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Biomedical subjects

A M Berg

Publications and source records attributed to A M Berg.

12 recordsLinked to original sources

Relapsing polychondritis and aseptic meningitis.

Aseptic meningitis is a rare complication of relapsing polychondritis. We describe a 60-year-old man who developed a prolonged episode of aseptic meningitis for which no cause could be determined and, that resolved spontaneously. He then developed classic relapsing polychondritis 14 months later. He subsequently had another episode of prolonged meningitis complicated by hydrocephalus. No infectious cause for the meningitis could be determined after extensive investigation including meningeal biopsy. The patient responded to corticosteroids and antituberculous therapy.

Biopsy

Localized amyloidosis of the larynx: evidence for light chain composition.

We report the biochemical characterization of amyloid fibrils from a patient with localized amyloidosis of the epiglottis and larynx. Biopsy specimens showed amorphous material consistent with amyloid deposits with a plasmacytic infiltrate. Both plasma cells and amyloid deposits stained positively by immunohistochemistry for kappa light chains. Amyloid fibrils were isolated. The major constituent resolved as a 13 kd band was sequenced and found to be consistent with a kappa 1 light chain. A tryptic digest was carried out and 3 tryptic peptides were sequenced defining the first 45 residues of the protein and residues 110 through 119. Four amino acid substitutions were found, 3 of which have not been described previously. This study defines the immunoglobulin origin of amyloid deposits in localized amyloidosis. The benign nature of localized amyloidosis suggests that a localized clone of plasma cells producing an amyloidogenic light chain may represent the pathogenetic mechanism of this disease, which appears to be a form of plasma cell dyscrasia.

Amino Acid Sequence

Established fibromyalgia syndrome and parvovirus B19 infection.

OBJECTIVE: To determine the seroprevalence of prior and persistent parvovirus B19 (B19) infection in a group of patients with fibromyalgia (FS) compared with controls. METHODS: Fifteen female patients with FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and eleven patients with FS who did not recall any such illness (-VP) were selected from a referral practice. We excluded patients with FS who described a history of trauma prior to the onset of FS symptoms. Twenty-six female medical workers served as controls. Serum IgM and IgG anti-B19 antibodies were measured by ELISA: Polymerase chain reaction (PCR) products from serum were analyzed by dot blot hybridization for B19 DNA. Fisher's 2-tailed exact test was used to compare the proportion of positive serologies in each group. RESULTS: No patient or control had positive IgM levels. For all patients with FS, the prevalence of prior B19 infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00) and that of the general population. No significant difference was found in the prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11, p = 0.25). None of the patients or controls showed evidence for persistent B19 viremia, as determined by PCR analysis. CONCLUSION: Our data do not suggest that B19 plays a pathogenic role in this population of patients with FS. Testing for IgM against B19 within 2-3 months of symptom onset may prove more helpful in further defining the role of B19 in FS.

Adult

Gamma-aminobutyric acid concentration in lumbar cerebrospinal fluid from patients with febrile convulsions and controls.

The cerebrospinal fluid (CSF) concentration of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) was analysed in 41 children with febrile convulsions (FC), 41 febrile controls of similar age (control group 1), and 59 controls, who had no fever and/or were outside the age range for FC (control group 2). A significant correlation between CSF-GABA and age was demonstrated for controls (1 + 2) (r = 0.63, p less than 0.00001), as well as for patients with FC (r = 0.42, p = 0.003). Patients with FC did not differ significantly from control group 1 in respect to CSF-GABA. Duration of FC was related to both CSF-GABA and age (GABA: r = -0.29, p less than 0.05; age: r = -0.32, p less than 0.05). For 56 controls (1 + 2) greater than 1 year of age, a significant negative correlation between CFC-GABA and body temperature was found (r = -0.34, p = 0.01). The low CSF-GABA in the FC-labile age group, the negative correlation of CSF-GABA to body temperature, and the negative correlation of the duration of FC to both CSF-GABA and age, all indicate that GABA could be of importance in the pathophysiology of FC.

Adolescent