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Tomoda, Takashi; Kurashige, Takanobu; Moriki, Toshiaki; Yamamoto, Hiroshi; Fujimoto, Shigeyoshi; Taniguchi, Taketoshi
doi: 10.1002/ajh.2830370402pmid: 1907096
Over‐expression of cellular protooncogenes has been proposed to function in the initiation and maintenance of malignancies. In order to distinguish malignant lymphoma from reactive proliferative diseases, we surveyed the expression levels of three protooncogenes(c‐myc, c‐fos and c‐myb) in malignant lymphoma and reactive proliferative diseases. An increased level of c‐myc or c‐fos mRNA was observed in one case, respectively, out of three malignant lymphomata. The other cases exhibited no enhancement in protooncogenes. These oncogenes are critically regulated during differentiation, but the half‐life of c‐myc mRNA was very short, and the level of the mRNA decreased to the initial level very quickly. Thus, the high level of the expression of these oncogenes may not always be maintained in all malignant cells. We then examined the level of mRNA for poly(ADP‐ribose) synthetase in those cases. An enhanced expression for the synthetase gene was observed in all five malignant lymphomata tested, but no increase in the level of the mRNA was observed in any reactive proliferative cases or normal lymph nodes. These results suggest that enhanced expression of poly(ADP‐ribose) synthetase gene seems to be a common characteristic of protopathic malignant lymphoma. By using the characteristics of malignant lymphoma, the level of mRNA for the synthetase may be applicable for differential diagnosis of malignant lymphoma from several pathologically indistinguishable diseases.
Ieko, Masahiro; Sawada, Ken‐Ichi; Sakurama, Shoki; Yamagishi, Ikuko; Isogawa, Shin; Nakagawa, Shoichi; Satoh, Masahiro; Yasukouchi, Taro; Matsuda, Michio
doi: 10.1002/ajh.2830370403pmid: 1830454
A new case of congenital hypodysfibrinogenemia associated with a thrombotic tendency (thrombosis of the peroneal artery, the pulmonary artery and the deep veins of the lower extremities), is reported. Clotting time using Reptilase was significantly prolonged. The low levels of plasma fibrinogen were demonstrated using both thrombin time (Clauss) method (45.0 mg/ml) and radial immunodiffusion technique (106.1 mg/ml). The fibrinogen is also characterized by a defective polymerization of fibrin monomers. Furthermore, the important functional property of this fibrinogen is that the patient's fibrin adsorbs approximately 31–38% of added tissue‐plasminogen activator (t‐PA) at the time of fibrin formation, whereas control fibrin can adsorb about 79% of added t‐PA. This result could provide an explanation for the thrombotic tendency in this patient. This variant fibrinogen appears to have unique characteristics and has been designated as “Fibrinogen Date,” according to the city where the proband has lived.
Capel, P.; Janssens, A.; Clumeck, N.; Gerard, M.; Feremans, W.; Vandevelde, D.; Fondu, P.
doi: 10.1002/ajh.2830370404pmid: 1907097
Anticardiolipin antibodies (ACA) and lupus‐like anticoagulant (LLAC) have been studied in a group of 142 non‐hospitalized and a group of 72 hospitalized HIV infected patients. We observed a variable frequency of ACA positivity ranging from 7.7% to 30.3% according to the groups of patients and the isotype of immunoglobulin fraction containing ACA activity. None of the patients investigated presented a prolongation of the activated partial thromboplastin time (APTT) compatible with the presence of a LLAC. Some patients presented a weak anticoagulant activity only detected by the tissue thromboplastin inhibition (TTI) test. No positive correlation was found between this latter test and ACA. We conclude that, like in syphilitic patients, ACA present in HIV infected patients are most often not associated with LLAC.
Ono, Kazutoshi; Kurohara, Kazuhiro; Yoshihara, Masahiro; Shimamoto, Yoshinori; Yamaguchi, Masaya
doi: 10.1002/ajh.2830370405pmid: 1858780
A 75‐year‐old female patient with agranulocytosis caused by ticlopidine is reported. She took the drug at 200 mg/day for 30 days to prevent recurrence of cerebral infarction. The leukocyte count at the nadir was 500/μl on the 34th day since she started to take the drug. Complete recovery of her peripheral leukocytes came 12 days after its withdrawal. In this patient, mechanisms of ticlopidine‐caused agranulocytosis were studied. The lymphocyte stimulation test using ticlopidine was negative. In the culture of marrow cells depleted of lymphocytes, ticlopidine directly inhibited the CFU‐C in a dose‐dependent manner. Neither the serum on the day of admission nor the T‐lymphocytes pre‐cultured with ticlopidine had any effect on the CFU‐C. The lymphocyte stimulation test is useless in an attempt to find the causal drug in agranulocytosis if it is caused in a directly toxic manner. Agranulocytosis caused by ticlopidine is rare, but careful follow‐up is necessary in the case of patients on the drug because there are some whose marrow cells are very sensitive to it.
