Extent of hypoechogenic area in the thyroid is related with thyroid dysfunction after subacute thyroiditis.

OBJECTIVE: To gain an insight into risk factors for hypothyroidism after subacute thyroiditis (SAT), we examined the correlation between initial laboratory and ultrasonographic findings and sequential thyroid dysfunction among treatment modalities. PATIENTS: We reviewed retrospectively the medical records of 252 patients (26 men and 226 women) with SAT who consecutively visited our thyroid clinic at Kuma Hospital for at least 6 months from 1996 through 2004. RESULTS: Throughout the course, 135 patients (53.6%) developed transient or permanent hypothyroidism. Levels of TSH were most often elevated (greater than 5 IU/ml) 2 months after SAT onset regardless of treatment, and 97.0% of patients who showed transient or permanent hypothyroidism clustered within 6 months from onset. During follow-up, patients treated with prednisone (PSL) were more likely to have normal thyroid function than patients not treated or those receiving anti-inflammatory drug therapy. In patients who developed hypothyroidism with PSL treatment or without treatment, the rates of bilateral hypoechogenic areas (HEA) were 6-fold higher than those of unilateral HEA. Moreover, permanent hypothyroidism occurred in 5.9% of patients, and all patients with permanent hypothyroidism presented initially with bilateral HEA and had consequently small thyroid size with or without abnormal autoimmunity. CONCLUSIONS: The rates of thyroid dysfunction after SAT were significantly lower in patients receiving PSL. Extent of HEA in the thyroid, but not laboratory findings, may be a possible marker for developing thyroid dysfunction after SAT.

Expression of angiogenesis-related genes regulates different steps in the process of tumor growth and metastasis in human urothelial cell carcinoma of the urinary bladder.

OBJECTIVE: This study was designed to determine the relative activity of angiogenesis-related genes in the regulation of tumorigenicity and subsequent metastases of urothelial cell carcinomas (UC) of the urinary bladder. METHODS: We selected the clones with the highest and lowest expression level of basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF)/vascular permeability factor or interleukin-8 (IL-8) in the highly tumorigenic and metastatic human UC cell line 253J B-V. Tumorigenicity and production of spontaneous lymph node metastases were evaluated 1, 2, 4, 8 and 12 weeks after orthotopic implantation of each specific expression clone into the urinary bladder of athymic nude mice. Moreover, the transitional changes in the expression of angiogenesis-related genes and neovascularization were determined in tumors and metastases. RESULTS: At the early stage of tumor growth following orthotopic implantation, tumorigenicity and metastases were significantly increased in the clones with the highest expression of bFGF and IL-8, while they were significantly inhibited in the clones with the lowest expression of bFGF and IL-8 compared to parental 253J B-V. In the tumors, specific expression of angiogenesis-related genes and intratumor neovascularity of each clone were gradually regulated to the same level as parental 253J B-V. In metastasized tumors of the highest and lowest IL-8-expressing clones, IL-8 expression was consistently high and low, respectively. CONCLUSIONS: These findings indicate that at the early stage of tumor growth, bFGF and IL-8 expression play important roles in the regulation of angiogenesis, tumorigenicity and subsequent metastases of human bladder cancer.

p53 induced by ionizing radiation mediates DNA end-jointing activity, but not apoptosis of thyroid cells.

To understand the effects of ionizing radiation on thyroid cells, we investigated the role of p53 in mediating apoptosis and in DNA repair following in vivo and in vitro irradiation of thyroid cells. In vitro exposure of human thyroid cells to ionizing radiation of up to 5-8 Gy failed to induce apoptosis in primary cells. The same results were obtained when the thyroid gland was irradiated in the intact rat. To explore the mechanism of failure of the wild-type p53 in inducing apoptosis in thyroid cells, we investigated the expression of apoptosis-related genes, bax, bcl-2 and fas/APO-1 following irradiation or induction of temperature-sensitive p53. The expression of Bax, Bcl-2 and Fas/APO-1 in human primary cultured thyroid cells did not change after irradiation. To further confirm the results, we established a clonal cell line (tsFRO) in which a temperature sensitive p53 (Val138) expression vector was stably transfected to a thyroid carcinoma cell line lacking endogenous p53. Incubation of tsFRO cells at the permissive temperature for three days, however, did not induce apoptosis although G1 arrest was noted. Although enhanced expression of the bax mRNA level was observed, the expression of Bax, Bcl-2 and Fas/APO-1 protein did not change by shifting tsFRO cells to permissive temperature as well as irradiated primary cells. Furthermore, DNA end-jointing ability was examined by transfection of linearized luciferase plasmid into tsFRO cells. Increased luciferase activity occurred when the cells were cultured at the permissive temperature, indicating that the wild-type p53 enhances DNA end-jointing activity. Our results indicate that the wild-type p53 does not lead to apoptosis but facilitates DNA end-jointing in thyroid cells. These results may reflect specific responses in thyroid cells following irradiation.

