Urticaria and Prodromal Symptoms Including Erythema Marginatum in Danish Patients with Hereditary Angioedema.

Erythema marginatum is a characteristic skin rash seen in patients with hereditary angioedema (HAE); however, it can be confused with urticaria, leading to delay in correct diagnosis. The aim of this study was to clarify how often erythema marginatum is misinterpreted as urticaria, potentially leading physicians to refrain from testing for HAE. Few studies have been published on urticaria and prodromal symptoms in HAE, thus the incidence of these parameters were also investigated. A total of 87 patients affiliated to the national HAE Centre were included. Retrospective and prospective data on skin eruptions and prodromal symptoms were collected. Fifty-six percent of 87 patients had a positive history of erythema marginatum. Half of the patients had experienced erythema marginatum being misinterpreted as urticaria. The most prevalent other prodromal symptoms were other skin symptoms, malaise, psychological changes, fatigue and gastrointestinal symptoms. HAE patients with erythema marginatum have a longer diagnostic delay, presumably caused by misinterpretation of the rash as urticaria.

Effect of l-glutamine on myenteric neuron and of the mucous of the ileum of diabetic rats.

The objective of this work was to investigate the effect of the L-glutamine supplementation to prevent - diabetes induced changes in myenteric neurons and also to verify the effect on the mucosa of the ileum of Wistar rats. The animals were divided in five groups (n = 5): untreated normoglycaemic (UN), normoglycaemic treated with L-glutamine (NG), untreated diabetics (UD), diabetics treated with L-glutamine, starting on the 4th (DG4) or 45th day following diabetes induction (DG45). The amino acid was added to the diet at 1%. The density and size of neurons, the metaphasic index in the crypt, the height of the villus, the depth of the crypt and the number of globet cells were determined. There was no difference in the neuronal density and in the cellular body area of the myosin-stained myenteric neurons of groups DG4 and DG45 when compared to group D. The metaphase index and the number of goblet cells showed no significant differences when all groups were compared (P > 0.05). The villi height of groups DG4 and DG45 were 45.5% (P < 0.05) and 32.4% (P > 0.05) higher than those in group UD, respectively. The analyzed crypts showed similar depth for all studied groups.

Neuroprotection and neurodegeneration in submucosal VIP-IR neurons in the jejunum of ascorbic acid supplemented aging Wistar rats.

The present work studied the effects of ascorbic acid supplementation (1 mg/ml in water daily) on submucosal vasoactive intestinal polypeptide-immunoreactive (VIP-IR) neurons in the jejunum of aging rats. Twenty-five male rats were divided into the following groups: Y90 (young, 90-day-old rats), A345 (aged, 345-day-old rats), A428 (aged, 428-day-old rats), AA345 (ascorbic acid-supplemented rats, 90-345-day old), and AA428 (ascorbic acid-supplemented rats, 90-428-day old). Whole mounts of the submucosal layer were subjected to immunohistochemistry for determination of VIP-IR. Morphometric analyses were carried out in 100 submucosal VIP-IR neuron cell bodies from each group. At 345 days, neurons from supplemented animals were larger than those of non-supplemented animals of the same age. These results indicate that ascorbic acid neutralized free radicals and played a neuroprotective role. At 428 days, no significant differences between cell body areas were seen with or without ascorbic acid supplementation, indicating that, from a certain age onward, the role of ascorbic acid as a VIP-IR antioxidant was reduced. This supposition is supported by the fact that both supplemented and non-supplemented animals had higher blood concentrations of ascorbic acid on Day 428 compared with Day 345. The possible neuroprotective and neurodegenerative effects of ascorbic acid appear to depend on the age of the animals, dose, and its interaction with other antioxidants.

Management of dens invaginatus type III with large periradicular lesion.

AIM: This study describes a clinical case of type III dens invaginatus with an extensive periradicular lesion treated successfully. BACKGROUND: Dens invaginatus is a maldevelopment of the dental germ which occurs as a result of the invagination of the enamel organ. These cases may present difficulties with respect to its diagnosis and treatment because of canal morphology. The success of endodontic therapy requires a knowledge of dental anatomy and its anomalies. CASE REPORT: A 17-year-old female patient is reported presenting right maxillary lateral incisor (tooth no. 7) classified as type III dens invaginatus with necrotic pulp and presence of an extensive radiolucid lesion. Endodontic treatment was recommended for tooth. However, intracanal exudate was present, suggesting a resistant infection. Enucleation of the lesion was performed as a complementary approach. The root canal obturation was carried out by the gutta-percha thermoplastification technique with root canal sealer, followed by restoration of the tooth. Healing of the lesion with hard tissue formation was confirmed at follow-up. CONCLUSION: A combination of endodontic and surgical treatments were fundamental to the maintenance of the tooth. The treatment was considered successful. CLINICAL SIGNIFICANCE: Root canal therapy of dens invaginatus should be based on a thorough clinical and radiographic evaluation. The knowledge of classification and anatomical variations of teeth with dens invaginatus are of great importance for correct treatment.

