Herpes simplex encephalitis and subsequent cytomegalovirus encephalitis after chemoradiotherapy for central nervous system lymphoma: a case report and literature review

Neurological complications during the treatment of hematological malignancies have a wide range of causes. Treatment-related leukoencephalopathy has been recognized as a major complication of combined chemotherapy and radiotherapy for central nervous system (CNS) lymphoma, and can complicate the diagnosis of CNS infection. Herein, we present a patient with diffuse large B-cell lymphoma who developed herpes simplex encephalitis (HSE) and subsequent cytomegalovirus encephalitis after chemoradiotherapy for CNS relapse. Although cerebrospinal fluid examination (CSF) showed no significant pleocytosis, brain magnetic resonance imaging and polymerase chain reaction analysis of the CSF were useful in the diagnosis. With a review of the literature on the association between HSE and radiotherapy for CNS malignancies, our case suggests that an awareness of viral encephalitis is important in the differential diagnosis of acute neurologic disturbance during chemoradiotherapy for CNS lymphoma.     

Immunoblastic lymphadenopathy-like T-cell lymphoma complicated by multiple gastrointestinal involvement

We report a rare case of immunoblastic lymphadenopathy (IBL)-like T-cell lymphoma complicated by multiple gastrointestinal involvement, which appeared to be ameliorated by chemotherapy but resulted in perforative peritonitis. A 66-year-old Japanese woman who had generalized lymphadenopathy and eruptions was admitted to our hospital because of bloody stool. Colonoscopic examination revealed hemorrhagic ulcers in the terminal ileum and a saucer-like ulcer in the cecum. Gastrointestinal endoscopy revealed several ulcerative or elevated lesions in stomach and duodenum. Biopsy specimens of these lesions and of a lymph node showed characteristic histological features of IBL-like T-cell lymphoma. The initial treatment with prednisolone (PSL) and cyclophosphamide (CPA) was effective. Six months after the treatment, however, she developed bloody stool again caused by multiple ulcerative lesions in the large intestine. The recurrence of the disease was determined histologically, and four courses of CPA, PSL, vinblastine sulfate and doxorubicin hydrochloride (CHOP) therapy were administered. One month after completing the CHOP therapy, she developed intestinal obstruction and then acute peritonitis resulting from perforation at an ulcer scar in the jejunum. Surgical treatment was successful, and histological examination demonstrated no lymphoma cells in the resected specimen. A gastrointestinal perforation should be recognized as a potential complication of IBL-like T-cell lymphoma, even during remission. (Received: June 24, 1998; accepted: Oct. 23, 1998)     

Colorectal Stenting for Malignant and Benign Disease: Outcomes in Colorectal Stenting

INTRODUCTION: Self-expanding metal stents are now an established treatment for malignant colonic obstruction. Favorable outcomes have been reported both for cancer palliation and treatment of acute obstruction as a bridge to surgery. However, little data exists regarding the use of stents for benign colonic obstruction.METHODS: All cases of colonic stent insertion occurring between December 1996 to October 2002 were reviewed. During the study period, 36 patients with malignant obstruction and 6 patients with benign obstructive disease underwent placement of self-expandable stents using a combined endoscopic and fluoroscopic technique.RESULTS: Stent placement was successful in 36 of 42 patients (86 percent). Complications occurred in 16 of 36 patients (44 percent): migration (n = 7), reobstruction (n = 5), perforation (n = 2), fistula formation (n = 1), and stent fracture (n = 1). Stent placement was successful in 100 percent of patients with benign strictures but poststent migration was frequent (2/6).CONCLUSIONS: Stent insertion provided an effective outcome in patients with malignant colonic obstruction as a palliative and preoperative therapy. Although a relatively high migration rate was observed in patients with benign strictures, stenting was still effective in providing luminal patency (median follow-up, 7.5 months). Stenting should be considered as a first-line treatment for malignant strictures and as a potential therapy for selected benign strictures.     

Aortic valve regurgitation in alkaptonuria

Aortic valve lesions associated with alkaptonuria tend mostly to be due to aortic valve stenosis, while aortic valve regurgitation is only rarely observed. Herein, a case is reported of severe aortic valve regurgitation and a fibrous strand in a patient with alkaptonuria. A 65-year-old male, with a history of inferior myocardial infarction, presented with symptoms of congestive heart failure. Alkaptonuria was diagnosed based on urine coloration, skin pigmentation and ochronotic arthropathy in the vertebrae and hip. Grade IV aortic valve regurgitation with mild aortic valve stenosis and occlusive disease in the right coronary artery indicated a need for aortic valve replacement and coronary artery bypass grafting. Sclerotic change in the cusps, and shrinkage of the non-coronary cusp, impeded normal coaptation of the aortic valve, and the left-coronary cusp also had a fibrous strand suspending the free margin of the cusp from the aortic wall just above the commissure. The sclerotic change in the cusps, and shrinkage of the non-coronary cusp, appeared to be the causative lesion of aortic valve regurgitation, implying that cardiovascular ochronosis may cause aortic valve regurgitation.     

