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The diagnosis of hemochromatosis requires liver biopsy and the quantification of hepatic iron. Magnetic resonance imaging (MRI) of the liver shows a characteristic decrease in tissue signal intensity in iron overload states, but its role in the diagnosis of hemochromatosis has not been fully delineated. Forty-three patients (31 men and 12 women) were referred for the evaluation of hemochromatosis based upon a fasting transferrin saturation55% and/or a serum ferritin400 ng/ml in males or300 ng/ml in females. Each patient prospectively underwent MRI of the liver prior to percutaneous liver biopsy and quantitative hepatic iron determination. Homozygous hemochromatosis was diagnosed in 10 patients based upon an hepatic iron/age indexor = 2. MRI was performed with a 1.5 Tesla system using standard spin-echo sequences (T1; TR = 300-500 ms, TE = 13-17 ms, PD; TR = 2,000-2,600 ms, TE = 30 ms). Signal intensity values were blindly determined for regions of interest in liver and skeletal muscle at T1 and proton density. Ratios of liver to muscle (LM) for T1 and proton density (PD) calculated from these values showed a significant correlation with quantitative iron by multiple regression analysis. The LMPD ratio provided the best correlation with hepatic iron (r = -0.6946; p0.001). Linear regression analysis also provides an equation that can be used to predict hepatic iron based upon the LMPD ratio; micrograms/g of hepatic iron = (-5,174 x LMPD) + 9,932. All patients with LMPD ratios of0.5 had hepatic iron/age indices of2.0, thereby excluding homozygous hemochromatosis. These results suggest that LMPD ratios derived from MRI of the liver can accurately predict hepatic iron content. These ratios can be clinically useful in the evaluation of hemochromatosis among patients who either refuse or have contraindications to liver biopsy.

Objective. To determine the prevalence of magnetic resonance imaging (MRI) lesions in systemic lupus erythematosus (SLE) patients without a history of neuropsychiatric symptoms and to correlate any MRI abnormalities with the patient's other disease manifestations or treatment. Methods. Prospective study of 32 consecutive patients with SLE without a history of neuropsychiatric symptoms, from inpatient and outpatient rheumatology services, who underwent MRI scan during a 3-year period. Results. Five patients had MRI abnormalities consisting of white matter lesions or periventricular hyperintensities; this is similar to the prevalence of these abnormalities in the general population. Conclusion. The prevalence of silent brain MRI abnormalities is not increased in SLE patients who do not have a history of neuropsychiatric manifestations.

It requires a high index of suspicion to make the diagnosis of dysphagia lusoria. Clinically, these adults will present with symptoms of intermittent solid food dysphagia, and a mediastinal abnormality may be seen on chest x-ray. Noninvasive imaging of the chest with either computerized tomography or magnetic resonance scanning are excellent methods for evaluating the mediastinum for solid tumors or vascular anomalies that can cause extrinsic esophageal compression. Dysphagia lusoria caused by a persistence of the right embryologic aortic arch and diverticulum of Kommerell with an aberrant left subclavian artery may be satisfactorily managed by dietary modification when the symptoms are mild.

A common finding on abdominal ultrasound and CT examinations is variation in the size of the inferior vena cava (IVC). On occasion the infrahepatic IVC even assumes a slit-like appearance. Though commonly related to respiratory change and to the degrees of intra-abdominal pressure, some have claimed the slit-IVC may be an indicator of hypovolemia. To study this phenomenon, we evaluated prospectively the IVC in 26 normal volunteers. These individuals were studied supine by dynamic image ultrasound at end-inspiration, end-expiration, and during the Valsalva maneuver. The size of the IVC was maximal with the patient supine and at end-inspiration (A-P 1.8 cm). The subhepatic IVC decreased in size at end-expiration (A-P 1.2 cm) and frequently collapsed with the Valsalva maneuver (A-P 0.7 cm). Dramatic changes in the size of the IVC with changes in ventilation are normal variants. The use of the slit-IVC to diagnose hypovolemia should be done with caution.

