This article has been retracted at the request of the Editors-in-Chief.Fig. 3a of this paper had previously been published in Int. J. Cancer, 118 (2006) 765–772, doi:10.1002/ijc.21389 and should have been appropriately cited as such.One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared or will not appear in a publication elsewhere (or that if an excerpt or illustration is used with permission it is acknowledged as such). As such this article represents a severe abuse of the scientific publishing system.

Two TRAbs: TSBAb and TSAb. TSBAb causes hypothyroidism. TSAb causes Graves’ hyperthyroidism. TSBAb and TSAb block TSH-binding to cells as TRAb, measured as TSH-binding inhibitory immunoglobulin (TBII). We reevaluate TSBAb and TSAb. We studied TSBAb, TSAb, and TBII over 10 years in 34 TSBAb-positives with hypothyroidism and in 98 TSAb-positives with hyperthyroidism. Half of the 34 TSBAb-positives with hypothyroidism continued to have persistently positive TSBAb, continued to have hypothyroidism, and did not recover from hypothyroidism. Ten of the 98 TSAb-positives with hyperthyroidism continued to have positive TSAb and continued to have hyperthyroidism. TSBAb had disappeared in 15 of the 34 TSBAb-positives with hypothyroidism. With the disappearance of TSBAb, recovery from hypothyroidism was noted in 13 (87%) of the 15 patients. TSAb had disappeared in 73 of the 98 TSAb-positives with hyperthyroidism. With the disappearance of TSAb, remissions of hyperthyroidism were noted in 60 (82%) of the 73. Two of the 34 TSBAb-positives with hypothyroidism developed TSAb-positive Graves’ hyperthyroidism. Two of the 98 TSAb-positive Graves’ patients with hyperthyroidism developed TSBAb-positive hypothyroidism. TSBAb and TSAb are TRAbs. TSBAb-hypothyroidism and TSAb-hyperthyroidism may be two aspects of one disease (TRAb disease). Two forms of autoimmune thyroiditis: atrophic and goitrous. We followed 34 TSBAb-positive patients with hypothyroidism (24 atrophic and 10 goitrous) over 10 years. All of the 10 TSBAb-positive goitrous patients recovered from hypothyroidism and 19 (79%) of the 24 TSBAb-positive atrophic patients continued to have hypothyroidism.

A 36-year-old woman with postpartum hypopituitarism(Sheehan's syndrome: SS) developed postpartum autoimmune thyroiditis (PPAT). She delivered a baby by Caesarean section (620mL blood loss). At 1 month post partum, she developed thyrotoxicosis due to painless thyroiditis (autoimmune destructive thyroiditis). She was positive for antithyroid antibodies. Postpartum and hypoadrenalism-induced exacerbation of autoimmune thyroiditis caused the thyrotoxicosis due to autoimmune destructive thyroiditis. ACTH was undetectable. She had ACTH deficiency and secondary hypoadrenalism. Hydrocortisone was started. At 6 months post partum, she was referred to us with hypothyroidism. Thyroxine was administered. She had thyrotoxicosis at 12 months post partum and then hypothyroidism. She was diagnosed with PPAT. She had hypopituitarism, ACTH deficiency (secondary hypoadrenalism), low prolactin with agalactia, and low LH with failure to resume regular menses. She had empty sella on MRI. She was diagnosed with SS. Three cases with SS have been reported to develop PPAT. Postpartum immunological rebounds and hypoadrenalism-induced immunological alterations (or a combination of the two) might have been responsible for the PPAT.

We report a rare case showing involvement with the cauda equina after autologous peripheral blood stem cell transplantation for primary plasma cell leukemia (PCL). A 55-year-old man was diagnosed with PCL(IgA-k type, stage III)in November of 2006. He was treated with VAD chemotherapy consisting of vincristine, doxorubicin, and dexamethasone. After achieving hematological remission, he received tandem high-dose melphalan supported by autologous peripheral blood stem cell transplantation. Five months after his second transplant, he complained of lumbago and bilateral leg pain. M-protein and Bence-Jones protein were not detected in serum or urine. An axial magnetic resonance imaging study revealed enlargement of the cauda equina nerve roots on T-1 weighted image. A sagittal T-1 weighted gadolinium-enhanced imaging study showed hyperintensities along the cauda equina. Leptomeningeal enhancement was also seen below the level of Th6. A cytological examination of the cerebrospinal fluid (CSF) with May-Giemsa stain showed atypical plasma cells. Immunoelectrophoresis of the CSF revealed monoclonal IgA-k type protein. A diagnosis of central nervous system (CNS)relapse was made. The patient died of pneumonia two months after relapse. It should be kept in mind that CNS relapse can occur during hematological remission in patients with multiple myeloma including PCL.

