respectively. Analysis of Q- and C-band polymorphisms suggested the clonal origin of the Ph¹ chromosome. Cytogenetic studies were also performed in blastic crisis of CML, where nummerical or structural changes of chromosome constitution were usually found prior to the clinical signs of blastic crisis.
The present study led to the conclusion that a variety of complex chromosome constitution found in leukemia and solid tumor would originate from a simple chromosomal rearrangement (e. g. 8/21- or 9/22-translocation) via clonal evolution.

抄録全体を表示

Utilization of chromosomal findings in the decision to treat or not to treat AML (acute myelogenous leukemia) or ANLL (acute nonlymphocytic leukemia) is introduced. Patients over 70 years of age should not be treated because of the high risk of the treatment related death. Chromosomal findings of bone marrow cells are useful in patients younger than 70 years old. In the latter age group, patients with an n-marrow (a bone marrow with normal metaphases only) or an an-marrow (a bone marrow with abnormal and normal metaphases) can be treated safely. In patients with an aa-marrow (a bone marrow with abnormal metaphases only), the karyotype analysis is helpful. Those with MIKA (minor karyotypic abnormalities) can be treated with relative safety, but those with MAKA (major karyotypic abnormalities) will be killed by chemotherapy. MIKA is characterized by a simple translocation or nondisjunction while MAKA by multiple such events, karyotypic instability etc., the latter type being preferentially associated with EL (erythroleukemia). In the bone marrow of patients with MAKA, when no normal metaphases are detected among 25 or so cells examined, no normal hemopoietic stem cells are expected to be remaining to repopulate the marrow after abnormal ones have responded to chemotherapy.

抄録全体を表示

The reported cases of so-called non-secretory myeloma were collected from the literature. We excluded doubtful cases, in which Bence Jones myeloma could not be denied by repeated examinations of the concentrated urine. Based on 42 definite cases, clinical, pathological and immunological spectrums of so-called non-secretory myeloma have been discussed, comparing with those of secretory myeloma. In addition, a typical case of non-secretory myeloma has been presented.
Frequency of so-called non-secretory myeloma seemed to be less than one per cent of multiple myeloma. In so-called non-secretory myeloma, proteinuria, elevated ESR, anemia, azotemia and thrombocytopenia were found only in the small number of cases, but marked skeletal involvement was demonstrated in all cases. Hypoproteinemia, hypogammaglobulinemia and suppression of each of serum immunoglobulins were present in most cases, as in Bence Jones myeloma. The plasma cell counts of the bone marrow and frequency of their appearance into circulation were not characteristic. The morphology of the plasma cells in so-called non-secretory myeloma was indistinguishable from that in secretory myeloma. Amyloidosis was present in one of ten autopsy cases of so-called non-secretory myeloma. Twenty cases were studied by the immunofluorescent technique. Twelve cases were non-secretory type producing cytoplasmic immunoglobulin or its fragment. Seven cases were non-producing type. It was undetermined whether the remainder was non-secretory or non-producing in type. The cause of death was infection in 61 per cent of so-called non-secretory myeloma. Data as to the survival time of so-called non-secretory myeloma was controversial.
Concerning the pathogenesis of so-called non-secretory myeloma, a variety of explanations has been offered as follows:
(1) Immunoglobulin can not be synthesized in the myeloma cells, because the cellular protein-synthesizing apparatus may not operate due to defective molecular machinery or the myeloma cell may be derived from stem cell or reticulum cell which can not produce immunoglobulin.
(2) The intracellular transport and/or secretory mechanism of immunoglobulin produced is disturbed, because the intracellular proteins do not assemble into whole immunoglobulin molecules or carbohydrate which may play a important role for intracellular transport of immunoglobulins will not be incorporated in immunoglobulin molecules.
(3) Non-antigenic immunoglobulin fragments are produced and they can not be detected by current methods.
The studies on the pathogenesis of so-called non-secretory myeloma will give us an important clue to the mechanism of antibody formation.

抄録全体を表示

Platelet aggregates induced by 3 μM ADP or 1 μg/ml of adrenaline on a screen, which was used in a screen filtration pressure method (SFP, Swank 1961), were observed by a scanning electron microscope. SFP method measured the resistence to flow of a fluid in mmHg as the blood is forced through the screen with multiple micropores (20 μ×20 μ). In 10 samples collected from four healthy volunteers and six patients suffering from Takayasu's disease, cerebral thrombosis, atherosclerosis obliterance, pancreatitis, typical figures of platelet aggregation were observed. There were little red and white blood corpuscles and fibrin nets. A close relationship was observed between the platelet aggregability measured by SFP and the morphological changes in platelet aggregates on the screen. The results suggest that the SFP value was mainly determined with the platelet aggregability.

