[A case of probable catastrophic antiphospholipid syndrome with multi-organ failure presenting as a transient increase of antiphospholipid antibody levels].

A 44-year-old woman was admitted to our hospital with shock, massive pneumonia and respiratory failure, liver and renal dysfunction, and cerebral infarction. Based on these symptoms, we suspected the presence of disseminated intravascular coagulation and multiple organ dysfunctions due to massive pneumonia or catastrophic antiphospholipid syndrome (CAPS). Therefore, the patient was placed on a respirator and was administered ciprofloxacin, doripenem hydrate, thrombomodulin, antithrombin III, and methylprednisolone pulse therapy. Because the patient's antiphospholipid antibody titer was low on the day of admission (day 1), we did not include CAPS in the differential diagnosis and discontinued prednisolone treatment on day 6. However, the anticardiolipin immunoglobulin M antibody titer was found to be elevated on day 7; in addition, a transient increase in the anticardiolipin anti-ß2 glycoprotein antibody titer was noted on re-examination. Moreover, on day 8, the thrombopenia and alveolar hemorrhage suddenly exacerbated. We finally diagnosed the patient with CAPS, and therefore resumed methylprednisolone therapy. Subsequently, the inflammation, respiratory failure, and thrombopenia rapidly improved, and the patient was extubated on day 12.

Cilostazol combined with aspirin prevents early neurological deterioration in patients with acute ischemic stroke: a pilot study.

Recent randomized trials have shown that cilostazol is superior to aspirin for secondary stroke prevention. We hypothesized that combining cilostazol with aspirin is more effective than aspirin alone in patients with acute ischemic stroke. This randomized study compared the effects of oral aspirin alone to aspirin plus cilostazol in patients with non-cardioembolic ischemic stroke within 48 h of stroke onset. NIH Stroke Scale (NIHSS) and modified Rankin Scale (mRS) scores were checked before and after 14 days and 6 months of drug administration. The primary and secondary endpoints were neurological deterioration or stroke recurrence (NIHSS score ≥ 1) within 14 days and 6 months, respectively. For statistical analysis, on-treatment analysis was conducted. Seventy-six patients were enrolled in the study. The primary endpoint was significantly higher in the aspirin group than in the aspirin plus cilostazol group (28% vs. 6%, relative risk (RR): 0.21, 95% confidence intervals (CI): 0.05-0.87, p=0.013). Among the patients who did not reach these endpoints, the mean improvement in the NIHSS score at day 14 tended to be better (-1.8 ± 1.2 vs. -1.2 ± 1.0, p=0.078) and the frequency of the favorable functional status of mRS 0-1 at month 6 was significantly higher (RR: 1.48, 95% CI: 1.07-2.06, p=0.0048) in the aspirin plus cilostazol group than in the aspirin group. Patients treated with aspirin plus cilostazol during the acute phase of stroke had less neurological deterioration and more favorable functional status than those treated with aspirin alone.

Behçet's disease initially presenting with meningitis and sudden hearing loss.

We report a patient with neuro Behçet's disease (BD) initially presenting with meningitis and severe hearing loss. A 51-year-old man with no noteworthy past history was hospitalized for evaluation of non-pulsating headache and high fever. Lumbar puncture on admission only showed slight pleocytosis (6 /microL, monomorphonuclear cells predominantly) but no evidence of meningitis. However, after admission, he continued to have a fever of over 38 degrees, and he developed painful oral aphthous ulcer and pseudofolliculitis on the upper limbs and trunk. Prior to admission he had often experienced oral ulceration and had bought commercially available mouthwash for prophylaxis. Subsequently, genital ulceration appeared. A small ulcer was observed at the blood collection site, leading to the diagnosis of BD. On the seventh hospital day, the patient developed sudden hearing loss, which was diagnosed as severe sensorineural hearing loss. Lumbar puncture was performed again. Cerebrospinal fluid (CSF) analysis showed mild pleocytosis (60 /microL, predominantly monomorphonuclear cells), with high CSF IL-6 levels. Neither edematous change nor atrophy of the brainstem was noted and there were no other abnormal findings on the brain MRI/MRA. Auditory brainstem response was normal, suggesting that the patient had developed hearing loss due to peripheral neuropathy. We speculate that the hearing loss was likely due to vasculitis associated with BD. This case is considered to be a rare case of Behçet's disease caused by severe hearing loss and meningitis.