A 75-year-old woman was found to be unconscious in hospital. She was febrile with a temperature of 38.4 degrees C. She had hypotension (blood pressure 80/40 mmHg) with serum Na 132 mEq/L and K 5.7 mEq/L (serum Na/K = 23.2), and serum cortisol 0.91 microg/dL, indicative of adrenal failure. She was admitted for the treatment of Graves' hyperthyroidism, and was found to be unconscious in hospital. We encountered a patient with unrecognized adrenocortical disease, in whom development of Graves' hyperthyroidism caused an adrenal crisis. The ACTH stimulation test indicated that she had 21-hydroxylase deficiency (21OHD); after ACTH stimulation, 17-OH-progesterone increased from 0.6 to 10.4 ng/mL (17.3 times), and 17-OH-progesterone/cortisol from 0.0049 to 0.045 (9.2 times). She did not have clinical signs of classical 21OHD. She had non-classical 21OHD (NC21OHD). Development of Graves' hyperthyroidism caused an adrenal crisis in a patient with previously unrecognized NC21OHD. A patient with unrecognized adrenocortical disease developed Graves' hyperthyroidism, which induced an adrenal crisis. She had NC21OHD.

Localized pretibial myxedema (PTM) is a sign of Graves' disease. A 53-year-old man with Graves' disease was admitted with the development of PTM following radioisotope (131)I treatment for Graves' hyperthyroidism. TSH receptor antibody (TRAb) titer was also increased after (131)I treatment. TRAb was measured as thyroid stimulating antibody (TSAb) or TSH-binding inhibitory immunoglobulin (TBII). PTM was noted several months after (131)I treatment. The PTM-development seems to be associated with the increased TRAb-activities. The localized pretibial myxedema was effectively treated with topical steroid (triamcinolone acetonide) ointment application with sealing cover (steroid occlusive dressing technique: steroid ODT). We also report our experience of PTM-treatment with steroid ODT in 5 other PTM patients with positive TRAb. PTM was successfully treated with steroid ODT in two patients. In these two patients, the treatment was started within several months of the appearance of PTM. In the other 4 patients, the treatment was started 5-10 years after the appearance of PTM without any beneficial effects. Early detection and early treatment are necessary for the remission of PTM.

We report a rare case of human immunodeficiency virus (HIV)- and human herpes virus-8 (HHV-8)-negative primary effusion lymphoma (PEL)-like lymphoma presenting with lymphomatous effusions complicated by cardiac tamponade. A 68-year-old woman was hospitalized with generalized weakness in June 2006. Echocardiogram revealed the presence of pericardial effusion and she had the signs of cardiac tamponade. Urgent pericardial drainage relieved her symptoms. Chest computed tomography showed bilateral pleural effusions along with pericardial effusion. Cytologic findings of both effusions were suggestive of malignancies, including malignant lymphoma. Immunocytochemical studies with a panel of antibodies, including CD20 and CD79a, could not provide a definite diagnosis. Flow cytometric analysis of pleural effusion revealed that tumor cells were positive for CD10 and CD19, but negative for CD20, CD23, surface immunoglobulin, and T-cell associated antigens. Clonal rearrangement of the immunoglobulin heavy chain gene was detected by Southern blot analysis. Polymerase chain reaction proved to be negative for HHV-8. The serology test for HIV was negative. After a diagnosis of HHV-8-negative PEL-like lymphoma, she was treated with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisolone). However, she died of progressive lymphoma 7 months after the diagnosis. PEL-like lymphomas are of B-cell origin. In some cases of PEL-like lymphoma, tumor cells may be negative for representative markers of B-cell phenotype such as CD20 and CD79a.

The development of Burkitt’s lymphoma (BL) is uncommon in elderly people. Most treatment-related hematological malignancies are of a myeloid lineage. Only a few cases with BL secondary to cancer treatment have been described. We report a rare case of an elderly patient with radiotherapy-related BL. A 71-year-old Japanese man, who had a past history of oropharyngeal cancer treated with local irradiation 15 years ago, presented with a left mandibular mass in December 2004. A partial mandibulectomy disclosed pathological features consistent with BL. Although the patient was initially treated with intensive chemotherapy, the development of complications precluded further anticancer drug treatment. Rituximab was administered once weekly for 5 consecutive weeks, with resolution of the mandibular mass. He remained in remission without further lymphoma treatment for more than 3 years after diagnosis. Rituximab monotherapy should be considered as a therapeutic option for elderly patients with BL.

