Automated computer-based CT stratification as a predictor of outcome in hypersensitivity pneumonitis.

BACKGROUND: Hypersensitivity pneumonitis (HP) has a variable clinical course. Modelling of quantitative CALIPER-derived CT data can identify distinct disease phenotypes. Mortality prediction using CALIPER analysis was compared to the interstitial lung disease gender, age, physiology (ILD-GAP) outcome model. METHODS: CALIPER CT analysis of parenchymal patterns in 98 consecutive HP patients was compared to visual CT scoring by two radiologists. Functional indices including forced vital capacity (FVC) and diffusion capacity for carbon monoxide (DLco) in univariate and multivariate Cox mortality models. Automated stratification of CALIPER scores was evaluated against outcome models. RESULTS: Univariate predictors of mortality included visual and CALIPER CT fibrotic patterns, and all functional indices. Multivariate analyses identified only two independent predictors of mortality: CALIPER reticular pattern (p = 0.001) and DLco (p < 0.0001). Automated stratification distinguished three distinct HP groups (log-rank test p < 0.0001). Substitution of automated stratified groups for FVC and DLco in the ILD-GAP model demonstrated no loss of model strength (C-Index = 0.73 for both models). Model strength improved when automated stratified groups were combined with the ILD-GAP model (C-Index = 0.77). CONCLUSIONS: CALIPER-derived variables are the strongest CT predictors of mortality in HP. Automated CT stratification is equivalent to functional indices in the ILD-GAP model for predicting outcome in HP. KEY POINTS: • Computer CT analysis better predicts mortality than visual CT analysis in HP. • Quantitative CT analysis is equivalent to functional indices for prognostication in HP. • Prognostication using the ILD-GAP model improves when combined with quantitative CT analysis.

Machine learning to identify lymph node metastasis from thyroid cancer in patients undergoing contrast-enhanced CT studies.

INTRODUCTION: We compared the diagnostic performance of morphological methods such as the major axis, the minor axis, the volume and sphericity and of machine learning with texture analysis in the identification of lymph node metastasis in patients with thyroid cancer who had undergone contrast-enhanced CT studies. METHODS: We sampled 772 lymph nodes with histology defined tissue types (84 metastatic and 688 benign lymph nodes) that were visualised on CT images of 117 patients. A support vector machine (SVM), free programming software (Python), and the scikit-learn machine learning library were used to discriminate metastatic-from benign lymph nodes. We assessed 96 texture and 4 morphological features (major axis, minor axis, volume, sphericity) that were reported useful for the differentiation between metastatic and benign lymph nodes on CT images. The area under the curve (AUC) obtained by receiver operating characteristic analysis of univariate logistic regression and SVM classifiers were calculated for the training and testing datasets. RESULTS: The AUC for all classifiers in training and testing datasets was 0.96 and 0.86, at the SVM for machine learning. When we applied conventional methods to the training and testing datasets, the AUCs were 0.63 and 0.48 for the major axis, 0.70 and 0.44 for the minor axis, 0.66 and 0.43 for the volume, and 0.69 and 0.54 for sphericity, respectively. The SVM using texture features yielded significantly higher AUCs than univariate logistic regression models using morphological features (p = 0.001). CONCLUSION: For the identification of metastatic lymph nodes from thyroid cancer on contrast-enhanced CT images, machine learning combined with texture analysis was superior to conventional diagnostic methods with the morphological parameters. IMPLICATIONS FOR PRACTICE: Our findings suggest that in patients with thyroid cancer and suspected lymph node metastasis who undergo contrast-enhanced CT studies, machine learning using texture analysis is high diagnostic value for the identification of metastatic lymph nodes.

Follistatin inhibits activin-induced differentiation of rat follicular granulosa cells in vitro.