Rapidly progressive thyroid failure in Graves' disease after painful attack in the thyroid gland.

We studied a new type of Graves' disease: rapidly progressive thyroid failure after painful attack in the thyroid gland. Four women with the mean (+/- SD) age of 51 +/- 3.2 years had newly diagnosed hyperthyroid Graves' disease. A severe painful episode developed in the thyroid glands of two patients and permanent hypothyroidism occurred spontaneously within 2 or 3 months thereafter. Two to three episodes of pain developed in the thyroid glands of the other two patients during antithyroid drug therapy. There was a transient rise in serum thyrotropin level after each painful episode and permanent hypothyroidism developed 6 to 8 months after the initial painful attack. The clinical picture is characterized by moderate to severe pain in the thyroid gland with tenderness. Patients responded to steroid or anti-inflammatory therapy. During painful attack, increased or normal thyroid radioiodine uptake, elevated levels of C-reactive protein, and an elevated erythrocyte sedimentation rate were found, but there was no cytological evidence of subacute thyroiditis. After painful attack, serum thyroid stimulation antibody began to decrease in three of the patients while thyroid stimulation blocking antibody developed in one patient. This is a rapid and self-destructive process of the Graves' thyroid gland, which appears to be associated with painful attack in the thyroid gland.

Thyrotropin regulates c-Jun N-terminal kinase (JNK) activity through two distinct signal pathways in human thyroid cells.

c-Jun N-terminal kinases (JNK) participate in cellular responses to mitogenic stimuli and environmental stresses. We investigated whether and how TSH, which promotes the proliferation and differentiation of thyroid cells, regulates JNK activity in primary cultured human thyroid cells. TSH stimulated JNK activity in cytosolic fractions of thyroid cells measured by in vitro kinase assay. A low concentration of TSH (10(-11) M) stimulated JNK activity but at a higher dose (10(-8)-10(-7) M), TSH suppressed JNK activity without any change of JNK protein level. Activation of JNK by TSH was also observed in CHO cells stably transfected with TSH receptor complementary DNA (cDNA), suggesting a ligand-receptor specific interaction. TSH stimulated JNK activity through a pertussis toxin-sensitive pathway. We next elucidated the signal transduction pathways in TSH-induced JNK activation by examining the involvement of four distinct intracellular signal molecules; protein kinase C (PKC), cAMP, Ca2+, and PI3-kinase. The stimulation of JNK by TSH was blocked by two PKC inhibitors and suppressed by 8-bromo-cAMP or forskolin. These findings demonstrate that TSH regulates JNK activity biphasically in human thyroid cells through an interaction between Gi-PKC and cAMP-PKA pathways.

Thyrotoxicosis after needle aspiration of thyroid cyst.

We report a new type of thyrotoxicosis (postaspiration thyrotoxicosis) that occurred after needle aspiration of thyroid cysts. In a retrospective study five patients with thyroid cysts developed transient thyrotoxicosis without significant symptoms of hyperthyroidism after needle aspiration. These patients had elevated serum thyroid hormone levels with suppressed serum TSH and thyroid radioiodine uptake. The thyroid hormone content in the cystic fluid was greater in patients who developed thyrotoxicosis than in patients who did not. In a prospective study we examined thyroid function tests after needle aspiration in 52 consecutive patients with thyroid cysts and 63 patients with solid thyroid nodules and confirmed an occurrence of postaspiration thyrotoxicosis in a patient with thyroid cyst. Our observation indicates that postaspiration thyrotoxicosis occurs only in patients with thyroid cyst and that the incidence of this disorder is probably less than 1% of patients who undergo thyroid needle aspiration. Although the exact mechanism of elevated serum hormone levels is unknown, an inflammatory process after needle aspiration might have triggered the release of thyroid hormone.

A long term clinical, immunological, and histological follow-up study of patients with goitrous chronic lymphocytic thyroiditis.

