Contrast Injection from an Intermediate Catheter Placed in an Intradural Artery is Associated with Contrast-Induced Encephalopathy following Neurointervention.

BACKGROUND AND PURPOSE: Contrast-induced encephalopathy can result from neurotoxicity of contrast medium in the affected area. The development of intermediate catheters has allowed guidance of catheters to more distal arteries. This study focused on the association between contrast-induced encephalopathy and contrast injection from an intermediate catheter guided into a distal intradural artery during neurointervention for cerebral aneurysms. MATERIALS AND METHODS: We retrospectively reviewed 420 consecutive aneurysms in 396 patients who underwent neurointervention for extracranial aneurysms and unruptured intracranial aneurysms at our institution from February 2012 to January 2023. Patients were divided into a group with contrast-induced encephalopathy and a group without. To identify risk factors for contrast-induced encephalopathy, we compared clinical, anatomic, and procedural factors between groups by multivariate logistic regression analysis and stepwise selection. RESULTS: Among the 396 patients who underwent neurointervention for cerebral aneurysms, 14 (3.5%) developed contrast-induced encephalopathy. Compared with the group without contrast-induced encephalopathy, the group with contrast-induced encephalopathy showed significantly higher rates of patients on hemodialysis, previously treated aneurysms, intradural placement of a catheter for angiography, nonionic contrast medium, and flow-diversion procedures in univariate analyses. Stepwise multivariate logistic regression analysis revealed intradural placement of a catheter for angiography (OR = 40.4; 95% CI, 8.63-189) and previously treated aneurysms (OR = 8.20; 95% CI, 2.26-29.6) as independent predictors of contrast-induced encephalopathy. CONCLUSIONS: Contrast injection from an intradural artery and retreatment of recurrent aneurysms were major risk factors for contrast-induced encephalopathy. Attention should be paid to the location of the intermediate catheter for angiography to avoid developing contrast-induced encephalopathy.

Intra-articular injection of hyaluronate (SI-6601D) improves joint pain and synovial fluid prostaglandin E2 levels in rheumatoid arthritis: a multicenter clinical trial.

OBJECTIVE: The relationship between clinicalfeatures and biochemical parameters of synovialfluid after serial intra-articular injections of sodium hyaluronate (SI-6601D) was investigated. METHODS: SI-6601D (sodium hyaluronate with an average molecular weight of 8.4 x 10(5); 25mg/2.5ml/syringe) was injected intra-articularly into the knees of 25 patients with rheumatoid arthritis (RA) every week for 5 consecutive weeks. Clinical and biochemical parameters were monitored before and after injection. Clinicalfindings included pain, as a summation of 3 categories (pain at rest, pain in motion and pain in passive motion, each assessed on a 4-step rating scale), and inflammation, also as a summation of 3 categories (swelling, patellar ballotement and local warmth, each assessed on a 4-step rating scale). Pain on walking of patient was qualitatively assessed by visual analogue scale (VAS). The aspirated volume of synovialfluid (SFV) was recorded and levels of prostaglandin (PG) E2, transforming growth factor beta-1, tumor necrosis factor alpha, interleukin I receptor antagonist, chondroitin 4-sulfate (C4S) and chondroitin 6-sulfate were measured. RESULTS: Significant improvement in pain symptoms (p < 0.0001), inflammation (p < 0.0001), VAS pain (p < 0.001) and SFV (p < 0.05) were observed after the 5 injections. Levels of PGE2 (p < 0.05) and C4S (p < 0.05) in the synovialfluid were significantly decreased. DISCUSSION: SI-6601D improved local clinical symptoms in RA patients by suppressing PGE2 and, therefore, may be a useful treatment for local inflammation in RA.

Dermatomyositis associated with rapidly progressive fatal interstitial pneumonitis and pneumomediastinum.

We describe two cases of dermatomyositis (DM), which subsequently developed into rapidly progressive fatal interstitial pneumonitis and pneumomediastinum during steroid therapy. Both cases showed the classical cutaneous manifestations of DM, but the muscular symptoms were absent or mild. Both rapidly progressive interstitial pneumonitis and pneumomediastinum can occur in DM showing less inflammatory changes in the muscles. Patients with this form should be treated with extreme caution.

