Localization of (99m)Tc HMDP in an extraskeletal myxoid chondrosarcoma: a case report.

Extraskeletal myxoid chondrosarcoma of the lower extremity is rare, and slowly progressive. The authors of this article present the case of a man with progressive enlargement of the right thigh that underwent bone scintigraphy. The bone images showed a diffuse, moderate increase in uptake in the swollen right thigh. Despite chemotherapy, the patient died 28 mo later. At autopsy, it was confirmed that he had extraskeletal myxoid chondrosarcoma of the right thigh, which had metastasized to the upper arms, left scapula, lungs, pleurae, and right lower quadrant of the abdomen. The myxoid chondroid matrix, a major feature of the extraskeletal myxoid chondrosarcoma, is thought to account for the localization of the bone-imaging agent.

Axillary lymph node uptake of Tc-99m MIBI resulting from extravasation should not be misinterpreted as metastasis.

Ipsilateral axillary lymph node visualization due to extravasation of Tc-99m MDP intravenous injection has been well documented. A patient with suspected angina underwent Tc-99m MIBI myocardial SPECT who had extravasation of Tc-99m MIBI in the antecubital region resulting in ipsilateral axillary lymph node uptake. This finding should not be misinterpreted as lymphatic nodal metastasis in a patient with breast cancer or lung cancer.

Bone agent localization in hepatic metastases.

We present the bone scintigrams of two patients, which demonstrate diffuse extraosseous uptake of a bone agent in metastatic masses in the liver, one from a primary lung tumor and one from a primary breast tumor. The bone imaging agent did not localize in the brain metastases in these patients. CTs of the abdomen in both patients showed massive metastases in the liver with multiple areas of tumor necrosis. The CT of the abdomen of the breast cancer patient showed multiple small hepatic calcifications. Autopsy revealed massive tumor necrosis with calcifications in the enlarged liver. In routine bone scintigraphy, diffuse uptake of bone agents in the liver of a patient with a known malignancy should be considered suggestive of massive hepatic metastases.

Morphine-augmented cholescintigraphy enhances duodenogastric reflux.

Morphine intervention in cholescintigraphy decreases imaging time to diagnose acute cholecystitis. Not infrequently we observe duodenogastric reflux during scintigraphy with and without morphine intervention. To evaluate occurrence of duodenogastric reflux related to morphine, we reviewed 55 patients who underwent cholescintigraphy with (32) and without (23) morphine intervention. Morphine was injected when there was bowel activity with non-visualization of the gallbladder at 60 min. Duodenogastric reflux was identified by the appearance of activity in the area just below or immediately adjacent to the tip of the left hepatic lobe laterally. Among 32 patients with morphine intervention, 19 had acute cholecystitis and 13 chronic cholecystitis. Eleven of 19 (58%) with acute cholecystitis had duodenogastric reflux and 6 of 13 (46%) had duodenogastric reflux in chronic cholecystitis. The total of duodenogastric reflux in the group with morphine injection was 53%. Two patients' duodenogastric reflux occurred before morphine injection and was more apparent after morphine was given. In the without morphine group, 3 had acute cholecystitis and 20 had chronic cholecystitis; 2 (one acute and one chronic cholecystitis) of these 23 (9%) had duodenogastric reflux. Our results indicate: (1) occurrence of DG reflux in morphine augmented cholescintigraphy is not significantly different in cholecystitis from that in chronic cholecystitis; (2) duodenogastric reflux in morphine augmentation occurs significantly more often than without morphine intervention (p < 0.001). We conclude that cholescintigraphy with morphine enhances duodenogastric reflux. The degree of duodenogastric reflux in the acute cholecystitis patients has been more severe than in the chronic cholecystitis patients.

Serum PSA and PAP measurements discriminating patients with prostate carcinoma from patients with nodular hyperplasia.

Prostatic specific antigen (PSA) and prostatic acid phosphatase (PAP) are the tumor markers for monitoring disease progression or improvement in patients with prostate adenocarcinoma. The clinical utility of PSA and PAP for early detection of prostate adenocarcinoma, however, requires distinction between prostate adenocarcinoma and prostate nodular hyperplasia. The serum PSA and PAP levels were measured in 20 men with histologically proven prostate adenocarcinoma and 28 men with histologically proven prostate nodular hyperplasia. Patients' blood samples were collected 1 to 7 days prior to the prostate examination, which included a rectal digital examination, transurethral resection, cytoscopy, and prostate biopsy. Sensitivity, specificity, and predictive values of positive and negative results for the discrimination of prostate adenocarcinoma from prostate nodular hyperplasia were 85%, 89%, 85%, and 29%, respectively, for serum PSA (cutoff level: 10 ng/mL) and 40%, 96%, 89%, and 69%, respectively, for serum PAP (cutoff level: 10 ng/mL). Results indicate that marked elevation of serum PSA suggests prostate adenocarcinoma and that serum PSA can discriminate prostate adenocarcinoma from prostate nodular hyperplasia better than serum PAP.

Prostate adenocarcinoma using Gleason scores correlates with prostate-specific antigen and prostate acid phosphatase measurements.