Goiter size, thyroid function, antimicrosomal and antithyroglobulin antibodies, and thyroid histology were compared in 43 patients with goitrous chronic lymphocytic thyroiditis (Hashimoto's disease) confirmed by biopsy before and after an interval of 10-20 yr. Although all were given thyroid hormone therapy, 13 patients took it infrequently, and are considered untreated. Among these 13 patients, 5 (38%) became hypothyroid, and 1 became thyrotoxic. Goiter size decreased in 17 (57%) of 30 patients during therapy and in 3 (23%) of 13 untreated patients, and the incidence of reduction was greater in treated than in untreated patients (P less than 0.05). However, in 13 (43%) of the patients, goiter size did not decrease even during treatment. Titers of antithyroid antibodies decreased in only 8 (21%) of 38 patients. There was no significant correlation between changes in antibodies and the size of goiter, and treatment with thyroid hormone did not decrease the titers of antibodies. In patients whose goiters were initially diffusely enlarged and regressed significantly in size during the follow-up period, the initial biopsies showed histological changes in diffuse lymphocytic infiltration and diffuse epithelial changes. Comparative studies of histological differences between patients who were treated with thyroid hormone and those who were not were made in the patients who had no change in goiter size during the observation period, which was greater than 10 yr. The histological changes were similar in both groups at the beginning of the study, and no significant histological changes during the period of greater than 10 yr were found in either group. In one patient who developed thyrotoxicosis after 20 yr and was rebiopsied, the histological picture was that of thyroid hyperplasia and lymphocytic thyroiditis. These data indicate that goitrous chronic lymphocytic thyroiditis changes little as a function of time in many patients regardless of whether thyroid hormone is administered.

The occurrence of thyrotropin binding-inhibiting immunoglobulins and thyroid-stimulating antibodies in patients with silent thyroiditis.

Silent (painless) thyroiditis has been recognized as a clinical entity for over a decade and is characterized by spontaneously resolving thyrotoxicosis. Its etiology is uncertain; however, a few reports have indicated the occurrence of TSH binding-inhibiting immunoglobulins (TBII) and thyroid-stimulating antibodies (TSAb) in some of the patients. The present study was undertaken to evaluate thyroid function and the occurrence of TBII and TSAb and thyroid autoantibodies (antithyroglobulin and antimicrosomal) in 53 patients with silent thyroiditis during the course of their disease. The patients were divided into 2 major groups: I) those who developed transient hypothyroidism and II) those who did not. All patients initially had significantly increased concentrations of serum T4, free T4, and free T3, suppressed TSH levels, and decreased thyroid radioiodine uptake. TBII and TSAb were initially positive in 8 (15.1%) and 10 patients (18.9%), respectively. Forty patients were available for follow-up. TBII was positive in 6 of 24 (25.0%), and TSAb was positive in 8 of 24 (33.3%) of the patients who developed transient hypothyroidism during the course of their disease. Among the patients who did not become hypothyroid at any time, TBII was positive in only 2 of 16 (12.5%), and none of the patients became TSAb positive. The findings indicate that increased TSAb and TBII activity may be detected in patients with silent thyroiditis and, when present, are associated with transient hypothyroidism during the course of the disease.

Treatment of methimazole-induced agranulocytosis using recombinant human granulocyte colony-stimulating factor (rhG-CSF).