Colombo, M.; Mannucci, P. M.; Brettler, Doreen B.; Girolami, A.; Lian, E. C. Y.; Rodeghiero, F.; Scharrer, Inge; Smith, P. S.; White, G. C.
doi: 10.1002/ajh.2830370406pmid: 1650134
A questionnaire‐based survey Involving 11,801 hemophiliacs from 54 hemophilia centers in the USA and Europe documented the occurrence of hepatocellular carcinoma(HCC) in 10 patients. The crude rate of HCC was 3.2/100,000 patients/year, at least 30 times higher than the background incidence of this tumor in the countries of origin of the patients. All patients were Caucasians with hemophilia A, 39 to 74 years of age, and had liver cirrhosis. All had one or more risk factor for cirrhosis and HCC: 5 were positive for serum hepatitis B surface antigen, 4 had the antibody to hepatitis C virus, and 4 had histories of alcohol abuse. Serum alpha‐fetoprotein, measured in 6 patients, was significantly elevated in 4 (range: 807‐1399 ng/ml), and only moderately elevated in 2 (25 and 171 ng/ml). The onset of HCC was asymptomatic in 5 patients, whereas it was accompanied by jaundice, abdominal pain, or ascites in the remaining patients. Thus, HCC seems to be a more important secondary disease for hemophiliacs than formerly recognized. Since HCC is often asymptomatic, screening hemophiliacs with chronic liver disease with periodic ultrasound scans might increase the chances of detecting HCC at a stage amenable to surgical treatment.
Adams, Paul C.; Chau, Luan A.; White, Martin; Lazarovits, Andrew
doi: 10.1002/ajh.2830370407pmid: 1858781
To assess whether an abnormality in transferrin receptor expression or regulation could represent an underlying metabolic defect in the reticuloendothelial (RE) system in hemochromatosis, monocytes were analyzed for the expression of the transferrin receptor using a monoclonal antibody (Act II) to the transferrin receptor (CD71) and flow cytometric analysis. Hemochromatosis patients (n = 14), and normal volunteers with no clinical evidence of iron overload (n = 14) were studied. A significant inverse relationship was observed for the relationship between the expression of transferrin receptor on monocytes and log(hepatic iron concentration) in hemochromatosis patients (r = −0.59, P < 02) and also for the relationship between the expression of transferrin receptor and log(serum ferritin) in normal volunteers (r = −0.90, P <.001). There was no significant difference in the mean expression of monocyte transferrin receptor between hemochromatosis patients and normal volunteers. However, the expression of the transferrin receptor in hemochromatosis patients was disproportionately higher than would be predicted from the relationship between serum ferritin and transferrin receptor expression in normal volunteers. The inverse relationship of the monocyte transferrin receptor relative to body iron stores in hemochromatosis is consistent with observations in other tissues, and suggests that non‐transferrin iron metabolism, including ferritin, requires further investigation in the RE cell in hemochromatosis.
Friedman, Samuel; Henry‐Amar, Michel; Cosset, Jean‐Marc; Carde, Patrice; Hayat, Marcel; Dupouy, Noelle; Tubiana, Maurice
doi: 10.1002/ajh.2830370408pmid: 1858782
An analysis was performed of all 57 early relapses (ER) (within 18 months of therapy initiation) seen in a group of 301 patients treated on three successive European Organization for Research and Treatment of Cancer (EORTC) protocols from 1964 to 1981; to determine whether a posttherapy elevated erythrocyte sedimentation rate (ESR) (⩾30mm) could predict the type of relapse and the effect upon the relapse of different therapies received. Overall most ER occurred in extranodal (EN) (42%) or irradiated transdiaphragmatic nodal (TDN) (40%) sites. Compared to patients with normal posttherapy ESR (n = 12), patients with elevated posttherapy ESR (n = 45) had the same proportions of outfield and late relapses; more frequent multiple sites of ER (38% vs. 25%), increased proportions of early EN relapses (16% vs. 3%), TDN relapses (17% vs. 2%), and other ER (6% vs. 1%). ER were most frequently observed between 1964 and 1971, and “modern” radiotherapy (Rt) decreased ER overall from 27% to 13% and for elevated posttherapy ESR patients from 54% to 25%. When chemotherapy (Ct) was used as either adjuvant or initial therapy, ER were greatly reduced vs. Rt alone (overall (6% vs. 28%) and for patients with elevated posttherapy ESR (10% vs. 39%)). Stepwise logistic regression showed Ct to be the most important factor “protecting” from EN relapse, but elevated posttherapy ESR was still significant. For early TDN relapse, elevated posttherapy ESR had the highest predictive value for relapse, greater than the types of radiation fields used and chemotherapy. An unexplained elevated posttherapy ESR, regardless of previous therapy, predicts for ER from aggressive HD, frequently in EN and irradiated areas, and warrants further early therapy.
Semple, John W.; Bruce, Suzanne; Freedman, John
doi: 10.1002/ajh.2830370409pmid: 1858783
Natural killer (NK) cell activity was studied in 17 patients with primary chronic idiopathic autoimmune thrombocytopenic purpura (ATP). Fifteen of 17 patients had a significantly reduced NK cytotoxicity against 51chromium labeled K562 target cells (mean LU20% = 18 ± 20 in patients versus 65 = 2 5 in controls, P < 0.001). NK activity was also significantly reduced in all of six patients with secondary ATP as compared with normal controls (LU20%28±15, respectively, P < 0.005). The NK activity in both patient groups correlated with the duration of therapy being received (r = 0.60, P < 0.001). Immunophenotypic analysis of peripheral blood mononuclear cells from patients with ATP revealed that CD8‐ cells bearing CD57 (HNK‐1, Leu 7) and CD3‐ cells bearing CD56 (Leu 19) were quantitatively within the normal range. These findings indicate that patients with ATP have a functional defect in NK cytolytic activity.
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