The effect of follistatin on activin-induced granulosa cell differentiation was investigated in freshly harvested granulosa cells from diethylstilbestrol (DES)-treated rats. Activin induced a remarkable change in granulosa cellular morphology from elongated fibroblast-like to round cells, which follistatin prevented. Follistatin itself had no influence on the cellular morphology. We studied the action of follistatin on activin-induced differentiation of granulosa cells cultured in a chemically defined medium. Addition of activin (30 ng/ml) to the culture increased the FSH binding site approximately 2-fold compared with the control (spontaneous expression) level, whereas follistatin reduced the activin-induced expression level to the control level in a concentration-dependent manner. Activin (30 ng/ml) markedly augmented FSH-induced hCG binding and progesterone production by approximately 20-fold, and these effects were suppressed by follistatin in a concentration-dependent manner. Similarly, addition of follistatin to the culture induced a concentration-dependent decrease of activin-enhanced inhibin-producing activity, but had no effect on FSH-induced inhibin production. These results suggest that follistatin/activin-binding protein binds to activin stoichiometrically to suppress the activin-induced differentiation of rat granulosa cell in vitro, but follistatin itself has no direct effect on activin-independent reactions.

Activin-binding protein is present in pituitary.

A binding protein for activin was purified from bovine pituitary by affinity chromatography on dextran sulfate-Sepharose CL-4B and activin-Affi-Gel 10. A 52,700-fold purification over the starting crude homogenate was achieved. The purified preparation showed two bands of 36 and 33 kilodalton in sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. The ability of each form of the protein to specifically bind activin was determined by ligand blot analysis and binding competition study. Each protein was found to have the same NH2-terminus and its sequence was identical to that of follistatin, which is a specific inhibitor of identical to that of follistatin, which is a specific inhibitor of FSH release. Moreover, the binding protein was shown to inhibit the spontaneous FSH release from cultured pituitary cells as does follistatin. These properties are the same as activin-binding protein that we have obtained from rat ovary. These results support a conclusion that activin-binding protein/follistatin exists also in the pituitary. Activin-binding protein has an ability to inhibit the activin-induced augmentation of FSH release from cultured pituitary cells as does inhibin. However, the inhibitory pattern by the binding protein was quite distinct from that of inhibin, suggesting that there may be different mechanism(s) for their antagonistic actions. Stoichiometric inhibition as shown by gel filtration analysis indicates that activin-binding protein binds activin to form an inactive equimolar complex having neither stimulatory nor inhibitory activity for FSH secretion by the pituitary. These findings suggest that activin is actually involved in FSH secretion in the pituitary and that the activin action in the pituitary is regulated by activin-binding protein/follistatin.

Purification and characterization of high molecular weight forms of inhibin from bovine follicular fluid.

High molecular mass forms [95 kilodaltons (kDa)] of bovine inhibin-A as well as the known forms of intermediate (55 kDa) and low (32 kDa) mass were purified from bovine follicular fluid by ion exchange chromatography on DEAE-Sepharose, immunoaffinity chromatography using a monoclonal antibody directed against bovine 32-kDa inhibin-A, gel permeation HPLC on TSK-gel, and reverse phase HPLC. The 95-kDa inhibin-A had similar suppressive activity on FSH secretion from cultured rat anterior pituitary cells as the 55- and 32-kDa inhibins. There is, however, a possibility that the inhibin activity detected with larger forms may be due to that of the 32-kDa form that results from proteolytic processing during incubation with rat pituitary cells. Both sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting analysis using monoclonal antibodies specific for 32-kDa inhibin alpha- or beta A-subunits revealed that the 95-kDa inhibin preparation contained two forms of inhibin (105 and 95 kDa), which were composed of either a 50- or a 40-kDa alpha-subunit linked by a disulfide bond(s) to a 55-kDa beta A-subunit. Amino-terminal sequence analysis showed that the 50-kDa alpha-subunit and the 55-kDa beta A-subunit were generated by removal of a signal peptide from each corresponding primary translation product [the first NH2-terminal 17 residues of the inhibin alpha-subunit (residues 1-360) and the first 20 residues of the inhibin beta A-subunit (residues 1-425)] and suggested that the 40-kDa alpha-subunit was formed by proteolytic processing of the 50-kDa alpha-subunit. On the basis of our findings, we propose that in bovine follicular fluid, the larger 105-kDa form of inhibin is processed successively to form the lowest molecular mass form, 32 kDa inhibin, through the smaller 95- and 55-kDa forms.

Immediate causes of death in thyroid carcinoma: clinicopathological analysis of 161 fatal cases.