Agranulocytosis, although extremely infrequent, is a serious complication of antithyroidal drug therapy in patients with hyperthyroidism. Presently, there is no specific therapy for this life-threatening complication, and recovery time is highly variable. Recently, recombinant human granulocyte colony-stimulating factor (rhG-CSF) was reported to be effective in shortening the recovery time of the neutropenia in patients undergoing chemotherapy. The present study was undertaken to determine the efficacy of rhG-CSF administration in patients with methimazole-induced (MMI) agranulocytosis. Thirty-four patients (7 males and 27 females, ages 16-68 yr) with MMI agranulocytosis were divided into 3 groups: group A (n = 11) was treated with antibiotics only; group B (n = 11) received antibiotics and dexamethasone, 8 mg/day; and group C (n = 12) was treated with antibiotics and im injections of rhG-CSF, 75 micrograms/day. Patients in groups A and B were studied retrospectively. When rhG-CSF became available, patients in group C were studied prospectively. Bone marrow sternal punctures were performed in all group C patients who were then divided into 2 subgroups according to the granulocyte to erythrocyte count ratio (G:E). Group C1 (n = 6) had a G:E ratio of less than 0.5, and group C2 (n = 6) had a ratio of more than or equal to 0.5. Recovery time in all groups was defined as the number of days required for the peripheral granulocyte count to be greater than 1.0 x 10(9)/L. There was no significant difference in recovery time between groups A and B: 10.1 +/- 2.2 and 12.3 +/- 1.9 days (mean +/- SE), respectively. P was not significant; the administration of dexamethasone proved to be ineffective in shortening the time for recovery from peripheral granulocytes. On the other hand, recovery time was significantly shorter in group C (6.8 +/- 1.2 days mean +/- SE) compared with groups A and B (P < 0.05). Group C2 recovered in 2.2 +/- 0.6 days whereas group C1 took much longer, 9.8 +/- 1.3 days (P < 0.001). There was a direct correlation between the G:E ratio and the peripheral leucocyte count, r = 0.806, P < 0.01. Furthermore, rhG-CSF significantly shortened recovery time when the peripheral granulocyte count was greater than 0.1 x 10(9)/L (group C2) compared with patients whose counts were less than 0.1 x 10(9)/L (group C1), 2.2 +/- 0.4 vs. 8.6 +/- 1.3 days, respectively (P < 0.001). These data indicate that administration of steroids is ineffective in shortening the duration of recovery in patients with MMI agranulocytosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Ovarian gonadoblastoma with dysgerminoma in a woman with two normal children.

An unusually rare case of unilateral gonadoblastoma with dysgerminoma occurring in the ovary of a 28-year-old woman with two normal children is reported.

Characteristics of "embryoid body" in human gonadal germ cell tumors.

The characteristics of so-called "embryoid body" appearing in gonadal germ cell tumors were studied histologically and immunohistochemically on serial sections of three cases (one ovary and two testes). The embryoid bodies were usually observed to be contiguous with immature or mature intestinal ducts, hepatic nests, or epidermal cell nests on serial sections, though they appeared to be isolated in one section. The "amniotic cavity"-like structure of embryoid body was continuous with intestinal duct, and rarely with squamous cell nests, while the "yolk sac" was continuous with hepatic tissue. In these immature or mature structures, differentiation was always found independently of "disc," and portions of "ectoderm" and "endoderm" remained less differentiated in comparison with others. These findings were in contrast with a normal embryo in which immature and/or mature structures are derived from the embryonic disc. The amniotic cavity connected frequently with yolk sac. From the present results, the embryoid body is not considered to be a real or teratomatous embryo, but only a product during a divergent differentiation into intestine and liver from the plastic epithelium, which seems to be derived from an embryonic gut.

Immunochemical study on PHI/PHM with use of synthetic peptides.

We have synthesized PHI and PHM (human PHI) as well as their fragments, PHI (1-6), PHI (1-15), PHI (14-19), PHI (14-27), PHI (20-27), PHM (1-15) and PHM (13-27), by the solution or solid-phase method for peptide synthesis. Using the highly purified synthetic peptides as immunogens or haptenic immunogens, five kinds of PHI/PHM specific antisera were produced. The major antibody-recognition sites of the five antisera were located respectively in the PHI C-terminal (R8201), in the PHI N-terminal (R8403), in the PHM C-terminal (R8502), and in the PHM whole molecule (R8702 and R8703). Radioimmunoassays (RIAs) with antisera R8201, R8403 and R8502, respectively, showed a wide distribution of immunoreactive (IR) PHI/PHM in porcine and human gastrointestinal and brain tissues. The concentrations of IR-PHI in the porcine gastrointestinal tissues, however, differed between the R8201 and R8403 RIAs employed for measurement. By using these two different PHI RIAs, the IR-PHI in the porcine brain tissue extract was shown to be almost a single component coeluting with synthetic PHI in gel filtration. The IR-PHI in the extract of porcine lower intestine on the other hand, contained, besides a PHI-like component, unidentified component(s) eluting immediately after synthetic PHI in gel filtration; this crossreacted with the PHI C-terminal specific R8201 antiserum but not with the N-terminal specific R8403 antiserum, suggesting the presence of the C-terminal-related fragment(s) of PHI in the tissues.

Granulocyte colony-stimulating factor (G-CSF) does not improve recovery from antithyroid drug-induced agranulocytosis: a prospective study.