抄録全体を表示

DIC was induced by infusion of provocative dose of endotoxin and tissue extract of gastric cancer into normal rabbits pretreated of the blockage of RES. But it was not induced after infusion of these substances into thrombocytopenic rabbits pretreated with Busulfan and with blockage of RES. DIC was not also induced after antiplatelet serum into normal rabbits without previous blockage of RES, but in these cases prominent drops of platelet counts and release of PF4 into plasma were observed. In the present study the attempt has been made to investigate the interrelation between the required level of platelet count, the requirements of trigger substances and the blockage of RES in the DIC.

抄録全体を表示

The fundamental study for the size distribution of red cells and platelets was performed by using the electronic cell counter- Coulter Counter, Model ZBI and Channelzyer. Blood counts by Coulter ZBI coincided well with those by the conventional hemocytometer. Edit switch was kept ON in order to eliminate irregular size distribution curves due to long impulses from cells passing through simultaneously into the orifice tube. No significant difference of size distribution curves of red cells was observed by the use of various anticoagulants such as ACD, citric acid, EDTA, heparin and Anglot ET or by the time duration after getting blood samples. However, significant decrease of platelet counts was observed 2 hours after the collection of samples. No significant difference was seen in platelet size distribution. The study was done just after the collection of samples.
The mean cell volume (MCV) from Channelyzer was compared to MCV calculated from red cell counts and hematocrit value. There was significant positive correlation between them (r=0.734, p<0.01) and MCV from Channelyzer was a little bit smaller than that from hematocrit. Average platelet diameter and volume in normal subjects were 3.41 μ±0.35 and 7.31 μ³±0.73, respectively, which coincided well with values reported by the other investigaters.
The application of Channelyzer to the clinical use was presented in the change of red cell distribution curves during the treatment of iron deficiency anemia.

抄録全体を表示

A case of α-methyldopa induced Coombs-positive hemolytic anemia with hyperdirect-bilirubinemia was reported. A 61 year-old man was admitted to the Bokuto Metropolitan Hospital on December 2 1974, with chief complaints of jaundice and anemia.
He had been administered α-methyldopa (750 mg/day) for 25 months before admission because of hypertension at outpatient clinic of his family doctor.
He had been suffered from jaundice with elevated transaminase on July 1974 during antihypertensive therapy.
Laboratory data on admission were the following; Hb 7.2 g/dl, reticulocytes 340‰ total bilirubin 24.9 mg/dl (direct bilirubin 16.9 mg/dl) and haptoglobin 0 mg/dl. Bone marrow aspiration revealed erythroid hyperplasia in marked degree. Both direct and indirect Coombs tests were positive. LE cell, parietal cell antibody, intrinsic factor antibody and thyroid antibody were all negative but ANF was positive.
Anemia and jaundice were improved and indirect Coombs test showed negative respectively since a month after stopping the α-methyldopa therapy.
On April 1975, α-methyldopa was readministered and 5 months later, reticulocytosis, decreased Hb value, positive indirect Coombs test and increased serum bilirubin were demonstrated again.
The etiology of α-methyldopa induced hemolytic anemia and the relationships between this hemolytic anemia and cholestasis were discussed.

抄録全体を表示

A case of primary acquired sideroblastic anemia was described, who died of bone marrow failure after a very short course of illness. The patient, 33 year-old Japanese male, was admitted with a history of anemia of 3 months duration.
On hematological examination at the onset of the disease, marked hyperchromic anemia with the dimorphic pattern of erythrocytes was noted without leukopenia and thrombocytopenia.
Three months later, hematological study revealed the presence of pancytopenia in this patient. Examination of bone marrow disclosed erythroid hyperplasia with minor megaloblastoid change. Iron stores in bone marrow were greatly increased predominantly with ringed sideroblasts. Serum iron was elevated and the ferrokinatic study indicated delayed iron clearance and depressed red cell iron utilization.
Eight months after the admission, the patient died of bleeding in the abdominal cavity. Autopsy revealed hypoplastic bone marrow and the deposition of large amount of hemosiderin in the heart, lungs, liver, spleen, pancreas and kidneys.

抄録全体を表示

Symptoms, signs and the results of pathological and laboratory examinations in thirteen patients in whom eosinophils were 2000/cmm or more in the peripheral blood during the course of their diseases were analyzed. Their pathological changes was remarkably various. Examinations of the bone marrow and peripheral blood revealed that there were certain stimuli to increase especially the myelocyte or more mature eosinophils in the bone marrow and stab or segmented eosinophils in the peripheral blood. The degree of eosinophilia was correlated neither with the lymphocyte count in the peripheral blood nor with the degree of hypergammaglobulinemia. High IgE levels (more than 500 I.U./ml) were found in two patients. Among four patients with asthmatic attacks, only one revealed the high IgE level in the serum. Enzymatic activities in a cell suspension (93% of which was eosinophil) derived from the peripheral blood of the patient with most prominent eosinophilia were measured. Another cell suspension (82% of which was neutrophil) derived from the synovial fluid of the patient with rheumatoid arthritis was used as a control. In the eosinophil suspension, stronger activities of peroxidase and arylsulfatase were found than in the neutrophil one, although the roles of these enzymes on the production or suppression of the multiple pathological changes were uncertain.

抄録全体を表示