Paul M. Weber

Detecting Unsuspected Thyroid Dysfunction by the Free Thyroxine Index

The free thyroxine index (FTI) was used in 2,704 adults to detect unsuspected thyroid dysfunction. Among 2,581 adults found to be clinically euthyroid without thyroid medication, 2,571 had a truly normal FTI (121 to 360) and ten had a falsely abnormal FTI (seven less than 121, three greater than 360). Among 25 subjects with newly diagnosed thyroid dysfunction, there were eight hyperthyroid (prevalence, 0.31%) and 14 hypothyroid (prevalence, 0.50%) subjects. The sensitivity of the FTI was 1.0, and the specificity was 0.996. The predictive value of an abnormal FTI with a prevalence of 0.81% was 67%. The cost to find a new case averaged

Diagnosis of acute cholecystitis using hepatobiliary scan with technetium-99m PIPIDA

127. The annual incidence of symptomatic hyperthyroidism was 0.05%; of hypothyroidism, about 0.08%. We conclude that the FTI is cost-effective for case finding in thyroid dysfunction.

The importance of perfusion imaging in brain scintigraphy for subdural hematoma.

Sixty patients were evaluated for acute abdominal pain using technetium-99m PIPIDA hepatobiliary imaging. The sensitivity of the test was 90.6 percent in all patients and the accuracy was 93.3 percent. In the evaluation of acutely ill patients with right upper quadrant pain, fever, nausea and vomiting, hepatobiliary imaging with PIPIDA is the preferred test for diagnosing acute cholecystitis. If the test is positive, disease of the gallbladder and probably acute cholecystitis are present. Early operation can proceed if desirable. If the test is negative and the bilirubin level is less than 5.0 mg/dl, acute cholecystitis is not present. In such cases conservative treatment is appropriate, and follow-up tests should be performed to evaluate the possibility of chronic cholecystitis. When the bilirubin level exceeds 5.0 mg/dl, the test is often indeterminate.

INDIUM LABELED LEUKOCYTES FOR ACUTE APPENDICITIS DETECTION

The authors report a case of subdural hematoma in a patient who showed bilateral perfusion defects, highly characteristic of subdural hematoma, but did not show the expected complementary static abnormalities. This appears to be the first such case in the literature.

Detection of the carrier of Wilson's disease

We report the successful use of Indium-111 labeled leukocytes to make the diagnosis of acute appendicitis. Clinical diagnosis has a false positive rate of approximately 20%. This has been accepted as the national standard to prevent the complication of ruptured appendix and peritonitis. Patients who present to the E.R. with symptoms and signs of possible appendicitis were screened by the surgical service and those with clear-cut appendicitis went to surgery. Those assigned to observation as possible but not definite acute appendicitis were selected for study. Using standard methodology leukocytes were harvested, labeled, and re-injected. Imaging was done at 2 hours. Scans were interpreted as supportive of the diagnosis or non-diagnostic. Surgical specimens were imaged to document the presence of Indium-111. Of 11 patients studied, there were 5 with positive scans all of whom had acute appendicitis proven at laparotomy. One non-diagnostic exam eventually went to laparotomy where a necrotic appendix was found. This patient had been an in-patient on I.V. antibiotics. Scan of the surgical specimen showed good labeling of the appendix. Four patients had negative early scans and were not operated on. One scan consistent with peritonitis without localized accumulation of tracer had this diagnosis confirmed at laparotomy. We have found that positive scans correlate well with acute appendicitis. Negative scans correlate well with negative pathology. Our 1 false negative so far indicates that this test may not be useful for cases where I.V. antibiotics have been used and delayed imaging is necessary.

Abnormalities of the Physiology of Copper in Wilson's Disease: III. The Excretion of Copper

SUMMARYWhole-body counting over a three- to four-week period following the intravenous administration of copper 67 in 11 normal volunteers, 2 neurological control patients, 7 control subjects with cirrhosis, and 10 homozygotes and 7 heterozygotes of Wilsons disease showed that whole-body retention of radio-copper was prolonged in the wilsonian subjects, both homozygous and heterozygous, and in cirrhotic patients with ascites or hepatocellular failure or both. If the latter can be excluded, prolonged whole-body retention of radiocopper serves to identify the presence of the abnormal gene or allele of Wilsons disease. Because of overlap, it is not possible to distinguish the heterozygote from the homozygote by whole-body counting alone. External probe counting over the liver and muscle, carried out in 5 control subjects, 8 homozygotes, and 5 heterozygotes, revealed abnormal hepatic uptake with little apparent release of radiocopper and usually evident uptake in muscle in the homozygotes and reasonably normal hepatic uptake with delayed release and no apparent muscle uptake in the heterozygotes, compared with the control subjects. It appears that external monitoring of hepatic and muscle radioactivity, in addition to whole-body turnover measurements after intravenous copper 67, permits more accurate determination of the genetic status of individuals in respect to Wilsons disease.