Embedding of laboratory wastes in clay or concrete blocks, with special reference to baking osmic acid and cacodylic acid wastes with clay.

Liquid laboratory waste containing osmic acid and cacodylic acid was mixed with potter's clay or hydraulic cement. The clay-waste product was kneaded into blocks and baked in a klin (1,200-1,400 degrees C). The cement-waste product was allowed to harden into concrete blocks. Some of the baked clay blocks and concrete blocks were ground, and immersed in 1 N NaOH or 10% HCI solutions for 3-6 months. X-ray microanalysis of the dried samples of these solutions showed that no leakage of osmium and arsenic occurred in the baked clay embedding, and that some leakage of these agents occurred in the concrete embedding. The present study indicates that the baked clay embedding method is useful for safe storage of dangerous laboratory wastes. Additional experiments suggested that glass embedding is also useful for safe storage of laboratory wastes or harmful metals.

Localization of membrane-associated sialomucin on the free surface of mesothelial cells of the pleura, pericardium, and peritoneum.

Strong anionic sites, as recognized by deposition of cationic colloidal iron even at pH 1.5, were distributed on the free surfaces of the mesothelia of the mouse pleura, pericardium, and peritoneum. Methylation inhibited colloidal iron staining on the surface, and successive saponification restored it. Digestion with neuraminidase or hydrolysis of sialic acid with H2SO4 erased the colloidal iron staining. Lectin Limax flavus agglutinin (LFA), which is specific for sialic acid, labeled the free surface of the mesothelium. All these findings strongly suggested that the surface substance contained sialic acid. Moreover, prior treatment with LFA inhibited the mesothelial surface stain with colloidal iron. In transmission electron microscopy, the colloidal iron (pH 7.3)-stained substance took the shape of fine strands of 50-300 nm in length. These characteristics of the substance on the mesothelial surface correspond well with biochemical properties of membrane-associated sialomucin, whose strong and abundant negative charges produce repulsive forces between facing serosal surfaces. This may contribute to prevent serosal adhesion and to reduce friction during movements of organs.

Characteristics of T cell lines established from skin lesions of Behçet's disease.

Hypersensitivity to a streptococcal antigen is postulated to be the pathogenesis of Behçet's disease. We analyzed T lymphocyte-phenotypes infiltrated in cutaneous pustular lesions in Behçet's disease and found that CD4+ T cells were predominant components although CD8+ T cells were also present in the lesion. In addition, we established T cell lines from pustular lesions of the four patients with a streptococcal antigen, KTH-1. Two of the cell lines showed the cell surface markers of CD8+TCR alpha beta +, and expressed mRNAs for interleukin (IL)-8, tumor necrosis factor (TNF) alpha, and perforin. Two other T cell lines expressed the cell surface markers for CD4+TCR alpha beta +. Cytokine expression pattern of the two CD4+ T cell lines revealed that one is Th1 type and the other is Th2 type. The Th2 type cell line showed marked proliferation with autologous peripheral blood mononuclear cells, suggesting that the self-reactive T cells play some role on the pathogenesis of Behçet's disease.

Development of ischemic colitis and scleroderma renal crisis following methylprednisolone pulse therapy for progressive systemic sclerosis.

We describe a patient with progressive systemic sclerosis who developed ischemic colitis and scleroderma renal crisis following steroid pulse therapy. The possible pathogenic mechanisms of ischemic colitis and scleroderma renal crisis development are discussed. We conclude that the administration of steroids in high doses, especially via steroid pulse therapy, should be undertaken with caution for progressive systemic sclerosis patients.

[Clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis in Japanese].

