[18F]-fluoro-2-deoxy-D-glucose positron emission tomography computed tomography is a useful tool to suggest the diagnosis of malignant processes. However, false positive results are known to occur in benign lesions that have a high metabolic activity. Here we describe the unusual diagnosis of a pulmonary endometrioma in a 47-year-old woman, presenting as a cavitary lung mass with intense (18)F-FDG uptake on PET-CT.

A 70-year-old male presented with hematuria and bruising of arms and legs for the last three days. He also complained of urinary frequency and hesitancy and weight loss of 40 pounds over a span of four months. Initial blood tests showed prothrombin time (PT) of 25.1 seconds, international normalized ratio (INR) of 2.5, partial thromboplastin time (PTT) of 43.9 seconds, fibrinogen of 60 mg/dl, fibrin degradation products (FDP) of more than 20 μg/ml, and platelets of 88,000/μl. The impression was disseminated intravascular coagulation (DIC). A search was initiated to determine the underlying etiology precipitating DIC. Due to urinary symptoms and weight loss, prostate-specific antigen (PSA) was ordered. PSA was elevated at 942 μg/dl. Computed tomography (CT) of the abdomen and pelvis without contrast showed an enlarged prostate with mass effect on the bladder base, left-sided hydronephrosis, and numerous enlarged pelvic lymph nodes. A bone scan of the whole body showed increased sclerosis of the L3 vertebral body. There was a concern for metastatic prostate cancer precipitating DIC. On first admission, our patient’s DIC was stabilized with FFP and cryoprecipitate transfusions. He refused chemotherapy, and degarelix was not economically feasible. Accordingly, he was started on androgen deprivation therapy (ADT), bicalutamide, and leuprolide as an inpatient, pending the tissue biopsy. The patient refused a prostate biopsy. A bone marrow biopsy was performed which confirmed metastatic prostate adenocarcinoma. The patient was stable for discharge with a plan for outpatient chemotherapy. Subsequently, he was lost to follow-up with the oncology. Six months after the initial presentation, he was readmitted with hematuria. Repeat PSA worsened to 1,970 μg/dl. Blood work was consistent with acute DIC. He refused chemotherapy again. So, he was restarted on ADT. However, his hematuria and DIC panel were worsening. He was emergently started on docetaxel as an inpatient (after patient agreement). Within three days of starting chemotherapy, his hematuria resolved and DIC panel showed consistent improvement.

A 52-year-old male presented with tinnitus and fullness in left ear for one day. Workup revealed a white blood cell count of 685 × 103/μL with marked increase in granulocyte series and myeloid precursors on peripheral smear. The initial impression was chronic myelogenous leukemia with hyperleukocytosis, and patient was started on hydration, hydroxyurea, and allopurinol. Patient tolerated bone marrow biopsy well but continued to bleed excessively from the biopsy site. Results confirmed Philadelphia chromosome positive chronic myelogenous leukemia (chronic phase). On day three of hospitalization, patient developed sudden slurred speech along with shaking movements involving extremities. Magnetic resonance imaging revealed multiple hemorrhages throughout the brain. Hydroxyurea was continued until insurance coverage for nilotinib was getting approved. On day nine of hospitalization, patient developed sudden bilateral sensorineural deafness. Repeat magnetic resonance imaging revealed multiple new hemorrhages throughout the brain. Computer tomography of the temporal bones showed inflammatory changes in right and left mastoid cells. Nilotinib was started on day eleven of hospitalization. Patient's white blood cell count continued to decrease, but there was no improvement in hearing. Four months later, patient was treated with bilateral transmastoid cochlear implants. This case highlights permanent deafness as a hemorrhagic complication secondary to chronic myelogenous leukemia.

We report a case of a 66-year-old female who presented to the hospital with abdominal discomfort for 3 months. Work-up revealed a 2.4 cm mass in the right adrenal gland. A laparoscopic resection of the adrenal mass was performed and the histopathology was consistent with a pheochromocytoma. Patient was under active surveillance for 8 years, until she developed local recurrence in the right adrenal bed. A right adrenal bed resection and right nephrectomy were performed. Although the tumor margins were positive, none of the sampled lymph nodes (0/6) were positive for metastasis. Patient refused any adjuvant therapy, and was discharged on surveillance from the hospital. A year later, patient was found to have metastatic disease involving her spine, iliac bones, bilateral hips and right dome of the diaphragm. Patient was offered a metaiodobenzylguanidine scan, and positive subsequent treatment with radioactive iodine was discussed with her. However, she denied any further intervention and was made hospice.

Precursor T-cell lymphoblastic lymphoma (LBL) and T-cell acute lymphoblastic leukemia (ALL) are considered same disease with different clinical presentations. Clinically, a case is defined as lymphoma if there is a mass lesion in the mediastinum or elsewhere and < 25% blasts in the bone marrow. Whereas, bone marrow with > 25% blasts with or without mediastinal masses is classified as T-cell ALL. Mediastinal masses caused by T-cell LBL can lead to complications such as superior vena cava syndrome, tracheal obstruction, pericardial effusion and tamponade. We report an unusual case of a 25-year-old male with no significant past medical history, who presented with clinical features of cardiac tamponade. Work-up revealed a massive pericardial effusion and a mass arising in the anterosuperior mediastinum. Patient underwent an emergent subxiphoid pericardial window and approximately 1 L of hemopericardium was drained. Histopathology (pericardial tissue) and flow cytometry on the pericardial fluid were compatible with a precursor T-cell LBL. Although pericardial involvement by lymphoma/leukemia is a very rare complication, cases have been reported with both lymphoma and acute/chronic leukemia. Our paper highlights cardiac tamponade as one of the life-threatening complications associated with a precursor T-cell LBL.