Lipid profile of cerebrospinal fluid in multiple sclerosis patients: a potential tool for diagnosis.

Multiple sclerosis (MS) is a complex multifactorial neuropathology. Although its etiology remains unclear, it has been demonstrated that the immune system attacks myelin, leading to demyelination and axonal damage. The involvement of lipids as one of the main components of myelin sheaths in MS and other demyelinating diseases has been postulated. However, it is still a matter of debate whether specific alteration patterns exist over the disease course. Here, using a lipidomic approach, we demonstrated that, at the time of diagnosis, the cerebrospinal fluid of MS patients presented differences in 155 lipid species, 47 of which were identified. An initial hierarchical clusterization was used to classify MS patients based on the presence of 25 lipids. When a supervised method was applied in order to refine this classification, a lipidomic signature was obtained. This signature was composed of 15 molecules belonging to five different lipid families including fatty acids (FAs). An FA-targeted approach revealed differences in two members of this family: 18:3n3 and 20:0 (arachidic acid). These results reveal a CSF lipidomic signature in MS patients at the time of diagnosis that might be considered as a potential diagnostic tool.

Raised serum alkaline phosphatase activity in one family.

Eleven members of the same family were studied after an incidental detection of raised serum alkaline phosphatase activity in one of them without any apparent underlying cause. Three other members were found to have the same abnormality; none of them had an associated disease. In the four cases with elevated serum alkaline phosphatase levels, its activity showed a preponderance of the bone isoenzyme. Studies of the erythrocyte and histocompatibility antigens in nine members of the family, as well as idiograms of karyotypes of four of them, did not show any relation between histocompatibility antigens and the raised levels of serum alkaline phosphatase. Also, no chromosomal abnormality is shown from karyotypes. The data suggest a probable autosomal dominant pattern of inheritance.

Remediastinoscopy after induction chemotherapy in non-small cell lung cancer.

BACKGROUND: This study was undertaken to evaluate the technical feasibility and the sensitivity, specificity, and accuracy of remediastinoscopy in restaging N2 bronchogenic carcinoma treated with neoadjuvant chemotherapy. METHODS: Patients presenting mediastinal lymph node involvement at mediastinoscopy received three or four cycles of neoadjuvant chemotherapy with mitomycin, iphosphamide, and cisplatin or cisplatin and gemcitabine. If there was no disease progression, these patients underwent remediastinoscopy and, if no residual extracapsular involvement or N3 disease was found, a thoracotomy was then carried out. RESULTS: Twenty-four patients underwent remediastinoscopy. In 12 (50%) remediastinoscopy was positive. The 12 remaining patients were operated on and the tumors resected: 5 pneumonectomies and 7 lobectomies. Lymphadenectomy specimens showed residual disease in mediastinal lymph nodes in 5 patients (pN2) and hilar lymph nodes in 1 patient (pN1). The other 6 patients were free of nodal disease, and 4 of them presented no involvement at lung level either. The sensitivity, specificity, and accuracy of remediastinoscopy were 0.7, 1, and 0.8, respectively. CONCLUSIONS: Remediastinoscopy is a technically feasible staging tool with high diagnostic accuracy that is useful in the selection of patients who can be served best by complete resection after neoadjuvant chemotherapy.