Most patients with thyroid carcinoma have a good prognosis. Due to the small number of fatal cases, it has not been clarified what conditions result in death for patients with thyroid carcinoma. To provide appropriate management for advanced thyroid carcinoma patients, we analyzed causes of death in 161 fatal cases. Clinical characteristics and immediate (final) causes of death based on pathological conditions were analyzed in 62 anaplastic carcinomas and 99 fatal differentiated carcinomas. Single fatal conditions could not be specified in 55 patients. In the remaining 106 patients, respiratory insufficiency (43%) was the most common specific fatal condition, followed by circulatory failure (15%), hemorrhage (15%), and airway obstruction (13%). Respiratory insufficiency due to remarkable pulmonary metastasis replacing lung tissue, massive hemorrhage and airway obstruction due to uncontrolled local tumors, and circulatory failure resulting from compression of the vena cava by extensive mediastinal or sternal metastases were found to be the most important immediate causes of death. Based on this knowledge, several palliative procedures may be worth considering to improve survival and quality of life in patients with advanced thyroid carcinoma.

Papillary carcinoma of the thyroid. Tall-cell variant with extensive lymphocyte infiltration.

Thirteen cases of tall-cell variant of papillary thyroid carcinoma (PTC) showing extensive lymphocyte and plasma cell infiltration within the fibrous stalks of the papillary architecture were compared with age-, sex-, and tumor size-matched cases of ordinary tall-cell variant without extensive lymphocyte infiltration and also with cases of PTC of the conventional type. All cases of the tall-cell variant of PTC with extensive lymphocyte infiltration exhibited the histologic features of chronic thyroiditis. Dissemination of tumor cells with the thyroid was significantly less frequent than in control cases, but there was no difference between the incidences of lymph node metastasis. Immunohistochemically, the lymphocytes infiltrating the carcinoma focus were mainly CD20+, CD45+, and CD45RO+ cells, that is, basically the same as those found in foci of chronic thyroiditis. No tumor recurrence was observed during the mean follow-up period of 3 years 8 months. The results of this study suggest that the tall-cell variant of PTC with extensive lymphocyte infiltration has less aggressive characteristics and a more favorable prognosis.

Surgery for patients with thyroid carcinoma invading the trachea: circumferential sleeve resection followed by end-to-end anastomosis.

BACKGROUND: Curative surgery can be accomplished by tracheal resection in patients with thyroid carcinoma invading the trachea; however, there is controversy regarding the extent of the tracheal resection. In this study we investigated by means of histologic examination the mode of tracheal invasion by thyroid carcinoma. METHODS: Twenty-one patients with thyroid carcinoma invading the trachea underwent circumferential sleeve resection of the involved trachea. The extent of invasion of the tracheal wall on the adventitial and mucosal sides was compared on histologic examination. RESULTS: Three to nine tracheal rings were resected. Assessment of longitudinal spread showed that one to six rings (mean; 3.1 rings) were invaded on the adventitial side but only zero to four rings (mean; 1.9 rings) on the mucosal side, with invasion on the mucosal side never exceeding invasion on the adventitial side. In contrast, examination of circumferential spread showed invasion on the mucosal side exceeding invasion on the adventitial side in five cases. CONCLUSIONS: Our results suggest that when the extent of invasion of the adventitia is considered, carcinoma tissue may be left behind on the mucosal side of the trachea when partial wedge resection is performed and that, whenever feasible, circumferential sleeve resection should be performed in patients with thyroid carcinoma invading the trachea.

The role of lipid peroxidation in endotoxin-induced hepatic damage and the protective effect of antioxidants.

Intraperitoneal injection of endotoxin (lipopolysaccharide, [LPS]) to mice at a dose of 15 mg/kg of body weight resulted in a survival rate of 31% 48 hours after administration. Simultaneous intramuscular administration of (10 mg/kg) coenzyme Q10 (CoQ10) increased the survival rates of LPS-administered mice to 69.7%. When LPS administration was increased to 30 mg/kg, no survivors were observed in the placebo group. Simultaneous intravenous injection of CoQ10 (10 mg/kg) or alpha-tocopherol (20 mg/kg) restored the survival rate to 52.9% or 42.9%, respectively. The adenosine triphosphate (ATP) level in the liver, which is the best index of the energy state, decreased gradually to 70% of the control ATP level 24 hours after LPS (15 mg/kg) administration. The lipid peroxide level in the liver increased fivefold 16 hours after LPS administration and then decreased to the control level in 8 hours. Simultaneous treatment of mice with antioxidants, such as CoQ10 or alpha-tocopherol, completely suppressed the lipid peroxide level in the liver and preserved the hepatic ATP level in the normal range. These results indicate that LPS induced hepatic damage in mice because of lipid peroxidation and that antioxidants suppressed lipid peroxidation, preserved energy metabolism in the liver, and enhanced survival of endotoxin-administered mice.