Catecholamines strongly promote lipolysis and thermogenesis, and play a central role in the regulation of body fat content. The β1 adrenergic receptor (BAR-1) is a major mediator of catecholamine-induced lipolysis and thermogenesis. To explore whether mutations in the BAR-1 gene contribute to morbid obesity in Japanese, we scanned for mutations in the coding sequence of the gene in 50 morbid obese [body mass index (BMI)≧35.0kg/m2; 99.7th percentile] Japanese subjects. Direct DNA sequencing was performed following polymerase chain reaction (PCR) amplification. Two common polymorphisms, Gly49Arg and Arg389Ser, were detected in these subjects. The frequencies of these polymorphisms, as determined by PCR-restriction fragment length polymorphism (RFLP) analysis, showed no significant difference between 180 severely obese subjects (BMI≧30.0kg/m2; 97th percentile) and 132 control (BMI<25.0kg/m2) subjects. This study represents the first investigations of genetic variations of BAR-1 in relationship to morbid obesity and suggests mutations in the BAR-1 coding sequence is not likely a major cause of morbid obesity at least in Japanese.

Objective: Programmed cell death-1 (PD-1) and its ligands (PD-L1 and PD-L2) inhibit T-cell proliferation and activation. This inhibition down-regulates the immune responses. The association of a PD-L1 polymorphism with Graves' disease (GD) was studied.Design: The association of an A/C polymorphism at position 8923 in PD-L1 intron 4 with GD was Studied.Patients: The study included 327 GD patients and 192 controls, of which 252 GD patients were followed over 5-10 years.Measurements: PD-L1 intron 4 position 8923 A/C polymorphism was typed using the PCR-restriction fragment length polymorphism method.Results: The A/C genotype frequencies were significantly different between GD patients and controls. The A/C and C/C frequencies were higher in GD patients than in controls. The A/A frequencies were lower in GD patients than in controls. C-allele frequency was higher in GD patients than in controls. A total of 2 52 GD patients were followed over 5-10 years; 200 had discontinued antithyroid drugs (ATD) while 52 continued to take ATD. Of these 200. 1.76 continued to be in remission and 24 had relapsed into hyperthyroidism. Significant. differences in the duration of positive TBII positive thyroid-stimulating antibodies, and ATD treatment were noted between the patients in remission and those that had relapsed. Significant differences in the A- and C-allele frequencies were noted between the two. The C-allele frequency was higher in GD patients who did not achieve remission than in those who achieved remission.Conclusion: An A/C polymorphism at position 8923 in PD-L1 is associated with GD. The PD-L1. polymorphism plays a role in GD development. GD patients with the C allele at position 892 3 in PD-L1, gene had difficulty in achieving remission.

Primary malignant lymphoma of the female genital tract is an extremely rare clinical entity. We report a case of primary non-Hodgkin lymphoma of the uterine cervix. A 68-year-old woman presented with abnormal genital bleeding in May 2002. A coloposcopic examination revealed a mass in the uterine cervix. Magnetic resonance imaging showed a bulky cervical tumor(7.5 x 8 cm)invading the right parametrium and adjacent levator ani muscle. Involvement of pelvic lymph nodes was also observed. The uterine lesion exhibited homogenous hypointensity on T1 weight image and isointense to hyperintense on T2-weight image. No other lesions were detected by the whole-body computed tomography, gallium scintigraphy, and bone marrow examination. Although cytology of the smear from the uterine cervix was nondiagnostic, the histologic examination of the punch biopsy material showed a diffuse proliferation of atypical lymphoid cells. Immunophenotypic studies revealed tumor cells were positive for CD19, CD20, CD30, and k-chain. A diagnosis of diffuse large B-cell lymphoma of the uterine cervix, clinical stage IIE was made. The patient was treated with 6 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone(CHOP)chemotherapy followed by the involved field irradiation. She remains alive and free of disease more than 5 years after the diagnosis.

We report a Japanese case of human herpes virus-8 (HHV-8)-associated multicentric Castleman disease(MCD) complicated by hemophagocytic syndrome(HPS). A 60-year-old man presented with persistent fever and progressive pancytopenia in June 2004. On physical examination, anemia, icterus, hepatosplenomegaly, and generalized lymphadenopathy were detected. Laboratory findings showed elevated levels of serum ferritin and soluble interleukin-2 receptor. Anti-human immunodeficiency virus (HIV) antibody was negative. Bone marrow aspiration revealed a normocellular marrow with an increased number of hemophagocytic histiocytes. Biopsy of cervical lymph node disclosed pathological features compatible with the plasmablastic variant of Castleman disease. HHV-8 DNA was detected in the specimen from lymph node by polymerase chain reaction. Thus, the diagnosis of HHV-8-associated MCD complicated by HPS was made. The patient was treated with immunotherapy and subsequent chemotherapy. However, he died of bacterial sepsis after one-month therapy. This case report provides some evidence that HHV-8 may be a causative agent of MCD even in HIV-seronegative Japanese patients.