The aim of this study was to determine if the anticytokine neuropeptide α-melanocyte-stimulating hormone (α-MSH) occurs, along with interleukin 1 receptor antagonist (IL-1ra) and soluble tumor necrosis factor receptor (sTNFr), in synovial fluid of patients with rheumatoid arthritis (RA), juvenile chronic arthritis (JCA), or osteoarthritis. The data show that α-MSH does occur in the synovial fluid and its concentrations are greater in patients with RA than in those with osteoarthritis. Synovial fluid concentrations of IL-1ra and sTNFr were likewise greater in RA. Further, concentrations of α-MSH, IL-1ra, and sTNFr were greater in patients with polyarticular/systemic-onset JCA than in those with pauciarticular disease, that is in patients with greater joint inflammation. Concentrations of α-MSH were greater in synovial fluid than in plasma in a substantial proportion of patients, suggesting local production of the peptide; this is the first indication that the anticytokine molecule α-MSH is produced within a site of inflammation. Further, it appears that local production of α-MSH is induced particularly in those arthritic joints that have more intense inflammatory reactions. This finding, combined with previous evidence of the marked anti-inflammatory activity of α-MSH, suggests that the peptide acts locally to modulate proinflammatory influences in rheumatic diseases.

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We studied circulating immune complexes (IC) in the serum and cerebrospinal fluid (CSF) of patients with clinically defined multiple sclerosis (MS), in order to establish a correlation with the clinical course of the disease and to investigate the molecular composition of the IC isolated from patients in active phase of the disease. Serum IC levels were found to be significantly increased in patients from the progressive and active relapsing-remittent subgroups with both the CIC-conglutinin and C1q-binding methods. High levels of IC in CSF were detected only in the subgroup consisting of the relapsing-remittent patients in disease exacerbation when IC were determined by the C1q-binding test. No significant increase in serum or in CSF were found using the mRF-I test. The preliminary results of a qualitative investigation on serum IC in MS indicated that they are heterogeneous in nature, their size is mainly of the intermediate type, and they contain IgG, IgM, complement components and beta 2-microglobulins, the latter presenting an observation both new and interesting for studies on serum IC in MS patients.

SUMMARY Clinical and laboratory findings of two patients affected by solitary myeloma, IgG3 lambda type, with peripheral neuropathy are reported. In both cases the same IgG isoelectrofocusing pattern was found in cerebrospinal fluid and serum samples. Data are consistent with damage of the blood-brain barrier.Peripheral neuropathy is a well-known complication of myelomaI-9 and other paraproteinaemias, such as Waldenstrom macroglobulinaemia,'°-12 benign gammopathies'3-" and cryoglobulinaemia, 16- Case 2 A 60-year-old man was admitted after a 14 months history of numbness in the feet followed by increasing difficulty in walking. Bilateral foot drop and wasting of distal muscles of the lower limbs were present. Deep reflexes were absent; vibration and position sense were impaired. Electromyographic findings confirmed peripheral nerve involvement. Serum IEP revealed a monoclonal IgG. Immunoglobulin levels were normal (IgA 2*26 g/l; IgG 12-5 gil; IgM 1.58 g/l). Cryoglobulins and Bence-Jones protein were absent. Total CSF protein (1.9 g/l), and albumin (0-9 gil) were increased; IgG index (0-49) was normal. No intrathecal synthesis of IgG was detected. IEP revealed a monoclonal IgG. Radiological examination showed an osteolyticosteosclerotic lesion of the 9th thoracic vertebra, suggestive of plasmocytoma. Bone marrow examination was normal. Biopsy and histological examination of the vertebral lesion led to the diagnosis of lymphoma with plasma cell differentiation; immunohistological stains showed IgG lambda light chains to be present within the tumour cells. In spite of local radiotherapy (total dose 4200 rads) followed by chemotherapy (melphalan and prednisone), his neurological condition detriorated: and 26 months after the onset, severe wasting, predominantly affecting the distal muscles was present.

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