Changes in the levels of endogenous antioxidants in the liver of mice with experimental endotoxemia and the protective effects of the antioxidants.

Gram-negative bacterial endotoxin (lipopolysaccharide) induces hepatic damage in mice caused by lipid peroxidation, and administration of antioxidants (coenzyme Q10 and alpha-tocopherol) suppresses this lipid peroxidation, preserves energy metabolism, and enhances the survival of endotoxin-administered mice. Therefore experiments were done to determine whether experimental endotoxemia in mice affected the levels of endogenous antioxidants and whether treatment with antioxidants altered these levels. Endotoxin produced decreases in hepatic endogenous antioxidants with time: reduced coenzyme Q9, alpha-tocopherol, and reduced glutathione were lowered to 29.9%, 27.1%, and 45.4% of the control levels, respectively, 24 hours after administration. Exogenously administered coenzyme Q10 (oxidized) accumulated in the liver and showed a maximal plateau between 8 and 16 hours after injection when 82% of coenzyme Q10 was converted to the reduced form. Coenzyme Q10 administered with endotoxin totally or partially prevented the decreases in these endogenous antioxidants, and furthermore, total coenzyme Q10 and the reduced form, both at levels of approximately 30 mg protein, were consumed during the period of elevated lipid peroxidation, 16 hours after endotoxin injection. These results indicate that coenzyme Q10 acts in vivo as an antioxidant after it has been converted to the reduced form. alpha-Tocopherol administered also showed an 84-fold accumulation in the liver 8 hours after injection, completely preventing any decrease in endogenous reduced coenzyme Q9 and partially preventing reduction of glutathione, which indicated an in vivo antioxidant action of alpha-tocopherol. These results support the assumption that administered coenzyme Q10 or alpha-tocopherol functions cooperatively with endogenous antioxidants to prevent tissue damage caused by lipid peroxidation in endotoxemia.

Factors affecting thyroid function after subtotal thyroidectomy for Graves' disease: case control study by remnant-weight matched-pair analysis.

In order to determine whether there are any predictive factors, other than the amount of remnant thyroid tissue, for subsequent thyroid function after subtotal thyroidectomy for Graves' disease, thyroid function was assessed in 329 patients 3 years after surgery, and a case control study was carried out in euthyroid, hyperthyroid, and hypothyroid groups by remnant-weight matched-pair analysis. Factors that affected thyroid function 3 years after surgery were thyroid gland infiltration by lymphocytes and the thyrotropin binding inhibiting immunoglobulin (TBII) value in the hyperthyroid and euthyroid groups, and the free triiodothyronine (FT3) value at the time of surgery and lymph follicle formation in the thyroid gland in the hypothyroid and euthyroid groups. It is concluded that no single factor studied at surgery, other than the amount of remnant tissue, can predict thyroid function after subtotal thyroidectomy for Graves' disease.

Follistatin and its role as an activin-binding protein.

Follistatin (FS), a specific binding protein for activin, neutralizes the diverse actions of activin by forming an inactive complex with activin. FS is a monomer derived from two polypeptide core sequences of 288 (FS-288) and 315 (FS-315) amino acids originated from alternatively spliced mRNA. We purified six molecular forms of FS from porcine ovaries. Their structural differences were caused by truncation of the COOH-terminal region and/or the presence of carbohydrate chains, resulting in the formation of FS-288, FS-315 and FS composed of 303 amino acids (FS-303) in various forms of glycosylation on the two potential Asn-linked glycosylation sites. All six molecular species have almost the same activin binding activity (Kd = 540-680 pM). By contrast, the COOH-terminal truncated form, FS-288, showed much higher affinity for heparan sulfate proteoglycans of the cell surface than FS-303, whereas the intact form of FS, FS-315, had no affinity. Furthermore, FS-288 more effectively blocked the suppression of follicle-stimulating hormone (FSH) secretion from rat pituitary cells by activin. This implies that activin binds to the cell surface through FS-288 which adheres to the cell surface. To clarify the physiological role of cell-associated FS, we then investigated the binding of activin to cell-associated FS and the fate of cell surface-bound activin and FS using primary cultured rat pituitary and ovarian granuloma cells. When the cells were incubated with 125I-activin A in the presence of FS-288 or 315, the binding of activin A to the cell surface was promoted much more markedly by FS-288 than by FS-315. The amounts of radioactivity recovered in trichloroacetic acid-soluble fractions (degraded activin) from the incubation medium were greatly increased by the addition of FS-288. This increase was abolished by heparan sulfate, monensin (an endocytosis inhibitor), chloroquine (a lysosome function inhibitor) and several lysosomal enzyme inhibitors. These results suggest that cell-associated FS-288 accelerates the internalization of activin into the cells, leading to its degradation by lysosomal enzymes, and that cell surface-associated FS therefore plays a role in the clearance system of activin.

