Diffuse Hepatic Uptake of Tc-99m MDP in Acute Hepatic Failure Caused by Excessive Use of Analgesic Drugs

The present case was a 74-year-old female with a history of diabetes mellitus, hypertension, breast cancer, and lumbar disc herniation.

She had undergone surgery (left mastectomy) 12 years previously and received chemotherapy for breast cancer. She was regularly followed up by oncology and no known metastases was reported.

The patient had undergone spinal instrumentation with metallic fixation hardware for lumbar disc herniation 4 years earlier.

Our patient had a history of intense low back pain and visited the neurosurgery outpatient clinic and emergency department multiple times.

On her most recent visit to the emergency department, she had complaints of vomiting and stupor. The physical examination revealed the signs of generalized abdomen sensitivity.

Biochemistry tests were performed and showed elevated liver enzymes (aspartate aminotransferase: 3595 U/L and alanine aminotransferase: 1503 U/L), urea (66 mg/dL), and creatinine (2.82 mg/dL) levels. Serum levels of alkaline phosphatase (72 U/L), gamma-glutamyl transferase (32 U/L), direct bilirubin (0.31 mg/dL), and indirect bilirubin (0.21 mg/dL) were all within the normal limits.

The patient was referred to internal medicine and the decision was made to admit her to the hospital with diagnoses of toxic hepatitis and acute kidney injury. It is important to note that 1 month before admission, contrast-enhanced computed tomography images of the abdomen were acquired, which showed no signs of metastases to liver and reported no other pathological findings in the abdomen.

An abdominal ultrasound performed at admission also did not show any pathological findings.

The possible cause for our patient’s diagnoses was thought to be excessive use of analgesic drugs; containing pharmaceutical agents such as tramadol, codeine, and paracetamol. During her stay, because of intense low back pain and history of breast cancer, bone scintigraphy was planned to rule out potential metastases.

Bone scintigraphy showed increased hepatic radiotracer uptake, without scintigraphic evidence of skeletal metastases [Fig 1]. Slightly increased uptake was observed at the L2–L3 vertebrae, likely related to a potential fracture in the L2 vertebra, which was also reported on subsequent magnetic resonance ımaging (MRI).

Close

Fig 1:

Diffuse hepatic uptake of Tc-99m MDP was observed on (a) whole-body images and (b) spot images in our patient with acute hepatic failure.

Export to PPT

It is important to emphasize that our patients’ previous bone scintigraphy reported neither bone metastases nor liver uptake. In addition, no liver uptake was observed in any of the other patients who underwent bone scintigraphy at our unit that day, thus possibility of radiopharmaceutical contamination was ruled out.

During the later days of her hospital stay, the patient’s condition improved, and liver enzymes and urea/creatinine levels returned to within the normal limits. The patient was discharged after 10 days in hospital.

Tc-99m MDP demonstrates high affinity for hydroxyapatite, particularly at sites of increased blood flow or osteoblastic activity. Capillary permeability, the local acid–base relation, fluid pressure within bone, hormones, vitamins, the quantity of mineralized bone, and bone turnover can also play a role in Tc-99m MDP uptake. Tc-99m MDP provides excellent target-to-nontarget ratio in 3–4 h after injection due to rapid blood clearence by renal excretion. Thus impaired renal function may result in increased soft-tissue activity.^[1,2]

Extraosseus uptake of Tc-99m MDP can be seen in variety of disorders. Mechanisms leading to increased extraosseous Tc-99m MDP uptake include elevated tissue calcium concentration, extracellular fluid expansion, enhanced regional vascularity, and permeability. Soft-tissue Tc-99m MDP uptake may seen in benign and malignant neoplastic entities, hormonal disturbances in calcium metabolism (e.g., hyperparathyroidism), tissue damage (from inflammation, infection, or physical trauma), urinary tract anomalies or dysfunction, and faulty radiopharmaceutical preparation.^[3]

Several causes for diffuse hepatic uptake of Tc-99m MDP were reported previously such as hepatic necrosis,^[4,5] hepatic failure due to thrombosis of vena cava inferior,^[6] hepatic metastases,^[7] high-dose methotrexate use,^[8] and history of gadolinium use for MRI.^[9] Given that the underlying causes of Tc-99m MDP are typically life-threatening, a significant proportion of reported cases has resulted in patient mortality.

Because of the correlation between hepatic uptake of Tc-99m MDP and relatively high mortality rate, hepatic uptake was considered a poor prognosis indicator by Hakim et al. in their case report.^[4] However, it is imperative to note that, in their case report, Wei-Jen et al. stated that hepatic uptake may not predict the outcome, and the patient’s condition might be reversible if the underlying disease is corrected in time.^[10]