Tumor liberated protein (TLP) is a protein that can be used to reveal the early development of a tumor. Besides being formed in the tumor, TLP is released in the blood when a patient starts producing cancer cells, which in turn enables the physician to intervene at a stage when the cancer is operable. To date, the available studies of tumor markers in lung cancer patients are CEA, NSE, TPA, Chromogranine, CA125, CA19-9, and Cyfra 21-1. The sensitivity and specificity for serum markers ranges between 50 and 90%, depending on the study and the clinical samples analyzed. Most of these markers show an increased rate of positivity as the stage advances. There are very limited data on TLP to draw any firm conclusion regarding the diagnostic value of this marker. TLP has been detected in 53.1% of non-small cell lung cancer (NSCLC) patients (N ¼ 534) with 75% being positive in the early stage (stage I) and dropping to 45% in the late stage (stage IV). However, 7.6% blood donor sera and 17.4% chronic lung disease sera have also tested positive. In a confirmation study, the specificity was 89.94% and the sensibility was 63.63% from stage III to IV NSCLC patients. In an initial study of TLP as a marker for early detection in stage I, NSCLC patients showed a sensitivity of 66.7% and a specificity of 80% for TLP compared to a sensitivity of 33.3% for CA19-9, 11.1% for Cyfra 21-1 and CA125, and 0% for CEA; the specificity for all four of the latter markers was 100%. Using immunohistochemical analysis with peroxidase anti-peroxidase (PAP), we observed that NSCLC cells were positive; we used the specific rabbit antiserum to TLP, which turned out negative in the presence of 1 mg/ml of the synthetized peptide. The pre-serum was also negative. The same reactivity was found early in the modified epithelial cells of interstitial lung fibrosis and might be a predictive marker of cell transformation. The site of the peroxidase positivity was cytoplasmic, of diffuse and/or granular type.

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Phenobarbital (PB) has a reputation for safety, and it is commonly believed that PB-related increases in serum aminotransferase levels do not indicate or predict the development of significant chronic liver disease. Here we report of two adult patients with a long history of epilepsy treated with PB who died suddenly: one as consequence of cardiac arrest, the other of acute bronchopneumonia. At autopsy, analysis of liver parenchyma revealed rich portal inflammatory infiltrate, which consisted of mixed eosinophil and monocyte cells, associated with several foci of necrosis surrounded by a hard ring of non-specific granulomatous tissue. Inflammatory reactions of internal and external hepatic biliary ducts were also seen. Our findings illustrate that PB may be associated with chronic liver damage, which may lead to more serious and deleterious consequences. For this reason, each clinician should recognize this entity in the differential diagnosis of PB-related asymptomatic chronic hepatic enzyme dysfunction.

Primary cerebral tumors rarely provoke sudden death. The incidence is often underestimated with reported frequencies in the range of 0.02 to 2.1% in medicolegal autopsy series. Furthermore, primary cerebral melanoma is an uncommon neoplasm. It represents approximately 1% of all melanoma cases and 0.07% of all brain tumors. This neoplasm is very aggressive, and its annual incidence is about 1 in 10 million people. In the present study, a 20-year-old male was admitted to hospital with vomiting, headache, paresthesia and aggressive behavior. A computed tomography (CT) scan of the head was performed showing a hyperdense nodule in the right parietal lobe with inflammation of the Silvian fissure. A complete autopsy was performed 48 h after death. A blackish material was displayed on the skull base, and posterior fossa. Microscopic examination diagnosed primary brain melanoma. A systematic review of the literature was also performed where no previous analogous cases were found. The forensic pathologist rarely encounters primary cerebral melanoma, and for these reasons, it seemed appropriate to describe this case as presenting aspecific clinical symptoms and leading to sudden unexpected death. Histopathological observations are reported and discussed to explain this surprising sudden death caused by a primary cerebral melanoma.

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