In order to examine the clinical characteristics and genetic background of secondary amyloidosis associated with rheumatoid arthritis, we analyzed clinical features and HLA typing of 85 patients in a multicenter study. Eighty-five patients with secondary amyloidosis associated RA were studied. The diagnosis of secondary amyloidosis were made on histological findings by biopsy or autopsy. The most common biopsy site was gastrointestinal tract (79.5%). Clinical symptom and the frequency at the time of diagnosis were; diarrhea (35 cases), abdominal pain (22 cases) and vomiting and nausea (16 cases). Abnormalities and the frequency in a laboratory test included proteinuria (49 cases), increased serum creatinine (32 cases), anemia (30 cases) and hematuria (15 cases). Twenty-eight patients were dead and 57 patients were alive at the time of the study. The average duration between diagnosis of amyloidosis and death was 19.4 +/- 18.5 (SD) months among the dead patients. The average duration after diagnosis of amyloidosis was 24.2 +/- 19.5 (SD) months in surviving patients. The causes of death were renal failure complicated with heart failure (6 patients), heart failure alone (3 patients) and renal failure alone (2 patients). Fifty-nine patients in the control group who were negative to amyloid deposition on biopsies at more than one site in the gastrointestinal tract, were clinically compared with patients in the amyloidosis group. No difference were noted in the age of RA occurrence and the stage between the two groups. As to the class, however, the number of patients with severe functional disorder (class 3 or severe) was larger in the amyloidosis group. There were no significant difference between the two groups in Lansbury's activity index. On hematology, biochemistry and urinalysis, the incidences of increased white blood cell count, anemia, increased platelet count, increased serum creatinine, hypoproteinemia, hypoalbuminemia, increased IgA, and increased urine and blood BMG were statistically significantly higher in the amyloidosis group than in the control group. HLA-A, -B, -C, and DR-locus antigens were compared in the 53 patients in the amyloidosis group and in the 59 subjects in the control group. There were no significant differences in frequency of HLA-A, and -B antigens between two groups. Frequency of CW7 antigen was significantly decreased in the amyloidosis group (13.2%) than in the control group (39.0%). Frequency of DR1 antigen was decreased in the amyloidosis group (3.8%) than in the control group (22.0%), although the difference was not significant. These findings suggest the possible involvement of genetic factors in the occurrence of amyloidosis. It is suggested that the occurrence of amyloidosis is suppressed by some genes which are linked with CW7 antigen.

[Cyclophosphamide-responsive subclinical Sjögren's syndrome in a patient with initial peripheral and central nervous system involvement].

A 36-year old woman was admitted because of painful dysesthesia of her extremities, suggesting the presence of mononeuritis multiplex. Laboratory data was almost within normal limits, with the exception of lupus anticoagulant positivity and increase of IgM level. We considered the possibility of connective tissue diseases and examined the patient accordingly. Keratoconjunctivitis sicca without dry eye symptoms, identified by rose-bengal and fluorescence testing, was the only recognizable abnormality. Oral sicca symptoms were not revealed although lip biopsy showed infiltration by a moderate number of plasma cells and lymphocytes. Under the diagnosis of subclinical Sjögren's syndrome, the following examination was carried out. Sural nerve biopsy specimens revealed wallerian degeneration and perivascular mononuclear cell infiltration of the vasa nervorum. We therefore concluded that the peripheral neuropathy was caused by subclinical Sjögren's syndrome. Magnetic resonance imaging (MRI) of the brain demonstrated multiple small lesions with increased spin echo images (T2 weighted) in the white matter. So, this patient was suffered from not only peripheral but also central nervous system complications. The mechanism of nervous system involvement was considered to be mononuclear cell-dependent ischemic damage caused by infiltration of the vasa nervorum. Both steroid pulse therapy and oral corticosteroid administration were ineffective in treatment of the peripheral neuropathy. Alternative use of cyclophosphamide (75 mg per day) was dramatically effective in relieving peripheral nervous system disorders. This was evident in the remarkable improvement of painful dysesthesia, grip strength and motor nerve conduction velocities. This case could be considered valuable for understanding the pathophysiology of Sjögren's syndrome and associated nervous system complications.

[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus].

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.

[Two cases of RA-like and SLE-like features similar to remitting seronegative symmetrical synovitis with pitting edema (RS3PE syndrome)].

