[Peripheral neuropathy involving cranial nerves in a patient with hepatitis C virus infection and mixed cryoglobulinemia].

A 75-year-old man developed subacute progressive muscle weakness and painful paresthesia of the left upper and right lower limbs. The patient had no history of diabetes mellitus. On physical examination, there was no evidence of icterus or hepatosplenomegaly. Palmar erythema without rash was noted. Neurologic examination revealed muscle atrophy and weakness in the left upper limb and mild muscle weakness in the right proximal lower limb. Dysesthesia, severe hypesthesia, and hypalgesia were found in the left upper limb. The tendon reflexes were decreased in the left upper limb and absent in the lower limbs. The cranial nerves were preserved on the day of admission, followed by the involvement of the right oculomotor nerve. Serological examination revealed a mixed IgG/IgM cryoglobulinemia and hepatitis C virus (HCV) infection with evidence of HCV virus replication by PCR for HCV RNA. The patient was diagnosed as having a mixed cryoglobulinemic neuropathy associated with HCV infection. Interferon-alpha therapy with 3 million units subcutaneously was initiated three times per week; however, there was no clinical improvement, although cryoglobulins became undetectable and the level of serum HCV RNA decreased remarkably. Intravenous immunoglobulin therapy 20 g per day for 5 days was also ineffective. The patient developed right facial nerve palsy, followed by right abducens nerve palsy. Treatment with prednisolone 40 mg per day improved and stabilized neurologic symptoms. Although interferon-alpha is considered to be a promising therapy for neurologic complications of HCV infection with mixed cryoglobulinemia, the optimal treatment remains unestablished.

Peptostreptococcal empyema in akinetic mutism.

Peptostreptococcal empyema occurred in a 54-year-old man who had suffered from diabetes mellitus and had been in akinetic mutism. Ultrasonic tomogram was useful to detect the space of empyema and to identify the decrease in volume of the empyema space with treatment.

Modulation by alpha 2-adrenergic stimulation of IgE-mediated 14C-serotonin release from rat mast cells.

The formaldehyde method was used to examine the effects of clonidine and methoxamine on IgE-mediated 14C-serotonin release from rat mast cells in vitro. Clonidine (10(-11) -10(-8) M) caused dose-related enhancement of the mediator release 7 min after the antigen challenge; yohimbine (10(-6) M) blocked this enhancement by clonidine (10(-6) M), but prazosin (10(-6) M) did not. Methoxamine did not enhance this immunological release reaction at concentrations up to 10(-6) M. PGE1 (2 X 10(-8) -2 X 10(-5) M), isoproterenol (10(-10) -10(-8) M), dopamine (4 X 10(-8) -4 X 10(-8) M) and aminophylline (6 X 10(-6) -6 X 10(-4) M) caused dose-related inhibition of this mediator release 1 min after antigen challenge. Clonidine (10(-13) -10(-12) M), but not methoxamine (10(-8) -10(-6) M), reversed dose-dependently this inhibition of mast cells by PGE1 (2 X 10(-6) M), isoproterenol (10(-8) M), dopamine (4 X 10(-6) M); yohimbine (10(-8) M) antagonized this reversing action of clonidine (10(-12) M), but prazosin (10(-10) M) did not. Neither clonidine (10(-14) -10(-11) M) nor methoxamine (10(-8) -10(-6) M) reversed the inhibitory action of aminophylline (2 X 10(-4) M). These results suggests that clonidine enhances IgE-mediated 14C-serotonin release from rat mast cells and also antagonizes the inhibition of mast cells by PGE1, isoproterenol and dopamine, but not by aminophylline in this immunological reaction through alpha 2-adrenergic receptors, and that the inhibition of adenylate cyclase of mast cells is one of the biochemical actions of alpha 2-adrenergic mechanisms.

Interactions of morphine with PGE1, isoproterenol, dopamine and aminophylline in rat mast cells; their effect on IgE-mediated 14C-serotonin release.

The formaldehyde method was used to examine the interactions of morphine with PGE1, isoproterenol, dopamine and aminophylline in rat mast cells by their effects on IgE-mediated 14C-serotonin release. PGE1 (2 x 10(-8) -2 x 10(-5) M), isoproterenol (10(-10) -10(-8) M), dopamine (4 x 10(-8) -4 x 10(-6) M) and aminophylline (6 x 10(-6) -6 x 10(-4) M) caused dose-related inhibition of the mediator release 1 min after an antigen challenge, and propranolol (10(-7) M) blocked the inhibition by isoproterenol (10(-8) M) but not that by dopamine (4 x 10(-6) M), while haloperidol (4 x 10(-6) M) blocked that by dopamine (4 x 10(-6) M) but not that by isoproterenol (10(-8) M). Morphine (3 x 10(-7) -3 x 10(-5) M) reversed the inhibitory effects of PGE1 (2 x 10(-6) M), isoproterenol (10(-8) M) and dopamine (4 x 10(-6) M) dose-dependently and stereospecifically; naloxone (2 x 10(-4) M) antagonized these reversing actions of morphine (3 x 10(-5) M). Morphine (10(-6) -10(-4) M) did not reverse the inhibitory action of aminophylline (6 x 10(-4) M). These results suggest that the inhibitory responses of mast cells to PGE1, isoproterenol and dopamine but not to aminophylline in immunological mediator release were reversed by morphine through opioid receptors, and that the inhibition of adenylate cyclase in mast cells is one of the biochemical actions of morphine.

IgE-mediated 14C-serotonin release from passively sensitized rat mast cells: comparative kinetic study with formaldehyde and ice-cold methods.

The kinetics of IgE-mediated release of serotonin from passively sensitized rat mast cells in vitro was studied by stopping 14C-serotonin release with the application of formaldehyde fixative or ice-cold mast cell medium (MCM). Antigen dose-release curves of 14C-serotonin and/or histamine were comparable when mediator release was terminated with either formaldehyde at a final concentration of 1% or ice-cold MCM 15 min after antigen challenge. However, the kinetic study of immunological mediator release stopped by formaldehyde showed that the addition of antigen resulted in a progressive increase of released 14C-serotonin for 7 min, the release curve being sigmoidal, whereas the application of ice-cold MCM artificially enhanced 14C-serotonin and histamine release in the first 2 min. The results suggest that stopping IgE-mediated release of 14C-serotonin with formaldehyde is a simple, rapid and accurate method of studying the kinetics of mediator release from mast cells.

IgE-mediated 14C-serotonin release from rat mast cells modulated by morphine and endorphins.

The formaldehyde method was used to examine the interaction of PGE1 with morphine, beta-endorphin and Met-enkephalin on rat mast cells by their effects on IgE-mediated 14C-serotonin release. PGE1 (2x10(-8) -2x10(-5) M) caused a dose-related inhibition of the mediator release 1 min after an antigen challenge, and morphine (3x10(-7) -3x10(-5) M) reversed this PGE1 effect dose-dependently and stereospecifically; naloxone (2x10(-4) M) antagonized this action of morphine. Beta-Endorphin (3x10(-7) -10(-5) M) and Met-enkephalin (3x10(-6) -10(-4) M) mimicked this morphine action dose-dependently and were antagonized by naloxone (2x10(-4) M). These results suggest that morphine and endorphins modulate immunological mediator release from rat mast cells through opioid receptors.