[A case of malignant lymphoma concomitant with multiple myeloma].

A 75-year-old woman was referred to us because of cough, high fever and skin erythema in April 1999. Malignant lymphoma (diffuse mixed cell type) was previously diagnosed in 1990 and she achieved complete remission after treatment with a series of CHOP regimen treatments. In 1998, multiple myeloma (IgG lambda type) was diagnosed and she was treated with a combination of melphalan and prednisolone. On physical examination, superficial lymphadenopathy and skin erythema were noted. Biclonal gammopathy (IgG kappa/lambda) was shown in serum, and Bence Jones protein in urine. Computed tomography showed pleural effusion and swelling of paraaortic lymph nodes. The bone marrow examination showed an increased number of abnormal plasma cells (19.2%) and no evidence of lymphoma. Left axillary lymph node biopsy revealed that she had non-Hodgkin's lymphoma (immunoblastic lymphadenopathy-like T cell lymphoma). She was treated with the CHOP regimen at reduced doses for both diseases. The lymphoadenopathy reduced after 6 courses of CHOP and 4 courses of CHOPE (CHOP + VP16), however, she had bone pain on November 1999 and received treatment with MCNU-VMP (MCNU + VDS + L-PAM + PSL). Her rib pain improved, but she died of systemic infection of herpes zoster virus. We report here a rare case of malignant lymphoma concomitant with multiple myeloma.

[Clinical characteristics of polycythemia vera in the elderly].

Of 43 elderly patients who were suspected to have polycythemia between October 1990 and July 1998, 12 patients showed an increased red cell volume measured by 51Cr-labeled red blood cells. We analyzed the clinical characteristics of the 12 patients consisted of 7 men and 5 women, with a median age of 71 (range: 57-92). Chief complaints were headaches and dizziness (3 cases), symptoms of other conditions than polycythemia (4 cases). Five patients had no symptoms. Five of 6 patients over 70 years old had no symptoms due to polycythemia. Seven cases (58%) showed splenomegaly and three cases (25%) showed hepatomegaly. Laboratory findings were as follows: WBC 9.7 +/- 3.9 x 10(3)/microliter (mean +/- SD, p < 0.02 vs normal control), Hb 17.9 +/- 4.2 g/dl (p < 0.001), Plt 39.7 +/- 26.0 x 10(4)/microliter, EPO 13.8 +/- 5.2 mU/ml (p < 0.0001), NAP score 258 +/- 114, Vit. B12 1,686 +/- 2,156 pg/ml, arterial O2 saturation more than 92% in all cases. The diagnosis of all cases was polycythemia vera according to the diagnostic criteria of Polycythemia Vera Study Group. Associated conditions included 8 cases of thrombosis (cerebral thrombosis 4, thrombophrebitis 2, myocardial infarction 1, ischemic colitis 1) and 3 cases of malignancy (esophageal cancer 1, breast cancer 1, renal cancer 1), none of which was therapy-related cancer. Six patients (50%) had only phlebotomy, three (25%) only chemotherapy, and three (25%) both phlebotomy and chemotherapy. Patients over 80 years old needed neither intensive nor continuous treatment. Only one patient died due to esophageal cancer at age 89.

Elevation of serum creatine kinase during treatment with antithyroid drugs in patients with hyperthyroidism due to Graves disease. A novel side effect of antithyroid drugs.

We describe 4 patients with Graves disease who had abnormal increases of serum creatine kinase (CK) concentrations during treatment with antithyroid medications. Three of the patients experienced myalgia and muscle cramps. All of the patients manifested an increase in serum CK levels 1 to 3 months after the administration of antithyroid drugs. Thyrotropin concentrations and cardiac systolic time indexes during the elevation of serum CK concentrations were not consistent with hypothyroidism. The mechanisms are not obvious, but it is likely that the rapid decrease of thyroid hormones in tissues may temporarily cause hypothyroid states, resulting in alterations in CK concentrations. It is suggested that hasty correction of thyrotoxicosis should be avoided in susceptible patients, unless the thyrotoxic conditions are critical.

3,5,3'-Triiodo-L-thyronine potentiates all-trans-retinoic acid-induced apoptosis during differentiation of the promyeloleukemic cell HL-60.

Although the programmed cell death mediated by thyroid hormone is not well evaluated in mammalian cells, thyroid hormone plays a crucial role in differentiation of the cells during the metamorphosis of Xenopus, suggesting that thyroid hormone has the potential ability to induce the apoptosis. To investigate the thyroid hormone-inducible apoptosis, we cultured HL-60 cells with various amounts of all-transretinoic acid (RA) and L-T3. T3 alone did not induce the apoptosis of the cells. T3, however, suppressed the proliferation of cells in the presence of RA. DNA ladder and microscopical examination showed that the reduction of cell number was due to the apoptosis induced by RA. These findings suggested that T3 affects the apoptotic process during the differentiation of HL-60 cells by RA. T3-inducible apoptosis may require the factors augmented by RA in HL-60 cells.

[Effects of traumatic subarachnoid hemorrhage on pathological properties in diffuse brain injury: a comparison with aneurysmal subarachnoid hemorrhage].

