Background: Neurofibromatosis type 1 (NF1) is an autosomal dominant condition with a high rate of new mutation and variable expression. Diffuse neurofibroma of the epidermis invading deeper organs is rare.We report a case of diffuse subcutaneous neurofibroma in the thoracoabdominal wall which had invaded the diaphragm and caused diaphragmatic eventration. Case presentation: We describe a patient with diffuse neurofibroma of the chest and abdomen who was admitted to the hospital due to sudden abdominal pain and a possible diaphragmatic hernia. We performed thoracotomy and found that the neurofibroma had invaded the diaphragm and caused diaphragmatic eventration. Conclusions: This occurrence has not been reported, and it shows that although neurofibromatosis is a benign disease, it still has the biological behavior of a malignant tumor and may cause a serious impact on and damage to other organs.

Peripheral neuropathy is a common side effect of cisplatin; however, there is no definitive treatment for this condition. In humans, beta-hydroxy-beta-methyl-butyrate (HMB) is an endogenous metabolite of leucine. To date, none data is available about the effects of HMB on cisplatin-induced peripheral neuropathy. Herein, oral administration of HMB considerably alleviated cisplatin-induced hyperalgesia in Wistar rats, a symptom of peripheral neuropathy affecting the extremities of the limbs. The primary mechanism of cisplatin-induced peripheral neuropathy (CIPN) is apoptosis in the sensory neurons of the dorsal root ganglion (DRG) arising from the accumulation of platinum (Pt). HMB mitigated CDDP-induced neurotoxicity in DRG neurons through reducing Pt accumulation within these cells, as evidenced by the recovery of cell viability and reduced apoptosis. In addition, HMB treatment down-regulated the levels of CTR1, a key molecule mediates the influx of cisplatin. And artificial recovery of CTR1 expression by CTR1-overexpression plasmids transfection abrogated the inhibition of HMB on Pt accumulation in DRG neurons. Moreover, enhanced ubiquitylation, arising from increased NEDD4L expression, mediated the down-regulation of CTR1 by HMB. Finally, as evidenced by the data from lung cancer model in vivo and in vitro, HMB did not interfere with cisplatin’s ability to induce tumor cells death. These findings suggest that HMB can alleviate CIPN by destabilizing CTR1 in DRG neurons without affecting cisplatin’s chemotherapy effects. Therefore, HMB could be developed as an adjuvant therapy to relieve neurotoxicity in cisplatin-based treatment protocols.

Background: Pulmonary sclerosing pneumocytoma (PSP) is a relatively rare benign tumor, and multiple pulmonary sclerosing pneumocytomas are even rarer. PSP is usually seen in adults over 50 years old, featuring a female to male ratio of 5:1. We report an extremely rare case of a 20-year-old male patient with bilateral multiple pulmonary sclerosing pneumocytoma. This rare benign disease also presents diagnostic challenges throughout the treatment process.Case presentation: A 20-year-old male was diagnosed with bilateral multiple pulmonary nodules on chest CT. The patient underwent regular chest CT reexamination over the course of six months, which indicated a tendency of slow enlargement of pulmonary nodules. After complete examination and exclusion of tumors in other parts of the body, he underwent two separate surgeries, and bilateral multiple nodules were removed. Intraoperative frozen section analysis suggested that some nodules were adenocarcinoma and the remaining nodules were considered benign tumors. Postoperative immunohistochemistry indicated that all nodules were pulmonary sclerosing pneumocytomas. Conclusions: Bilateral multiple pulmonary sclerosing pneumocytoma are rare in young men. In clinical practice, the differentiation of this disease from malignancy is challenging, and surgical treatment is a safe option for pulmonary nodules with a tendency to become larger.