Central nervous system involvement in the eosinophilia-myalgia syndrome.

A patient with eosinophilia-myalgia syndrome developed progressive central nervosa system involvement that did not improve despite discontinuation of L-tryptophan therapy. Neurologic impairment was manifested initially by spastic monoparesis, which was improved by treatment with methyl-prednisolone and hydroxyurea. Recurrence of weakness was accompanied by gait ataxia, dysphagia, and complaints of a gradual decline in memory and concentration. Neuropsychological testing identified a broad pattern of cognitive deficits suggestive of a subcortical dementia, and magnetic resonance imaging demonstrated multiple high-signal lesions in the white matter. Cognitive deficits appear to be underrecognized in patients with the eosinophilia-myalgia syndrome. The response of our patient's initial symptoms to corticosteroid therapy suggests a possible role for autoimmune mechanisms in the pathogenesis of central nervous system involvement in the eosinophilia-myalgia syndrome. Neuropsychological evaluation should be performed in patients with cognitive complaints to delineate the full spectrum of central nervous system impairment associated with the eosinophilia-myalgia syndrome.     

Intestinal absorption of the octapeptide SMS 201-995 visualized by fluorescence derivatization

The absorption of an intact oligopeptide was investigated in rat and dog small intestine using the metabolically stable somatostatin analogue SMS 201-995. The synthetic octapeptide was coupled to 4-nitrobenzo-2-oxa-1,3-diazol to have a fluorescent label for the direct visualization. The 4-nitrobenzo-2-oxa-1,3-diazol-labeled peptide was active in displacing the corresponding hormone 125I-Tyr3-SMS 201-995 (Sandostatin; Sandoz Pharmaceuticals, Basel, Switzerland) from its high-affinity binding site in rat cortex membranes with an IC50 = 4.6 x 10(-10) mol/L. The release of growth hormone from cultured anterior pituitary cells was inhibited by the fluorescent somatostatin analogue with the same potency as by somatostatin 14 (IC50 = 6 x 10(-10) mol/L). Incubation with mucosal scrapings followed by high-performance thin-layer chromatography analysis showed that the peptide was stable against proteolysis. 4-Nitrobenzo-2-oxa-1,3-diazol SMS 201-995 was well absorbed from enterocytes of rat small intestine. The absorption was highest into jejunal cells and it could be inhibited by an excess of unlabeled peptide. A significantly lower absorption was detected in crypts compared with villus tips. No fluorescence could be seen in intestinal mucin and goblet cells. After oral administration, the 4-nitrobenzo-2-oxa-1,3-diazol-labeled peptide rapidly appeared in the blood of rats and dogs, reaching a bioavailability of 4.3% and maintaining pharmacological activity. This suggests that enterocytes are able to absorb intact oligopeptides being stabilized against proteolytic degradation through a transcellular mechanism.     

Expression of Schwann cell and peripheral T-cell activation epitopes in hereditary motor and sensory neuropathy

To evaluate possible immune-mediated mechanisms in hereditary motor and sensory neuropathy (HMSN-I, Charcot-Marie-Tooth syndrome), we examined class II major histocompatibility complex antigen expression (MHC-II, HLA-DR) in Schwann cells and peripheral lymphocyte T-cell (Ta1, CD26) activation in five unrelated adults with HMSN-I. Evidence of increased activation expression was found in both compartments but the pattern did not suggest a general state of hyperimmunity or appear related to clinical characteristics of HMSN. Significantly increased CD26+ T-cell activation and greater than normal fluctuation of values occurred intermittently in sequential tests of eight HMSN patients and at single time points in 24 others. The combined data, consistent with repeated stimulations of an immune reaction under normal feedback control, suggest that HMSN-I expresses some characteristics also found in autoimmune polyneuropathies.     

国产檀香中α-反式香柠烯醇化学结构研究

从国产檀香木Santalum ablum L.分得一个新倍半萜醇,根据光谱(IR,MS,¹H-¹H COSY,¹³C-¹H COSY和¹H-¹H NOESY)解析,确定了它的化学结构和相对立体化学为9(10)-顺,α-反式香柠烯醇[9(10)Z,α-trans-bergamotenol](Ia)。     

Comorbidity of hospital-treated psychiatric and physical disorders with special reference to schizophrenia: a 28 year follow-up of the 1966 Northern Finland general population birth cohort

We studied the comorbidity of psychiatric and physical disorders in a sample (n = 11017) from the unselected, general population, Northern Finland 1966 Birth Cohort. During the period 1982–1994, hospital-treated psychiatric patients were more likely than people without psychiatric diagnoses to have been treated for physical disease in hospital wards, 298 out of 387 (77.0%) vs 6687 out of 10 630 (62.9%) (OR = 2.0, 95% CI = 1.6−2.5). Injuries, poisonings and indefinite symptoms were a more common reason for hospital treatment in people with schizophrenia or other psychiatric disorder as compared with people without a psychiatric disorder. Men with psychiatric disorder had more than a 50-fold risk for poisoning by psychotropic drugs (OR = 52.6, 95% CI = 27.7−99.8), women with psychiatric disorder a 20-fold risk (OR = 19.0, 95% CI = 9.5–38.1) and schizophrenics more than a 30-fold risk (OR = 37.5, 95% CI = 19.1–73.8). Men with psychiatric disorders were more commonly hospitalised for a variety of gastrointestinal disorders and circulatory diseases (OR = 2.3, 95% CI = 1.2–4.4), as compared with men with no psychiatric disorder. Respiratory diseases (OR = 2.2, 95% CI = 1.2–4.2), vertebral column disorders (OR = 4.2, 95% CI = 1.8–9.9), gynaecological disorders (OR = 2.1, 95% CI = 1.2–3.6) and induced abortions (OR = 1.8, 95% CI = 1.2–2.7) were more prevalent in women with psychiatric disorder than in other women. Epilepsy was strongly associated with schizophrenia (OR = 11.1, 95% CI = 4.0–31.6). Nervous and sensory organ diseases in general (OR = 2.5, 95% CI = 1.1–5.8) and inflammatory diseases of the bowel (OR = 12.8, 95% CI = 3.8–42.7) were also overrepresented in schizophrenia when compared with people without a psychiatric disorder. Our results indicate that physicians must be alert for psychiatric disorder, and mental health professionals must be aware of the considerable physical morbidity in their patients.     

Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria

Over a 10-year period, we followed up 60 patients (35 men and 25 women) with chronic inflammatory demyelinating polyradiculoneuropathy. Diagnosis was based on previously outlined criteria. Patients were treated in a uniform manner and the overwhelming majority, 56 (94.9%) of 59 treated patients, initially responded to immunosuppressive therapy. The time for initial improvement was 1.9 +/- 3.6 months while the time to reach a clinical plateau was 6.6 +/- 5.4 months. The course was monophasic in 32 patients (53.3%) and relapsing in 28 (46.6%). Despite the initial responsiveness, only 24 (40%) of 60 patients are in partial or complete remission, receiving no medication. Two patients died. We were unable to identify specific clinical or laboratory features at the time of diagnosis that predicted outcome. Our data analysis, along with previous reports, suggests that chronic inflammatory demyelinating polyradiculoneuropathy may be more heterogeneous than previously emphasized. In this light, we have proposed diagnostic criteria that allow for the heterogeneity but at the same time provide for a more consistent approach to better establish the natural history of this condition.