Percutaneous microwave coagulation therapy for primary or recurrent hepatocellular carcinoma: long-term results.

BACKGROUND/AIMS: To clarify the indication of percutaneous microwave coagulation therapy for hepatocellular carcinoma. METHODOLOGY: Thirty-three hepatocellular carcinoma patients who underwent percutaneous microwave coagulation therapy were enrolled in this study, including 18 primary and 15 recurrent hepatocellular carcinoma patients. We examined the local recurrence rates and the long-term results after the treatment. RESULTS: The overall survival rates of the primary group at 1, 2, 3, 4 and 5 years were 94.4%, 77.8%, 77.8%, 77.8% and 48.6%, respectively, whereas those of the recurrent group were 100%, 85.7%, 66.7% and 50.0% at 1, 2, 3 and 4 years, respectively. Local recurrence after percutaneous microwave coagulation therapy was found in about 50% of patients in both groups. Seventeen of the 27 patients (63.0%) with a moderately or poorly differentiated hepatocellular carcinoma tumor had local recurrence, while none of the 6 patients with a well-differentiated hepatocellular carcinoma tumor did (P = 0.005). CONCLUSIONS: Irrespective of primary or recurrent hepatocellular carcinoma, the indication of percutaneous microwave coagulation therapy as an alternative to hepatic resection should be limited to cases of a well-differentiated hepatocellular carcinoma tumor smaller than 2 cm in diameter.

Fe2+ and ascorbic acid induced oxidation of cholesterol in phosphatidylcholine liposomes and its inhibition by alpha-tocopherol.

Fe2+ and L-ascorbic acid induced oxidation of cholesterol was investigated in liposomes of egg yolk phosphatidylcholine (PC). Cholesterol 5,6-epoxide, 7-hydroxycholesterol, 7-oxocholesterol, and cholestane-3,5,6-triol were detected as the oxidation products by gas chromatography, indicating that epoxidation and hydroperoxidation took place independently in cholesterol. Oxidation of cholesterol was accompanied with oxidative loss of unsaturated fatty acid moiety of PC. When egg yolk PC was replaced by dimyristoyl-PC, little oxidation was observed in the cholesterol fraction. These results indicate that cholesterol oxidation depends on peroxidation of polyunsaturated fatty acids in liposomal phospholipids. alpha-Tocopherol incorporated into liposomes at a level of 1.0 mol% to egg yolk completely suppressed not only the loss of unsaturated fatty acid moiety, but also oxidation of cholesterol. alpha-Tocopherol may inhibit cholesterol oxidation by suppressing phospholipid peroxidation. tert-Butyl hydroxytoluene, a synthetic antioxidant, was less effective against the oxidation of both PC and cholesterol.

Clinico-pathologic study of pulmonary metastasis of differentiated thyroid carcinoma: age-, sex-, and histology-matched case-control study.

From 1952 to 1984, 70 primary cases of differentiated thyroid carcinoma with pulmonary metastasis were treated. Of these, histopathological sections were reviewed in 59 cases (metastasis group). Fifty-nine age-, sex- and histology-matched cases without pulmonary metastasis were chosen as controls (control group). Poorly differentiated features of tumor cells were observed in 57.6% of the cases in the metastasis group but in only 27.1% of the control group (P < 0.001). In contrast, solid and/or trabecular growth patterns were noted in 45.8% of the cases in the metastasis group and 52.5% of the control group (P > 0.30). No difference in the incidence of vascular or capsular invasion was seen between the two groups. These findings suggest that the poorly differentiated features of tumor cells rather than the solid and/or trabecular growth pattern or vascular invasion of the tumor are more important as histopathologic characteristics of differentiated thyroid carcinoma with pulmonary metastasis.

