The stiff-person syndrome. Case report.

The stiff-person syndrome is a rare and disabling disorder, characterized by muscle rigidity with superimposed painful spasms involving axial and limb musculature. The clinical symptoms are continuous contraction of agonist and antagonist muscles caused by involuntary motor-unit firing at rest and the spasms that are precipitated by tactile stimuli, passive strach, volitional movement of affected or unaffected muscles, startling noises and emotional stimuli. Both the rigidity and the spasms are relieved by sleep, general anaesthesia, myoneural blockade and peripheral nerve blockade. The cause of the stiff-person syndrome is unknown but an autoimmune pathogenesis is suspected because 1) the presence in the cerebrospinal fluid (CSF) of antibodies against glutamic acid decarboxylase (GAD), the rate-limiting enzyme for the synthesis of the inhibitory neurotrasmitter gamma-aminobutyric acid (GABA), 2) the association of the disease with other autoimmune disorders, 3) the presence of various autoantibodies and 4) a strong immunogenetic association. The stiff-person syndrome is clinically elusive but potentially treatable and should be considered in patients with unexplained stiffness and spasms. Drugs that enhance GABA neurotransmission, such as diazepam, vigabatrin and baclofen, provide modest relief of clinical symptoms. Immunomodulatory agents such as steroids, plasmapheresis and intravenous immunoglobulin, seem to offer substantial improvement.

Cefodizime once daily in the treatment of lower respiratory tract infections.

Cefodizime (CAS 69739-16-8, HR 221) is a new third-generation cephalosporin with pharmacokinetic properties that make it suitable for once-daily administration in the treatment of lower respiratory tract infections (LRTI). Ninety-nine adult hospitalized patients (66 males, 33 females, median age 57.5 years) received a once-daily injection of 2 g cefodizime for LRTI. Median treatment duration was 8 days. Forty-two patients received cefodizime intravenously and 57 intramuscularly. Indications for treatment were as follows; primary lobar pneumonia (n = 36), bronchopneumonia (n = 14), secondary pneumonia (n = 3), aspiration pneumonia (n = 5), acute exacerbation of chronic bronchitis (n = 21), and of bronchiectasis (n = 9) and acute purulent bronchitis (n = 11). General condition was good in 29 patients and poor in 58; 12 patients were critically ill. The following pathogens were isolated at baseline (source: bronchial secretions, sputum or blood): S. pneumoniae (n = 47), Haemophilus spp. (n = 17), M. catarrhalis (n = 6), Streptococcus spp. (n = 9), Staphylococcus spp. (n = 5), Klebsiella spp. (n = 4), Pseudomonas spp. (n = 1), A. calcoaceticus (n = 1) and anaerobic organisms (n = 7). Fifty-nine patients were evaluable for bacteriological response and 82 for clinical response. Bacteriological outcome was satisfactory in 29/30 patients having LRTI with parenchymal involvement (97%) and in 29/29 patients without parenchymal involvement (100%). Clinical cure was achieved in 41/43 evaluable patients with parenchymal involvement (95%) and in 37/39 patients without parenchymal involvement (95%) in the per-protocol analysis and in 54/58 patients (93%) and 37/41 patients (93%), respectively, in the clinical intention-to-treat analysis. Three of the patients with an unsatisfactory clinical response died of infection during the study. Cefodizime was well tolerated. Adverse reactions--all of mild intensity--were tachycardia, lumbalgia and dizziness, each occurring in one patient. Cefodizime 2 g once daily either i.m. or i.v. was effective in the treatment of lower respiratory tract infections in hospitalized patients.

Human immunodeficiency virus infection search for musculoskeletal manifestations and mimicking of rheumatologic disorders.

This study involved 50 human immunodeficiency virus (HIV)-positive patients in various stages of the disease to identify signs and symptoms suggestive of rheumatologic disorders and to determine how frequently such findings mimic rheumatologic pictures. Control subjects were 25 ambulatory HIV-negative patients with similar risk factors, mostly drug abuse. Although arthralgias and myalgias were reported in both groups, arthritis was only detected in the HIV-positive group. Twenty-four HIV cases presented two or more signs or symptoms suggestive of rheumatic disorders versus only six non-HIV cases (p < 0.04). Some features were suggestive of systemic lupus erythematosus, vasculitis-panarteritis nodosa, Sjögren's syndrome, Behcet's syndrome and rheumatoid arthritis, although no patients met criteria for these diseases. Reiter's syndrome was diagnosed in two (4%) HIV-positive patients. On correlating CD4 lymphocyte levels and rheumatic symptomatology, the more severely immunocompromised cases were found to present musculoskeletal manifestations with greater frequency. Potential HIV infection should be considered in differential diagnosis of questionable cases of rheumatic disease to avoid both misdiagnosis and the institution of therapies liable to worsen the immunodeficiency syndrome.