The pulmonary mass was reduced by 30% and he presented a complete remission of the cervical lymphadenopathy. diagnosis and treatment of lung malignancy. and were undetectable. The PNS serum antibody panel came out to be positive for anti-SOX1 antibody. The CT scan showed a 68?mm mass on the right upper lobe and a 45?mm right hilar lymphadenopathy compressing the superior vena cava practically in its entire diameter (figures 2 and 3).?Fine needle aspiration (FNA) of his cervical lymphadenopathy resulted positive for malignant cells. The anatomical pathology statement confirmed a high-grade neuroendocrine carcinoma, suggestive of an SCLC. The immunohistochemistry resulted positive for TTF1, CK7, synaptophysin and showed a 90% ki67 nuclei positive staining in tumour cells. Open in a separate window Physique 2 CT shows the 45?mm lymphadenopathy in the axial view (A) and the pulmonary tumour in the right upper lobe of the coronal view (B). Open in a separate window Physique 3 CT scan shows the lymphadenopathy surrounding the right pulmonary artery in the coronal view (A) and the sagittal view shows the compression of the superior vena cava by the pulmonary tumour (B). In this context, we performed another EMG with single fibre electromyography (SFEMG), which showed a pathological jitter sign in 100% of the proximal muscle tissue analysed and more than 50% of registered transmission blockage. The SFEMG also showed post-maximum voluntary contraction facilitation (physique 4A), a null sympathetic skin response (physique 4B) and a decremented response to slow repetitive Difloxacin HCl stimuli 3?Hz (physique 4C), all of which were compatible with LEMS. Open in a separate window Physique 4 Electromyography displays a post-maximum voluntary contraction facilitation (A), a null sympathetic skin response (B) and a decremented response to slow repetitive stimuli 3?Hz (C). Arrows show the pathological response to stimuli. Differential diagnosis The differential diagnosis for our patients paraesthesia, proximal muscle mass strength loss and excess weight loss included a polyneuropathy of carential, metabolic or alcoholic origin. Despite Difloxacin HCl his interpersonal, economic background and the results from the first EMG, the lab work showed no alterations in any of the parameters excluding common causes of polyneuropathies such as diabetes mellitus, hypothyroidism, alcoholism or hypovitaminosis. The only alteration was a moderate hyponatremia that did not improve his neurological symptoms after it was corrected. A viral or bacterial infection with myelin sheath tropism could be another cause that was excluded by undetectable serologies. An autoimmune disorder such as Sjogrens syndrome, lupus and rheumatoid arthritis could also explain a peripheral polyneuropathy, but they would be accompanied by dry mouth or dry eyes, rash or fever and arthralgia, respectively, and the autoimmunity panel was also unfavorable. Another possibility could be a paraproteinaemia-related disease, but the SPIEP was not altered, excluding amyloidosis, lymphoma, cryoglobulinemia and multiple myeloma. No new drugs were launched recently and Difloxacin HCl all toxins evaluated in urine were unfavorable. After excluding common causes of demyelinating neuropathies, we made the decision that a potential PNS could better explain the weight loss, mixed polyneuropathy and asthenia in a smoker patient with a pulmonary opacity in the chest X-ray. In light of this, we chose to add a full-body CT scan with intravenous contrast and the PNS serum antibody panel. The anti-SOX1 antibody was positive, which has a good sensitivity and specificity for LEMS related to SCLS, and the CT scan revealed a right pulmonary mass, suspicious for malignancy. A diagnosis of SCLC was confirmed on FNA of the cervical lymph node. After performing?all these tests, we obtained the three requisites to identify a PNS: neurological symptoms, anti-SOX1 antibody positivity and the evidence of a tumour within 5 years of the neurological clinical onset. The most probable PNS was LEMS since our individual had proximal muscle mass strength loss, loss of reflexes, a positive specific onconeuronal antibody and an SCLC. Finally, a pattern compatible with LEMS was confirmed by SFEMG, supporting the diagnosis of Lambert-Eaton myasthenic syndrome (LEMS)?produced by an SCLC. Treatment The patient received palliative treatment with carboplatin, taking into account the neurological alteration, and etoposide chemotherapy for four cycles. He received 500?mg intravenous infusion of carboplatin (AUC 5) on day 1 along with etoposide (100?mg/m2) on days 1 and Rabbit Polyclonal to BL-CAM (phospho-Tyr807) 3. The cycle was repeated every 21 days. End result and follow-up The patient was seen in the medical center 2 months after discharge with a CT scan and lab work, presenting a partial radiological response after 2 cycles of chemotherapy. The pulmonary mass was reduced by 30% and he offered a complete remission of the cervical lymphadenopathy. He also showed an.