Interaction between ACE and ADD1 gene polymorphisms in the progression of IgA nephropathy in Japanese patients

An interaction effect between the angiotensin-converting enzyme insertion/deletion (ACE I/D) and alpha-adducin (ADD1) Gly460Trp polymorphisms (G460W) on blood pressure regulation has recently been suggested, although its significance in the prognosis of renal function in IgA nephropathy (IgAN) has not been fully investigated. Therefore, we evaluated the clinical manifestations and renal prognosis in 276 Japanese patients with histologically proven IgAN with respect to their ACE I/D and ADD1 G460W polymorphisms. The prognosis of renal function was analyzed by Kaplan-Meier survival curves and multivariate Cox proportional-hazards regression models. Baseline data, including blood pressures, proteinuria, renal function, and incidence of hypertension, were similar for the different genotypes of ACE and ADD1. The individual genotypes taken alone were not associated with the progression of renal dysfunction. However, renal survival of patients with the 460WW polymorphism of ADD1 was significantly worse within the group with the II genotype of ACE (Kaplan-Meier, log rank test; chi2=6.062, P=0.0138) but not for those with other ACE genotypes. In the Cox proportional-hazards regression model with adjustment for clinical risk factors, including hypertension, proteinuria, and no administration of an angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, the 460WW variant of ADD1 was a highly significant and independent risk factor only for patients with the ACE II genotype, with a hazard ratio of 3.65 (P=0.0016), but not for those with other ACE genotypes (hazard ratio=0.65, P=0.2902). These findings suggest an interaction between ACE and ADD1 polymorphisms not only on blood pressure regulation but also on the progression of renal dysfunction in patients with IgAN.     

Acid-suppression Therapy Offers Varied Laryngopharyngeal and Esophageal Symptom Relief in Laryngopharyngeal Reflux Patients

It is widely accepted that laryngopharyngeal reflux requires more aggressive and prolonged therapy than gastro-esophageal reflux disease. Otolaryngologists often observe that laryngopharyngeal symptoms, such as throat clearing, hoarseness, cough, and globus pharyngeus, are slower to resolve than esophageal symptoms, such as heartburn and regurgitation. The aim of this was to provide empirical evidence to support this observation and to carry out a detailed investigation of the differences between these symptoms. Forty-five patients with laryngopharyngeal and esophageal symptoms received acid-suppression therapy that involved the continuous administration of a proton-pump inhibitor for up to 6 months. We investigated the differences in response to acid-suppression therapy between patients suffering from laryngopharyngeal and esophageal symptoms, respectively, who received upper gastrointestinal endoscopy and were assayed for serum Helicobacter pylori antibodies. The significance of the rate of symptom improvement was estimated by Kaplan-Meier analysis and the logrank test. Laryngopharyngeal symptoms improved significantly more slowly than esophageal symptoms following acid-suppression therapy (49.8 vs. 78.3%, 60 days after the start of acid suppression; P = 0.003). These differences were observed both in patients with erosive esophagitis (P = 0.008) and in H. pylori-seronegative patients (P = 0.001).     

Association study between a novel single nucleotide polymorphism of the promoter region of the prostacyclin synthase gene and essential hypertension.

The purpose of this study was to investigate whether an association exists between the promoter region of the prostacyclin synthase gene and essential hypertension (EH). Using the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) method, we discovered a novel single nucleotide polymorphism (SNP), T-192G, in the 5'-flanking region. We performed an association study using the SNP in 200 patients and 200 controls. The allele frequency distribution in the two groups was not significantly different. Thus, this SNP in the PGIS gene is not associated with EH.     

An autopsy case of desmoplastic malignant mesothelioma]

On November 15, 2000, a 60-year-old man was admitted to our hospital with progressive dyspnea and right chest pain. He had a 40-year history of occupational asbestos exposure, which began when he was 20 years old. On admission, his chest radiographs showed pleural effusion on the right side, and asbestos bodies were detected in his sputum. Neither a cytological examination of the pleural effusion nor a histological examination of the pleura by percutaneous pleural biopsy revealed malignant cells. In addition, we could not find any other cause for the pleural effusion (such as tuberculosis, collagen disease, or heart failure). In May 2001, the patient also developed pleural thickening and pain in the right hypochondrium, and he was readmitted to our hospital on May 21, 2001. On readmission, an enhanced abdominal CT showed multiple liver tumors, and percutaneous pleural and liver biopsies were performed. The histological findings in the pleura and liver specimens revealed hypocellular collagen tissues without malignant cells. Thus, we could not determine the main cause either of the pleural effusion or of the patient's disease. However, his condition rapidly deteriorated, and he died on August 12, 2001. At the autopsy, bilateral pleural thickening, predominantly on the right side, and invasion of the lungs were observed. The histological findings in the pleural and hepatic tissues revealed hypocellular collagen fibers with a striate pattern and areas of neoplastic spindle cells. He was diagnosed as having malignant desmoplastic mesothelioma with liver metastasis. Cases of malignant desmoplastic mesothelioma have rarely been reported in Japan.