In 1985, McCarty et al reported 10 patients with a symmetrical synovitis affecting predominately the wrists and flexor digitorum tendon sheaths associated with marked pitting edema of the dorsum of both hands and both feet. It was insisted on the clinical entity as remitting seronegative symmetrical synovitis with pitting edema (RS3PE syndrome). These patients were mostly elderly men whose sera revealed negative rheumatoid factor and had a benign clinical course. Patients with RS3PE syndrome remitted completely within 3-36 months and the remission was maintained even after all medications were discontinued. We experienced 2 interesting cases which were similar to RS3PE syndrome. One case with SLE-like conditions evolved into RA-like conditions. On the contrary, the other which had been effectively treated as RA developed into SLE-like conditions. Both cases were seronegative and had the characteristic pitting edema of both hands and feet demonstrating the symmetrical synovitis without bony erosions. They went into complete remission by corticosteroid therapy, although it did not continue for a long time. We should consider that such cases are similar to RS3PE syndrome and must be distinct from it.

[A case of cyclosporin A-induced myopathy].

A 40-year old man with Behçet's disease was admitted for severe decrease of visual acuity. Since 1987, he had suffered from oral aphtha, retinitis, erythema nodosum, genital ulcer and epididymitis. He was diagnosed as complete Behçet's disease and has been administered cyclosporin A (CYA) and colchicine (Col). Because of repeated ocular attacks and reduced visual acuity, CYA was increased from 3.49 mg/kg/day (220 mg/day) to 6.35 mg/kg/day (400 mg/day) and Col, 0.5 mg/day to 1.0 mg/day. 2 weeks later, he revealed fever, generalized myalgia, muscle weakness and general fatigue, accompanying marked elevation of creatine kinase (4962 IU/l). CYA was discontinued and Col was diminished to 0.5 mg/day. The myalgia disappeared in 4 days and general conditions including creatine kinase were normalized within 2 weeks. We concluded that CYA was highly suspected of the cause of myopathy considering his clinical course.

[Gold-induced severe cholestatic jaundice in rheumatoid arthritis patient and effect of repeated steroid pulse therapy].

A 32-year-old female with early stage of rheumatoid arthritis (RA) developed anorexia, pruritus, dark urine, pale stool and jaundice 3 weeks after initiation of chrysotherapy. She was administered a total of 35mg of gold sodium thiomalate (GST) intramuscularly and auranofin 6mg per day orally. Liver function tests and biopsy specimens showed severe cholestatic jaundice. Prednisolone 30mg per day and plasma exchange were started. No response however was obtained and the total bilirubin level gradually increased. Steroid pulse therapy, 1000mg methylprednisolone for successive 3 days as one therapy unit, was repeated 4 times. Liver functions were then gradually improved. Gold induced hepatotoxicity is a rare complication. We concluded that the hepatotoxicity in this case was caused by allergic reaction against GST and repeated steroid pulse therapy was very effective to these conditions.

Effects of solute hydrophobicity and phospholipid composition on permeability of composite membranes containing phospholipids.

Permeabilities of several solutes through the composite membranes containing phospholipids have been measured. They were inversely proportional to the content of the phospholipids in the membrane. Both the permeability of solutes and the degree of permeability change around the phase transition temperature of the phospholipids for the hydrophobic solutes such as n-butanol and salicylamide were larger than those for the hydrophilic solutes such as amino acids and pyridoxine. These results suggest that the permeation path of hydrophobic solutes is different from that of hydrophilic ones. The addition of phosphatidyl ethanolamine, phosphatidyl serine, or phosphatidic acid to the composite membrane influenced the solute permeability due to the introduced negative charge and/or the change in the molecular packing of phospholipid.

Purification of antilymphocyte antibody (ALA) from patients with systemic lupus erythematosus (SLE)-immunoabsorption and elution.

Purification of antilymphocyte antibody (ALA) from patients with systemic lupus erythematosus (SLE) was achieved by immunoabsorption and elution. Human tonsil cells or thymocytes were used as absorbents. Complement dependent microcytotoxicity tests showed that, in comparison to the parent sera, the eluate from tonsil cells was eight times, and that from thymocytes four times, more active. Antinuclear activity was eliminated by elution. The ALA was almost entirely IgM, IgG being involved in only a few cases. IgA lacked cytotoxic activity. ALA was directed at both T- and B-cell surface determinants, which suggests that, in SLE, it has a heterogeneous biological composition.