As a result of recent advances in continuous monitoring equipment, it has been reported that vasospasm (VS) and delayed ischemic neurological deficit (DIND) occur as frequently in traumatic subarachnoid hemorrhage (TSAH) as in subarachnoid hemorrhage due to ruptured intracranial aneurysm (ASAH), and these VS and DIND have been reported to affect the outcome of TSAH adversely in many cases. When we compared TSAH secondary to diffuse brain injury (DBI) with ASAH, however, these two conditions were evidently different from each other in nature. Then we compared laboratory data, clinical course, and outcomes of TSAH associated with DBI with those of ASAH, to determine whether TSAH results in poor outcomes of DBI. On CT scans, patterns of SAH distribution were different from each other, and SAH was detected in 76% of the patients with ASAH on day 4, whereas only 2.0% of the patients with TSAH had detectable SAH on day 3. The incidence rates of detectable SAH in both groups remained significantly different from each other after day 2. The cerebral blood flow (CBF) decreased to around 75% of the normal flow in the acute stage of ASAH, and it decreased further to around 65% in the subacute stage. In TSAH, in contrast, CBF varied widely among the patients. The average CBF decreased to about 70% in the acute stage, and then it increased to around the lower limit of the normal range in the subacute stage. The urinary output and serum concentration of low molecular protein compositions in TSAH were markedly different from those in ASAH. In addition, the contour of a low density area (LDA) in CT scans in the subacute-chronic stage was the same as that of the area supplied by the artery being constricted due to cerebro-vascular spasm in ASAH. In TSAH, in contrast, hardly any LDA had a form that was suggestive of this conjuction, with cerebro-vascular spasm and the incidence rate of LDAs was significantly different from that for ASAH. About 30% of the patients with ASAH had ventricular enlargement, which was diagnosed as normal pressure hydrocephalus by cisternography, in the chronic stage. Surgical shunting was effective for these patients. In TSAH, ventricular enlargement was observed in more than 50% of the patients, but almost none of these patients underwent surgical shunting, because it resulted from cerebral atrophy. Regardless of causes of SAH, the severer SAH was, the more often patients had a poor outcome. The outcome of TSAH was, however, significantly poorer than that of ASAH. When SAH was traumatic, it disappeared by the time VS developed and, in addition, changes in CBF and the form and incidence rate of LDAs were different from those in ASAH. We concluded that, although TSAH is an adverse prognostic factor for DBI, it does not contribute to poor outcomes of DBI by giving rise to DIND caused by VS.

Reversible G1 arrest induced by dimethyl sulfoxide in human lymphoid cell lines: dimethyl sulfoxide inhibits IL-6-induced differentiation of SKW6-CL4 into IgM-secreting plasma cells.

We have previously found that dimethyl sulfoxide (DMSO), a known inducer of differentiation in several kinds of myeloid cells, arrests proliferation of human lymphoid cells including Raji and Akata Burkitt's lymphoma cells at the G1 phase. We investigated whether DMSO affects cell proliferation and differentiation of the lymphoid cell line SKW6-CL4, which is capable of differentiating terminally into IgM-producing cells. As in the case of Raji, Akata, and Molt-4, the proliferation of SKW6-CL4 was reversibly arrested at the G1 phase by treatment with 2% DMSO for 5 days even in the presence of interleukin-6 (IL-6). DMSO inhibited spontaneous IgM secretion as well as IL-6-induced IgM production in SKW6-CL4 at a concentration lower than that affecting cell proliferation. Of the cell-surface differentiation markers CD10, CD20, CD21, and CD23, the expression of CD20 was suppressed by DMSO treatment, and partial restoration of the expression was observed 24 to 48 h after release from DMSO. The level of IL-6 receptor protein was not affected by DMSO treatment. These results indicate that DMSO not only arrests the cell cycle of a human lymphoid cell line SKW6-CL4 at the G1 phase but also inhibits the differentiation into IgM-secreting cells at a concentration lower than that affecting cell proliferation and that DMSO overcomes the effect of IL-6 on terminal differentiation of SKW6-CL4. As a whole, proliferation of human lymphoblastoid cell lines was revealed to be reversibly arrested at the G1 phase by DMSO, which is known to induce differentiation in several myeloid cells, without inducing cell differentiation.

[A report of four cases of intrathoracic meningocele].

Intrathoracic meningocele is regarded as an uncommon pathological entity frequently associated with von Recklinghausen's disease. In this paper, four cases of intrathoracic meningocele, treated between 1966 and 1986, are presented. There were three males and one female, all between the ages of 40 and 50. These were referred to our clinic for further evaluation of an asymptomatic lesion which had been seen on a routine chest roentgenogram. There was definite evidence of von Recklinghausen's disease in three cases: two males and one female. All four cases had no pain, dyspnea or neurological disorder. Chest and vertebral tomograms revealed masses in the posterior mediastinum and enlarged vertebral canals at the location of the lesion which varied from T-3 to T-11; three on the left side and one on the right side. None of them revealed scoliosis or kyphosis of the spine. In three cases, myelography was performed and showed an egg-shaped mass dorsolaterally. In two cases, metrizamide computed tomographic myelography was carried out and demonstrated deformity of the vertebral bone and passage of the contrast material through the enlarged vertebral canal into the paravertebral mass. Furthermore, magnetic resonance imaging was performed in two cases, and showed a homogeneous low signal intensity paravertebral mass communicating with the spinal canal on T1-weighted image. In two cases, the meningoceles were ligated or wrapped surgically. Postoperatively one presented a paraparesis and severe meningitis, and died; the other had an uneventful postoperative course. Two patients were followed conservatively without developing any symptoms or signs.(ABSTRACT TRUNCATED AT 250 WORDS)