[A case of transverse myelitis caused by primary antiphospholipid antibody syndrome].

A 14-year-old man was admitted with sudden onset of paralysis in his lower extremities paralysis and of sensory loss below Th10 level. On admission, linear high intensity signals was seen in the spinal cord from Th 8 to Th 12 level on thoracic MRI T2 weighted image. Laboratory data on admission indicated existence of lupus anticoagrant in the patient's serum. Systemic lupus erythematodes was negative in his past history. The diagnosis of transverse myelitis caused by primary antiphospholipid syndrome was made accordingly. Plasmapheresis was performed to remove the lupus anticoagrant. After plasma pheresis coagulopathy was normalized with disappearance of the lupus anticoagrant. The lesion of the spinal cord is too extensive to be caused by single obstruction of any one blood vessel branch of the spinal cord. The transverse myelitis may be aggravated by the direct invasion of the lupus anticoagrant into nervous tissue from the vasculature whose blood brain barrier had been compromised by intravascular coagulation of this substance.

Study of the pharmacokinetics of cefpirome sulphate in the elderly.

OBJECTIVE: To determine the appropriate method of administration of the cephem antibiotic cefpirome sulphate in elderly patients. METHOD: We studied cefpirome's pharmacokinetics in patients with urinary tract infections. Patients received cefpirome sulphate 0.5 g by intravenous drip infusion over 30 mins. RESULTS: Patients with a creatinine clearance rate (Ccr) of 80 ml/min had an AUC of 96.7 microg.h/ml and a T1/2 of 2.36 h, whereas those with Ccr of 40-80 ml/min had an AUC of 172.0 microg.h/ml and a T1/2 of 3.45 h and those with Ccr of < 40 ml/min had an AUC of 152 microg.h/ ml and a T1/2 of 4.86 h. CONCLUSION: These results indicate that decreased kidney function can cause increases in the AUC and T1/2 of cefpirome. Thus in elderly patients and perhaps also in other patients with decreased kidney function, cefpirome should be administered at an initial dose of 0.5 g.

Cerebellar ataxia and polyneuropathy in a patient with IgM M-protein specific to the Gal(beta 1-3)GalNAc epitope.

A 79-year-old man with sensory dominant polyneuropathy, cerebellar ataxia, and palatal myoclonus had serum IgM M-protein that specifically bound to GM1, GD1b, and asialo-GM1. IgM with the same specificity was detected in his cerebrospinal fluid. Results of immunohistochemical studies showed specific binding of this monoclonal IgM to the cerebellar granular layer, dentate nucleus, inferior olive, and gray matter of the cerebrum and spinal cord. Monoclonal antibody GGR12, monospecific to GD1b, had an immunostaining distribution similar to that of the patient's IgM M-protein. The binding of M-protein may be associated with the development of cerebellar ataxia and palatal myoclonus in this patient.