Central nervous system vasculitis is a rarely described complication of rheumatoid arthritis. We report a case of cerebral vasculitis in a 55-year-old woman with a 7-year history of seropositive, nodular rheumatoid arthritis. Striking multifocal abnormalities of the white matter on magnetic resonance imaging led to a suspicion of vasculitis despite lack of clinical evidence of extracranial vasculitis and normal findings on cerebrospinal fluid studies and cerebral angiography. After institution of treatment with glucocorticoids and azathioprine, she survived in stable condition for 14 months from the onset of symptoms. Postmortem examination of the brain revealed vasculitis and chronic ischemic changes.

Quantitative bone scan (QBS), computed tomography (CT), and magnetic resonance imaging (MRI) have each been used to confirm the diagnosis of active sacroiliitis (SI) in patients with low back pain (LBP). The authors prospectively evaluated 19 patients referred for symptoms of possible inflammatory LBP (group I), 26 seronegative spondyloarthropathy (SNSP) patients with LBP (group II, inflammatory or mechanical), and 5 SNSP patients without LBP (group III) to determine which radiological scan, alone or in combination with other serological tests (Westergren erythrocyte sedimentation rate, C-reactive protein, HLA-B27, immunoglobulin A) was most useful in confirming a clinical diagnosis of active inflammatory SI. All patients were followed up for a minimum of 1 year to confirm the clinical diagnosis and evaluate response to therapy. Eight of 19 group I patients had active SI clinically or on plain radiographs on follow-up evaluation. Of these patients, 5 had abnormal QBS (71%), 3 had abnormal CT scans (38%), and 8 had abnormal MRI scans (100%, type I lesions). These type I MRI lesions were indicative of active inflammation manifested as subcortical bone marrow edema. The remaining 11 group I patients had negative scans for SI. Ten of 26 group II patients with LBP had SI diagnosed clinically and confirmed with positive QBS (60%), CT (100%), and MRI (100%, type I lesions). The remaining 16 group II patients had mechanical LBP without active SI clinically and had negative QBS (88%), CT (19%), and MRI (100%, normal or type II lesions). These type II MRI lesions represented old postinflammatory lesions with either fibrosis or fat replacement. All 5 group III patients had negative scans for active SI. Three patients (2 group I and 1 group II) with inflammatory SI treated with sulfasalazine showed marked improvement on serial MRI scans. Westergren erythrocyte sedimentation rate, C-reactive protein, immunoglobulin A, and CT scan alone or in combination with other tests were not reliable predictors of active SI. Positive QBS and HLA-B27 tests were the best combination of screening tests with 82% predictability of inflammatory SI in whites, and QBS alone had an 80% predictability in black patients. However, MRI, which had 100% predictability, was the best single test for confirming active inflammatory SI.

We performed a retrospective study of symptomatic peripheral vascular malformations to determine if MR imaging can be used to distinguish slow-flow venous malformations from high-flow arteriovenous malformations and arteriovenous fistulas. Twenty-seven MR examinations in 25 patients with malformations outside the CNS were reviewed. Sixteen venous malformations, nine arteriovenous malformations, and two arteriovenous fistulas were included. In all cases, the MR findings were correlated with the results of angiography. The distinction between slow-flow venous malformations and high-flow arteriovenous malformations and arteriovenous fistulas was made primarily on T2-weighted MR images, which showed high signal intensity in venous malformations and flow voids in high-flow lesions. In addition to the previously described MR features of venous malformations (serpentine pattern with septations, associated muscle atrophy, and typical T1 and T2 signal intensities), several new MR features were apparent. Venous malformations had a propensity for multifocal involvement (37%), orientation along the long axis of extremities or affected muscles (78%), and adherence to neurovascular distributions (64%). Prominent subcutaneous fat was commonly seen adjacent to the malformation. MR images of arteriovenous malformations and arteriovenous fistulas also commonly showed muscle atrophy and subcutaneous fatty prominence. Our results show that slow-flow venous malformations can be distinguished from high-flow arteriovenous malformations and fistulas on the basis of spin-echo MR signal characteristics. The associated imaging characteristics help in the differential diagnosis in problematic cases.