Agranulocytosis is the most serious side effect of antithyroid drug (ATD) therapy. We conducted prospective and randomized studies to examine whether granulocyte colony-stimulating factor (G-CSF) is actually effective for ATD-induced agranulocytosis. Twenty-four patients with Graves' disease who developed agranulocytosis during ATD therapy were randomly divided into a G-CSF group (n = 14) and an untreated group (n = 10). Subcutaneous injection of G-CSF (100 to 250 microg) was given daily until neutrophil counts rose to greater than 1000/microL. The untreated group received antibiotic therapy only. Recovery time, which is defined as the number of days required for neutrophil counts to exceed 500/microL, was monitored by daily complete blood count (CBC). Recovery time in the G-CSF-treated group did not differ from that of the untreated group in those patients with moderate and severe agranulocytosis; thus, prolonged use of G-CSF treatment is generally ineffective for ATD-induced agranulocytosis.

Increased serum concentration of interleukin-12 in patients with silent thyroiditis and Graves' disease.

We previously reported that interleukin-5 (IL-5), secreted from Th2 cells, was increased in patients with Graves' disease, but not in patients with silent thyroiditis. In this study, we investigated serum levels of interleukin-12 (IL-12) in order to examine the role of Th1-type immune response in the pathogenesis of autoimmune thyroid diseases. Serum levels of IL-12 were determined by a highly sensitive sandwich enzyme-linked immunosorbent assay in 68 patients with Hashimoto's thyroiditis (26 of whom had silent thyroiditis), 74 patients with Graves' disease, 8 patients with subacute thyroiditis, and 27 normal controls. Serum levels of IL-12 in thyrotoxic patients with silent thyroiditis (385.2 +/- 164.5 pg/mL, mean +/- SD), and in thyrotoxic patients with Graves' disease (343.6 +/- 163.8 pg/mL) were significantly increased compared with serum levels in normal subjects (163.9 +/- 66.8 pg/mL, p < 0.0001, p < 0.0001, respectively) or in thyrotoxic patients with subacute thyroiditis (241.9 +/- 46.5 pg/mL, p < 0.01, < 0.05, respectively). The ratio of IL-12 to IL-5 in thyrotoxic patients with silent thyroiditis (64.2 +/- 39.7) was significantly higher than that in normal controls (33.7 +/- 13.3, p < 0.01) or in thyrotoxic patients with Graves' disease (40.6 +/- 36.0, p < 0.05). These data suggest that Th1-type immune response is predominant in silent thyroiditis, and that not only Th2-type immune response but also Th1-type immune response is important in the pathogenesis of Graves' disease.

Differences in response of thyrotropin to 3,5,3'-triiodothyronine and 3,5,3'-triiodothyroacetic acid in patients with resistance to thyroid hormone.

This study investigated the response of TSH secretion to 3,5,3'-triiodothyronine (T3) and 3,5,3'-triiodothyroacetic acid (Triac) in patients with resistance to thyroid hormone, and compared the responses with those in patients with TSH-secreting pituitary adenoma and normal subjects. A short-term administration of 75 microg of T3 daily for 7 days suppressed serum TSH concentrations almost completely in normal subjects, but suppressed TSH only partially in patients with resistance to thyroid hormone and TSH-secreting pituitary adenoma. A single-dose administration of 75 microg of T3 gave similar results in regard to TSH suppressibility in these three subjects groups. In contrast, a single-dose administration of 1.4 mg of Triac remarkably suppressed serum TSH concentrations after 2 hours in not only normal subjects (-34 +/- 11% [mean +/- SD] from the basal value) but also in patients with resistance to thyroid hormone (-31 +/- 9%), and this TSH suppression continued for 4 hours. After 24 hours, this TSH suppression persisted in normal subjects (-62 +/- 12%) but was relieved in patients with resistance to thyroid hormone (-23 +/- 14%). After the Triac administration, molar ratios of alpha-subunit to TSH in serum were decreased in patients with TSH-secreting pituitary adenoma but increased in patients with resistance to thyroid hormone. Because the Triac therapy for patients with resistance to thyroid hormone suppressed pituitary-TSH secretion during the early phase of drug ingestion, this drug should be given several times within a day to obtain continuous TSH-suppressive effects.

Natural course of Graves' disease after subtotal thyroidectomy and management of patients with postoperative thyroid dysfunction.