Myenteric neurons and intestinal mucosa of diabetic rats after ascorbic acid supplementation.

AIM: To investigate the effect of ascorbic acid (AA) dietary supplementation on myenteric neurons and epithelial cell proliferation of the jejunum of adult rats with chronic diabetes mellitus. METHODS: Thirty rats at 90 d of age were divided into three groups: Non-diabetic, diabetic and diabetic treated with AA (DA) (1 g/L). After 120 d of treatment with AA the animals were killed. The myenteric neurons were stained for myosin-V and analyzed quantitatively in an area of 11.2 mm(2)/animal. We further measured the cellular area of 500 neurons per group. We also determined the metaphasic index (MI) of the jejunum mucosa layer of about 2500 cells in the intestinal crypts, as well as the dimensions of 30 villi and 30 crypts/animal. The data area was analyzed using the Olympus BX40 microscope. RESULTS: There was an increase of 14% in the neuronal density (792.6 +/- 46.52 vs 680.6 +/- 30.27) and 4.4% in the cellular area (303.4 +/- 5.19 vs 291.1 +/- 6.0) respectively of the diabetic group treated with AA when compared to control diabetic animals. There were no significant differences in MI parameters, villi height or crypt depths among the groups. CONCLUSION: Supplementation with AA in the diabetic animal promoted moderate neuroprotection. There was no observation of alteration of the cellular proliferation of the jejunum mucosa layer of rats with chronic diabetes mellitus with or without supplementation with AA.

Alterations of the number and the profile of myenteric neurons of Wistar rats promoted by age.

The objective of this study was to analyze the morpho quantitative behaviour of duodenum myenteric neurons of Wistar rats (Rattus norvegicus), aged 21, 60, 90, 210, 345 and 428 days, using wholemount preparations of the muscular tunica obtained by dissecting the intestinal tunica for neuronal revealing, through the Giemsa non-histochemical and Myosin-V immunohistochemical techniques. The neurons were quantified in 80 microscopic fields (14.832 mm(2)) for each animal and neuronal cell body morphometry was carried out on 100 neurons/rat. Duodenal samples were submitted to histological routine processing, stained by hematoxylin-eosin method in order to perform morphometric analysis of the muscular tunica. An increase in the length of the small intestine was observed up to the age of 60 days, which was maintained up to 210 days, with a reduction in this parameter from 345 days. Muscular tunica thickness was maintained independently of the animal age. During the course of the study, there was a reduction in the mean neuron population in both techniques used. However, in all of the ages evaluated, the use of the Myosin-V technique lead to a reduced mean number of neurons compared to the Giemsa method. The cellular profile morphometry revealed, with both techniques, the predominance of smaller neurons in young animals, and bigger neurons in animals from higher age groups. It was concluded that advanced age is a determinant factor in the number reduction of myenteric neurons, with maintenance of the intrinsic intestinal innervation by the remaining neurons and that the use of the Giemsa non-histochemical technique showed itself more adequate to determine the total neuronal population.

Effects of a hypoproteic diet on myosin-V immunostained myenteric neurons and the proximal colon wall of aging rats.

The objective of this work was to analyze the morphoquantitative behavior of neurons of the myenteric plexus, as well as the morphometry of elements of the proximal colon wall of Wistar rats (Rattus norvegicus) fed a normoproteic (22%) and a hypoproteic (8%) diet, and sacrificed at 360 days of age. To perform the neuronal evaluation, we used whole-mount preparations of the proximal colon immunostained with the antibody anti-myosin-V. The neurons were quantified in 80 microscopic fields (16.98 mm(2)/animal). The neuronal cell body morphometry was performed in 100 neurons/animal. Samples of the proximal colon were weighed and measured, and then submitted to routine histological processing. They were later stained using the hematoxylin--eosin method in order to carry out morphometric analysis on the mucosa and external muscular layers. The number of neurons and the neuronal cell body morphometry did not present significant differences between the studied groups. A significant reduction in the weight and length of the proximal colon and in mucosa layer thickness was observed in the animals fed with the hypoproteic diet. We concluded that the neuronal and non-neuronal components of the proximal colon adapted to the imposed nutritional condition, which guaranteed the maintenance of their functions.