To the Editor. —We read with great interest the letter by Seiff et al1in the March 1991 issue of theArchives. We faced a similar predicament and tested gold weights in addition to lid springs. We want to share two points. See also p 1503. Although stainless steel is generally considered to be nonmagnetic, it can become magnetic when bent or formed, as is done for palpebral springs.2We tested a formed palpebral spring (0.010-in stainless steel wire, Catalog No 200-104, Unitek Corp, Monrovia, Calif) in a high-field-strength 1.5-T magnetic resonance imaging (MRI) system (Signa, General Electric, Milwaukee, Wis). It was held in a palm in front of the magnet before it was placed in the bore of the magnet without any noticeable movement or heating. The stainless steel wire of 302 grade was then taped onto the eyelid of a volunteer (K.M.R.), and an MRI was

One hundred twenty-eight patients were examined prospectively to determine the significance of mucosal thickening seen in the paranasal sinuses during routine MR imaging of the brain. On the basis of responses to a questionnaire, each patient was categorized as symptomatic (n = 60) or asymptomatic (n = 68) for paranasal sinus disease. Patients were categorized further on the basis of the maximal mucosal thickening seen by MR in any paranasal sinus. A modified t test was used to compare the prevalence of various degrees of mucosal thickening between symptomatic and asymptomatic groups. Statistically significant differences between the groups were seen only in those patients with normal sinuses and in those with 4 mm or more of mucosal thickening. We conclude that mucosal thickening of up to 3 mm is common and lacks clinical significance in asymptomatic patients. An ancillary finding is that 1- to 2-mm areas of mucosal thickening in the ethmoidal sinuses occur in 63% of asymptomatic patients. This minimal mucosal thickening in the ethmoidal sinuses is thought to be a normal variant, possibly a function of the physiologic nasal cycle.

Arteriovenous fistulas (AVFs) can be posttraumatic or congenital vascular malformations. In the initial arteriographic evaluation, chronic AVFs potentially can be confused with arteriovenous malformations (AVMs). The authors studied five patients with a single AVF and one patient with numerous AVFs. Three patients had undergone surgery for treatment of their AVFs, one patient had undergone isobutyl-2-cyanoacrylate (IBCA) embolization, and two patients had undergone no prior therapy. The AVFs recurred in the three patients who had undergone surgery and in the patient who had undergone IBCA embolization. All patients underwent ethanol embolization of their AVFs. Angiograms obtained immediately after embolization documented closure of all AVFs. At follow-up, none of the embolized lesions have recurred. The authors conclude that ethanol embolotherapy can cure these problematic lesions. Extreme caution, however, must be employed with the use of intravascular ethanol because nontarget embolization can potentially result in tissue devitalization. In this study, two patients developed a small focal area of skin necrosis that did not require skin grafting and healed with conservative management.

Absolute ethanol was used to treat 20 patients with symptomatic vascular malformations (SVMs) (ie, venous malformations, arteriovenous malformations, and congenital and posttraumatic arteriovenous fistulas) in whom previous surgery or standard embolotherapy had failed or who were not candidates for surgery. All large complex lesions required multiple embolizations as staged procedures. Immediate thrombosis was achieved in all patients; complications (13% of cases) were generally minor and were treated conservatively. Follow-up studies, performed in 19 of 20 patients, showed persistent occlusion of the SVM in all cases. Ethanol embolization of SVMs, performed according to strict techniques, has proved efficacious in SVM management and is emerging as a definitive form of therapy.