Does total thyroidectomy induce metabolic bone disturbance?

Bone mineral content of 38 thyroidectomized patients with well differentiated thyroid carcinoma were determined. Seventeen patients were totally thyroidectomized and 21 patients were non-totally thyroidectomized (lobectomy). Thirty-eight healthy males and females were served as age-matched controls. Trabecular bone mineral content of lumbar vertebra was evaluated by quantitative CT method. Bone metabolic parameters in serum were measured. No significant differences were observed in the mean bone mineral content and BMC-index of totally thyroidectomized patients compared with non-totally thyroidectomized patients and control. Serum calcitonin level was not reduced in totally thyroidectomized. It is concluded that after total thyroidectomy, bone metabolic disturbance was not significant, and that when calcitonin remained at its basal level, it had no effects on bone metabolism.

Laparoscopy-assisted hepatectomy for a large tumor of the liver.

We performed a laparoscopy-assisted hepatectomy on a 52-year-old woman with a large hepatic cavernous hemangioma (longest diameter, 8.5 cm). With the use of Pringle's maneuver, the left lateral segment of the liver was resected with a Cavitron ultrasonic surgical aspirator (CUSA) while lifting the abdominal wall. Postoperative hepatic dysfunction was mild and transient, resolving spontaneously early after surgery. We intend to expand the indications of this minimally invasive procedure for hepatic resection.

Granular cell tumor of the breast: report of a case.

A case of granular cell tumor of the breast in a 43-year-old woman is described. The patient presented with a painless mass in the upper-outer quadrant of her right breast. Mammography showed a spiculated tumor and ultrasonography demonstrated a hypoechoic mass with an irregular border. Magnetic resonance (MR) mammography revealed a homogeneous enhanced mass in T1-weighted images using Gd-DTPA and a ringed high-intensity area around the mass in T2-weighted images. Fine-needle aspiration cytology failed to show any malignant cells. A partial resection of the breast was performed and histological examination revealed a granular cell tumor. Granular cell tumors are generally always benign, but they may be misdiagnosed as malignant tumors because of their mammographic and ultrasonographic findings. MR mammography did not reveal a typical breast cancer in either T1- or T2-weighted images in the present case. This case illustrates the need for care in preoperative examinations in order to avoid overdiagnosis of breast cancer.

A patient with a large hepatocellular carcinoma alive 13 years after repeated transcatheter arterial chemoembolization and hepatectomy.

We describe a rare case of a large hepatocellular carcinoma (HCC) in a patient who survived 13 years after repeated transcatheter arterial chemoembolization (TAE) and hepatectomy. The patient was a 41-year-old woman found in March 1985 to have a large HCC, measuring 14 x 12 cm in diameter and associated with obstruction of the main portal trunk. She underwent TAE 8 times over a period of 1 year. The serum alpha-fetoprotein level decreased from 18342 to 1871 ng/ml. The patient subsequently underwent left hepatectomy on October 9, 1986. Thirteen years after hepatectomy, the patient is being followed up on an outpatient basis and has had no evidence of recurrence.

A case of abdominal aortic aneurysm associated with systemic lupus erythematosus.

A case of abdominal aortic aneurysm associated with systemic lupus erythematosus (SLE) is reported. A 45-year-old woman with a 18-year history of SLE was admitted with severe lumbago radiating to the bilateral inguinal region. CT and DSA showed a dumbbell shaped true aneurysm of the abdominal aorta. An aorto-biiliac Y shaped graft replacements was performed. SLE is rarely associated with aneurysm of the great arteries. We could find only 4 reports of abdominal aneurysm associated with SLE. Common features were the young age of the patient, the long term of the systemic disease, and administration of corticosteroid therapy for a relatively long period of time. We speculate that atherosclerosis, hypertension, and corticosteroid may all work in concert, possibly together with aortic wall involvement or vasculitic damage, to produce the rare abdominal aneurysm in SLE.