The Natural course of Graves' disease after subtotal thyroidectomy was studied in 67 patients who had subtotal thyroidectomy for Graves' disease and did not receive any medical treatment for 8 to 12 years after surgery. Postoperative thyroid status was determined by serum free thyroxine (T4), free triiodothyronine (T3), and thyrotropin (TSH) levels in the first period (1 year after surgery), second period (3.9 +/- 1.0 years), and third period (8.8 +/- 1.5 years). Serum thyroid stimulating antibody (TSAb) and TSH binding inhibitor immunoglobulin (TBII) activities were also measured. A total of 53 patients (79%) changed thyroid status during the observation period. One year after surgery, 50 percent of euthyroid subjects developed abnormal thyroid function in the next period. Reversible latent hypothyroidism was the most common type of thyroid dysfunction seen in up to 46% of patients. Interestingly, hyperthyroidism and hypothyroidism that developed in the postoperative period were temporary disorders in most cases. Serum TSAb and TBII activities did not help predict the postoperative changes of thyroid status. Our study indicates that the instability of the thyroid function is common after subtotal thyroidectomy.

Mucosal dysplasia in the bile duct after choledochoduodenostomy: a case report.

A 60-year-old woman who had undergone cholecystectomy, choledocholithotomy and choledochoduodenostomy 21 years previously for cholecystolithiasis and choledocholithiasis, presented with nausea and vomiting. With a preoperative diagnosis of recurrent common bile duct stones, the extrahepatic bile duct was excised and choledochojejunostomy was performed. Histologic examination of the resected specimen disclosed chronic cholangitis, papillary epithelial hyperplasia, and mild dysplasia. Choledochoduodenostomy predisposes to reflux of duodenal contents, resulting in chronic mechanical and chemical irritation likely to induce histopathologic alterations in the bile duct mucosa. Since bile duct dysplasia induced by chronic inflammation may be a precursor of cancer, indication for choledochoduodenostomy should be specific and limited, and careful long-term follow-up is mandatory.

Percutaneous transhepatic balloon dilation for papillary stenosis.

In this study, a case of primary common bile duct stone due to papillary stenosis is reported. The patient was a 68-year-old man with complaints of epigastric pain and fever who had undergone gastrectomy at age 55 and cholecystectomy with choledocholithotomy at age 62. Laboratory data revealed elevation of the transaminases acid biliary enzymes. Both abdominal ultrasonography and CT scan revealed dilatation of the common bile duct with stones. Since endoscopic retrograde cholangiopancreatography could not visualize the bile duct, percutaneous transhepatic biliary drainage was carried out. After lithotripsy by percutaneous transhepatic cholangioscopy a diagnosis of papillary stenosis was made following percutaneous transhepatic manometry of the sphincter of Oddi, and balloon dilatation through the PTBD fistula was successfully performed. In this case report, emphasis is placed on the diagnosis and treatment of papillary stenosis.

[Small cell carcinoma of the urinary bladder with synchronous esophageal cancer and incidental lung cancer: a case report].

We present a case of triple primary cancers occurring synchronously in the urinary bladder, esophagus, and incidentally in the lung. A 65-year-old man with a chief complaint of gross hematuria was admitted to our hospital. Cystoscopy, computed tomography (CT) and magnetic resonance imaging (MRI) revealed a non-papillary broad-based bladder tumor. Histological diagnosis was transitional cell carcinoma of the urinary bladder and he underwent one course of neoadjuvant chemotherapy (M-VAC) with the preoperative diagnosis of T3bN0M0. After one course of chemotherapy, chest CT, lymph node biopsy and esophagoscopy revealed squamous cell carcinoma of the esophagus. He first underwent radiochemotherapy (total 70 Gy, CDDP 5 mg x 41, 5-FU 250 mg x 24) for esophageal cancer and achieved complete remission. Then, he underwent radiotherapy for a total of 60 Gy for bladder cancer. However, his general condition gradually became worse and he died from metastatic cancer. The autopsy proved that he died from multiple metastases of small cell carcinoma of the urinary bladder and incidentally squamous cell carcinoma of the lung was identified.

[Female paraurethral cyst: a case report].

We experienced a case of paraurethral cyst in a 42-year-old woman. A paraurethral cyst, the diameter of which was about 2 cm, was observed in the septum between urethra and vagina. No communication between the cyst and urthra or vagina was detected. The resected cyst did not reveal malignant findings. Sixty-one cases of paraurethral cyst in the Japanese literature are also reviewed.