To evaluate a relationship between Gleason scores of histopathology of prostate carcinoma and concurrent serum prostate-specific antigen (PSA) and prostate acid phosphatase (PAP) values, 65 men with prostate carcinoma were studied. These patients' cumulative Gleason scores were obtained by totaling the primary and secondary patterns, resulting in two groups: 42 patients received high (6-10) and 23 received low (2-5) Gleason scores. Serum PSA and PAP values were measured by radioimmunometric assay 1 to 7 days before surgical procedures or biopsy for prostate carcinoma. Mean serum PSA for patients in the high Gleason score group was 134.39 ng/mL (normal range: 0 to 4), and the mean serum PSA for patients in the low Gleason score group was 23.62 ng/mL. Mean serum PAP for patients with high scores was 28.08 ng/mL (normal range: 0 to 5), and the mean serum PAP for patients with low scores was 18.19 ng/mL. Patients with high Gleason scores showed significantly greater elevation of serum PSA than those with low Gleason scores (P = .047), using two samples to test for groups having unequal variants. Prostate acid phosphatase levels of patients with high scores were not significantly higher than the levels in patients with low scores (P = .60). These results indicate that PSA levels but not PAP levels correlate with Gleason scores.

Prediction of radionuclide bone imaging findings by Gleason histologic grading of prostate carcinoma.

To evaluate a relationship between Gleason scores and Tc-99m HMDP bone imaging findings, data from 48 men (aged 45 to 77; mean, 67) with prostate carcinoma who had a bone imaging study at the time of presentation were reviewed. Cumulative Gleason scores were divided into two groups: high scores (6-10), 32 men; low scores (2-5), 16 men. Of the 32 men with high Gleason scores, 15 tested positive for multiple metastases and 17 tested negative. Tumors of the 16 men with low Gleason scores were negative for metastasis. A chi-square association between Gleason scores and the presence of metastases, either of a superscan pattern or multiple metastases, was 10.9 (1 df, P less than 0.001). The results indicate that a superscan pattern or multiple metastases were found exclusively in the bone images of patients with high histologic grades; bone images negative for metastases were associated with low-grade tumors. We conclude that positive bone imaging for metastases at the initial scan occurs only in patients who have high Gleason scores, that patients with high Gleason scores might or might not have skeletal metastasis, and that skeletal metastasis is not predictable in patients with low Gleason scores.

Tc-99m HMDP bone scintigraphic findings in association with concurrent serum osteocalcin measurements.

Osteocalcin is a noncollagenous bone protein produced by osteoblasts. Increase in serum osteocalcin level reflects osteoblast activity with acceleration of bone formation. To evaluate the correlation of Tc-HDP bone scintigraphic findings and concurrent serum osteocalcin, serum osteocalcin values of 40 consecutive patients were measured by radioimmunoassay at the time of initial referral for bone studies. These patients, all males aged 23-93, were studied for various disease entities, including prostate carcinoma. The results of the assay were categorized into three groups (gp) as follows: 17 at normal (1.8 to 6.6 ng/ml) level (gp 1), 21 low (gp 2), and two high (gp 3). Only one bronchogenic carcinoma patient with a high level had a right iliac lesion suggesting metastasis. The bone scans of nine patients with normal or low levels showed positive metastases. Two patients with stress fractures as shown on bone scans had normal levels. The images of patients with disparity between serum osteocalcin and positive bone lesions may be interpreted as follows: Instead of osteoblastic activity resulting in the synthesis and/or release of osteocalcin, area(s) of increased uptake in the bone scan may be predominantly reflecting increased regional blood flow and decreased sympathetic tone, resulting in an increase in bone-agent deposition.

Serum osteocalcin measurements in prostate carcinoma patients with skeletal deposits shown by bone scintigram: comparison with serum PSA/PAP measurements.

The correlation of technetium-99m-HMDP bone scintigraphic findings, serum osteocalcin as a measure of bone turnover and prostate-specific antigen (PSA) and/or prostate acid phosphatase (PAP) was determined in 19 men with bone metastasis due to prostatic carcinoma. Six of the 19 patients with metastases on bone scan showed elevation of osteocalcin. These patients had extensive metastatic disease. All 19 men with positive bone scans had high serum PSA and/or PAP levels. Serum osteocalcin measurement is less sensitive to detection of bone deposits than PSA/PAP measurements (p less than 0.0008).

Correlation of prostate-specific antigen and technetium-99m HMDP bone imaging.

For an evaluation of the clinical utility of prostate-specific antigen (PSA), 32 prostatic carcinoma patients (ages 54-76) and 13 nonprostatic carcinoma patients (ages 60-70) underwent PSA measurements and bone imaging. At the time of bone imaging, each patient's PSA value was measured by a monoclonal immunoradiometric assay. All 13 nonprostatic carcinoma patients (11 bronchogenic, 1 colon, and 1 urinary bladder) gave normal PSA values, although 6 had metastatic bone disease. The 32 prostatic cancer patients were divided into 2 groups of 16 each; PSA levels in Group 1 were abnormal (greater than or equal to ng/ml): PSA levels in Group 2 were normal (less than 4 ng/ml). In Group 1, bone images of 14 patients showed bone metastases; 6 of the 14 showed progression of metastases in a 6- to 12-month period. Two patients in Group 1 were negative for skeletal metastases. Twelve patients in Group 2 were negative for skeletal metastases; bone imaging in 1 showed regression of skeletal metastases; and 3 patients had unchanged bone lesion(s). The data indicate that PSA measurements may enhance bone imaging interpretation and provide valuable clinical monitoring of prostatic carcinoma. In the case of a patient with positive bone imaging and an unknown primary, PSA measurements may definitively determine if metastases originated from prostatic carcinoma.