Effects of topical ropivacaine on eicosanoids and neurotransmitters in the rectum of patients with distal ulcerative colitis.

BACKGROUND: Topical administration of lidocaine has been suggested to have beneficial clinical effects in patients with active ulcerative colitis, but the mechanism of action, if any, remains obscure. As local anaesthetics may exert anti-inflammatory actions through their inhibition of nervous reflexes, we have studied the local effects of a single rectal dose of ropivacaine gel on rectal concentrations of eicosanoids and neurotransmittors in patients with relapsing ulcerative colitis. METHODS: In a randomized, double-blind, placebo-controlled study, concentrations of leukotriene B4, thromboxane B2 and prostaglandin E2 in rectal dialysates and concentrations of substance P, neurokinin A, somatostatin, vasoactive intestinal polypeptide and calcitonin gene-related peptide in rectal biopsies from 19 patients with active, distally located, ulcerative colitis were measured before and after rectal administration of a 200-mg dose of ropivacaine- or placebo-gel by use of radioimmunoassays. For comparison with normal conditions, concentrations of neuropeptides were measured in another 19 patients with relapsing ulcerative colitis and 14 controls with non-inflamed colon. RESULTS: No significant changes in concentrations of eicosanoids or neuropeptides were observed after ropivacaine or placebo administration. Baseline concentrations of all neuropeptides, except somatostatin, were significantly lower in active ulcerative colitis than in controls with non-inflamed colon. CONCLUSIONS: These findings reveal no evidence of anti-inflammatory actions by ropivacaine in active ulcerative colitis and thus provide no rationale for topical treatment with local anaesthetics.

Aspects of skeletal development in fragile X syndrome fetuses.

The purpose of the present investigation was to describe the skeletal development in prenatal fragile X syndrome. We studied fetuses (4 males, 2 females), with gestational ages (GA) 12-14 weeks, from 5 unrelated, different, known carrier mothers. Because of trauma to the fetus during abortion, different parts of the 6 fetuses were available for investigation. The vertebral column and the facial skeleton of all the fetuses were examined, the feet and hands of 5 fetuses, and the cranial base of 3 fetuses. The tissue remnants were examined radiographically and histochemically, and the results compared with previously published normal findings. Radiographic findings included normal ossification sequence, except for 1 fetus where there was an abnormal sequence in the first finger; normal morphology of ossification centres; and nasal bones were absent in the 5 fetuses and present in 1 (14 weeks of gestation). The histological study suggests presence of an acid mucopolysaccharide malfunction in the supporting tissue, because the normal cartilage resorption and orthochromatic cartilage reactions do not appear during the initial enchondral ossification. In addition, the apoptosis of ectodermally derived cells (notochord and palatal epithelial layers) appears delayed or abnormal. The sella turcica was malformed in the 2 fetuses investigated for sella turcica morphology.

A new craniofacial disorder involving hypertelorism and malformations of external nose, palate and pituitary gland.

The aim of the present study was to describe and pathologically evaluate an apparently unreported craniofacial malformation, based on comparison of the cranial midsagittal components with similar components under normal developmental conditions. A severely malformed fetus with a gestational age of about 17 weeks underwent whole body and special craniofacial radiography. Following autopsy dissection, the midsagittal segment of the cranial base, including the eyes, was radiographed in different projections. Midsagittal tissue blocks were serially sectioned for microscopy. Routine stains and immunohistochemical stains were applied. The face was characterized by hypertelorism, absence of external nose but with open shell-like cavities medio-cranially to the eyes, and by a palate fused in the midline and with extensive bony ridges laterally. There was absence of normal nasal cavities, presence of nasal septum and vomer, normal eyes, and nasal ducts covered with nasal mucosa ending blindly in the cartilage. No olfactory bulbs were found. The palatal ridges consisted of bony tissue. The pituitary gland was severely malformed and consisted solely of adenopituitary gland tissue, located in its full extent in the pharyngeal mucosa. There was no sella turcica. From a pathogenetic point of view, it is suggested that the neural crest cells in the frontonasal region of the crest were reduced in amount or late in migration to the midfacial region compared to the neural crest cells to the maxillary region. Therefore, we believe that the malformations observed in the nasal placodes and in the pituitary placode, combined with abnormal migration or abnormal timing of neural crest cells during the craniofacial development, are important factors behind this disorder.