Diffuse alveolar haemorrage as initial presentation of systemic lupus erythematosus: a case report.

Diffuse alveolar haemorrhage (DAH) is a rare life-threatening complication of systemic lupus erythematosus (SLE), associated with high mortality rates. It usually occurs in patients with an established diagnosis of SLE. It has been reported as the initial presentation of SLE in 11-20% of cases. It occurs most frequently in females. We describe the case of a child, aged 14 years, with fever, asthenia, haemoptysis, dyspnea, anaemia, increased inflammatory markers, positivity to ANA, nDNA, direct Coombs tests, anticardiolipin antibodies and complement factors consumption. Computed tomography (CTscan) of the chest showed bilateral pulmonary alveolar infiltrates. He also developed renal involvement with nephritis later in the course of the disease. He was started on the treatment approved by the Euro Lupus Protocol for critical patients. After starting Mycophenolate Mofetil the clinical and radiological features were improved as was the survival outcome.

Effect of muscimol on ethanol-induced central nervous system depression.

In male Sprague-Dawley rats acute ethanol (1.0 and 2.0 g/kg) produced impairment of motor coordination and induced hypnosis (4.0 g/kg). Muscimol (1.25 mg/kg, IP) prior to ethanol administration enhanced motor impairment as measured by the aerial righting reflex. The rate of ethanol disappearance from the blood was unaltered by muscimol. Functional tolerance to the effect of ethanol on sleep time was produced by a 24 hr ethanol inhalation procedure. Animals tested 48 hr after ethanol inhalation exhibited a reduced sleep time from ethanol (4.0 g/kg). Muscimol (1.75 mg/kg) was administered along with ethanol 48 hr following 1 day of ethanol inhalation. Although the animals exhibited tolerance to ethanol-induced hypnosis, they did not manifest tolerance to the effect of muscimol.

An inhalation procedure to produce tolerance to the behavioral effects of ethanol.

In male Sprague-Dawley rats the acute effect of ethanol administration (1.0, 2.0, or 3.0 g/kg, IP) on motor coordination was measured by the aerial righting reflex. Ethanol in doses of 2.0 and 3.0 g/kg produced significant impairment of motor coordination with corresponding elevated blood ethanol levels. The rate of ethanol dissappearance from the blood was 0.32 +/- 0.03 mg/ml/hr. Functional tolerance to the effect of ethanol on motor coordination and hypnosis (sleep time) was produced in rats by a 24 hr period of exposure to ethanol vapor (28 mg/liter of air) in a chamber. Animals tested 48 hr after the ethanol inhalation period showed less motor impairment from acute ethanol (3.0 g/kg, IP) and other animals exhibited a reduced sleep time from ethanol (4.0 g/kg, IP) when they were compared with controls. The rate of ethanol elimination from the blood was unchanged in ethanol vapor treated animals (0.30 +/- 0.01 mg/ml/hr) and air-treated animals (0.33 +/- 0.02 mg/ml/hr).

Acute effects of taurine and a taurine antagonist on ethanol-induced central nervous system depression.

Sprague-Dawley rats received taurine intracerebroventricularly (i.c.v.) 30 min prior to ethanol (4 g/kg, i.p.). The duration of ethanol-induced sleep time was increased with taurine at doses of 7.5, 14.0 and 25.0 mumol/kg. In another experiment, TAG (a taurine antagonist, i.c.v.) was given 5 min prior to taurine (i.c.v.) and ethanol was administered 30 min later. TAG antagonized the effect of taurine to enhance ethanol-induced sleep time. These results suggest an interaction between taurine and the depressant effect of ethanol in the brain.

Sampling of orbital sinus blood closely reflects brain ethanol content in rats.

It was demonstrated that the aerial righting reflex can be used as an index of acute ethanol-induced impairment of motor coordination in rats, and was found to directly correlate with blood ethanol content from the infraorbital plexus. A study of ethanol within the blood and its distribution in brain regions showed that the ethanol content of orbital sinus blood closely reflected that in the cerebral cortex, midbrain, and cerebellum. Ethanol administration by intraperitoneal (IP) injection (2, 3 or 4 g/kg) produced the same distribution as 24 hr ethanol vapor inhalation (28 mg/l). Blood ethanol concentrations were slightly higher than brain ethanol concentrations when measured at 10, 30, and 60 min after IP injection and immediately following ethanol vapor administration. Also, in rats 48 hr following ethanol vapor inhalation when tolerance to ethanol is exhibited, the distribution and concentrations of ethanol in blood and brain from acute ethanol (2 g/kg, IP) were unaltered when compared with controls. These data suggest that ethanol distribution within the brain does not play a role in the phenomenon of tolerance to ethanol.