Liver uptake of 99mTc-pyrophosphate

Abstract

A 56-yr-old chronic schizophrenic with a prior history of anterior myocardial infarction was hospitalized with a 2-day history of progressive abdominal pain and shortness of breath. Physical examination revealed an agitated male with regular pulse of 100/min, blood pressure of 112/70, respiratory rate of 30/rain, and slightly elevated temperature of 100~ The jugular veins were distended to the level of the jaw and bibasilar rates were ausculted in the lungs. The liver was enlarged, firm, and mildly tender. The chest roentgenogram showed pulmonary interstitial edema and pulmonary venous congestion. On admission, creatine phosphokinase (CPK) was 2464, lactate dehydrogenase (LDH) 1110, glutamic oxalactic transaminase (SGOT) 1210, bilirubin 0.8, and alkaline phosphatase 177. The prothrombin time and partial thromboplastin time were elevated at 22.5 and 45.4 sec, respectively. Serum urea nitrogen (BUN) was 66 with creatinine level 1.9. The EKG showed right bundle branch block, old Q waves in the precordiaI leads, and new Q waves in leads I1, lI1, and AVF. Diagnosis on admission was recent inferior MI, rightand left-sided congestive heart failure, congestive hepatopathy, and acute renal failure. Subsequent CPK isoenzyme fractionation failed to support the diagnosis of acute myocardial infarction, and a 99mTc-pyrophosphate myocardial scintigram was performed on the third hospital day that showed intense labeling of the liver without demonstrable myocardial activity. (Fig. 1). It was postulated that the patient's myocardial infarction had occurred 3-5 days prior to admission, and that the persistent elevation of CPK was due to rhabdomyolysis. Right heart catheterization performed after correction of coagulation parameters with fresh frozen plasma revealed markedly elevated right-sided pressures, with right atrial pressure 23 mm Hg, RV 47/20, and pulmonary artery wedge 28. The cardiac output was 2.8 liter/min. On nitroprusside and dopamine, the hemodynamic parameters improved somewhat with diuresis and concomitant improvement in hepatic function. On the seventh hospital day, the patient developed supraventricular tachycardia, which progressed to ventricular fibrillation. Resuscitation was performed; however, a downhi|l course ensued and the patient expired 3 days later. Permission for autopsy was not granted. This case demonstrates diffuse hepatic labeling by 99mTc-pyrophosphate in a clinical setting with high likelihood of central hepatic necrosis secondary to severe congestive heart failure. Liver uptake of bone imaging agents is unusual; in a study of 250 consecutive bone scans, liver uptake occurred only in 5 cases, 2 of which were associated with metastases and the remaining 3 due to poor radiopharmaceutical quality. ''~ Diffuse hepatic uptake of 99roTe-phosphate compounds has since been shown to occur in massive liver necrosis, 2 in the presence of high serum AI +§ levels, 3 and in amyloidosis. 4 Animal studies have shown elevated liver uptake with increased phosphate salt concentration: and with combination of tin and 99mTc-reagents prior to the addition of the phosphate-chelating agent during radiopharmaceutical preparation. 6 In liver necrosis and amyloidosis, labeling occurs presumably due to phosphate localization at sites of cellular damage by mechanisms to be discussed, while in the other cases, reticuloendothelial uptake of microcolloidal particles is the postulated mechanism: ~ Focal uptake of 99roTe-phosphate compounds by hepatic metastases from adenocarcinoma of the colon, breast carcinoma, oat cell carcinoma of the lung, malignant melanoma, and esophageal squamous cell carcinoma has been reported. 7-~~ A single case of uptake by cholangiocarcinoma has also been described. 8 Tumor localization of phosphate compounds probably