Mast cells and T lymphocytes in chronic urticaria

Mast cells are considered to be the primary effector cells in urticaria but it is possible that lymphocytes contribute to the formation of weals by secreting histamine releasing factors. The aim of this study was to examine the population of mast cells and to quantify the T cell subsets and their activation status in delayed pressure urticaria (DPU), chronic idiopathic urticaria and normal controls. Three biopsies were obtained from each of four patients with chronic idiopathic urticaria but not DPU. Three biopsies were taken from each of 13 patients with DPU, from a combination of unchallenged skin and at 0, 2, 6, 24, 48 and 120 h after weighted steel rods (diameter 1.5 cm) had been applied to the thighs. Three biopsies were similarly obtained from each of four normal controls before an identical pressure challenge and at 6, 24 and 48 h afterwards. The chloracetate esterase stain was used to demonstrate mast cells and an alkaline phosphatase anti-alkaline phosphatase immunohistochemical technique to assess the phenotypic and activation characteristics of the T cell infiltrate. The mast cell count did not differ significantly between unchallenged skin from DPU patients and normal controls. Following a pressure challenge to the DPU patients, the number of stainable mast cells decreased significantly to a level comparable with that in spontaneous weals of chronic idiopathic urticaria. Investigation of T cell subsets showed a preponderance of CD4+ cells over CD8+ cells. There was no evidence of T cell activation in chronic idiopathic urticaria or DPU when compared with normal controls. These data support the view that mast cell degranulation occurs in chronic idiopathic urticaria and suggest that it may also play a role in the pathogenesis of DPU. There was no evidence that lymphocyte activation occurs in either condition.     

Atypical Nekam's disease—keratosis lichenoides chronica associated with porokeratotic histology and amyloidosis

A patient with atypical Nekam's disease is described. Although the histological appearances were lichenoid, the presence of porokeratosis and amyloid deposition, previously reported in this condition, argue against the view that Nekam's disease is a subset of lichen planus.     

Enumeration of Absolute Numbers of T and B Lymphocytes in Human Blood

A new immunofluorescence test permits the direct enumeration of T and B lymphocytes in unseparated blood. B cells were identified with antiimmunoglobulin sera and T cells by a rabbit anti-human brain serum rendered unreactive with B cells by sequential absorption with erythrocytes, liver, and either chronic lymphocytic leukaemia cells or a cell line, BRI-8, with B-cell surface characteristics. T and B cells were also enumerated with lymphocyte suspension purified by either Ficoll-lsopaque density sedimentation or by a two-step gelatin-polystyrene bead column method. T cells in Ficoll-purified suspension were also enumerated by rosette formation with sheep erythrocytes. Comparison of the T-B proportions evaluated with the different cell preparation showed that the cell separation procedures can give rise to a deviation in the T:B ratio in favour of B cells. The extent of this induced bias related inversely to lymphocyte yield. Staining of whole blood preparations or high-yield purified cells enables absolute numbers of T and B lymphocytes to be calculated. We consider this measurement considerably more informative than relative proportions of T and B cells.     

INHIBITION OF PROSTACYCLIN RELEASE BY ENDOTHELIAL BINDING ANTICARDIOLIPIN ANTIBODIES IN THROMBOSIS-PRONE PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS AND THE ANTIPHOSPHOLIPID SYNDROME

IgG from 18 patients with SLE, eight with the primary antiphospholipidsyndrome and 19 controls was examined for its effect on thrombin-inducedprostacyclin (PGI₂) release from human umbilical vein endothelialcells in relation to both the titre of anticardiolipin (ACA)and antiendothelial activity (AEA) and clinical thrombotic events.Although no significant inhibition of PGI₂ release was foundoverall, examination of subgroups revealed that IgG from patientswith ACA produced significant inhibition of PGI₂ release (meanstimulation index IgGM, 0.74 ± 0.12, P = 0.02) when comparedwith patients without ACA (1.18 ± 0.12). Further analysisrevealed a significant positive correlation between ACA andAEA (r = 0.52, P = 0.006) in the total patient group which wasreflected in significant negative correlations between inhibitionof PGI₂ release and increasing titre of both ACA (r = –0.42,P = 0.032) and AEA (r = –0.57, P = 0.002). However, onlyincreasing titre of AEA showed a significant negative correlationwith inhibition of PGI₂ release when patients with (r = –;0.74,P = 0.0005) and without (r = 0.23, N.S.) thromboses were compared.The titre of ACA failed to show any significant correlationwith inhibition of PGI₂ release in either patients with (r =–0.42, N.S.) or without (r = –0.16, N.S.) thromboses. These findings suggest that previous, sometimes conflicting,reports of an association between inhibition of PGI₂ releaseand ACA may be explained by the co-incidence of AEA with ACA. KEY WORDS: Prostacyclin, Endothelium, Anticardiolipin antibodies, Antiendothelial antibodies     

Children of mothers with mental ilness: attachment, emotional and behavioural problems

This study describes the pattern of emotional and behavioural difficulties of children whose mothers have mental illness, and explores the relationship between children's behavioural and emotional difficulties and maternal perceptions of attachment. Thirteen mothers previously admitted to psychiatric hospital for mental illness completed a measure of their own symptoms (Brief Symptom Inventory), their children's emotional and behavioural problems (Strengths and Difficulties Questionnaire (SDQ)), and attachment security (Parent/Child Reunion Inventory) (n = 21). Mean scores for child SDQ profiles were found to be within the 'normal' range, although (on some indices) mothers reported more 'case' scores for their children, than would be expected from standardized norms. It was found that there were significant positive correlations between 'insecurity' scores and all problem scales of the SDQ. Best predictors from the Parent/Child Reunion Inventory factors for each SDQ scale are reported and discussed.     

Using Intraindividual Variability to Detect Malingering in Cognitive Performance

The utility of measures for detecting malingering was evaluated using a simulation design in which half the participants were encouraged to do their best and half were asked to feign head injury. Particular attention was focused on the utility of repeated assessment (intraindividual variability) in discriminating the groups. Participants were tested on three occasions on measures commonly used to detect malingering including a specific symptom validity test (SVT). The results indicated that multiple measures of malingering obtained in single assessment (occasion one) discriminated the groups effectively. In addition, however, intraindividual variability in performance, particularly of indicators from the SVT, provided unique information beyond level of performance. The results suggest that response inconsistency across testing sessions may be a clinically useful measure for the detection of malingering.     

SERUM MASKS THE INHIBITION OF THROMBIN-INDUCED PROSTACYCLIN RELEASE PRODUCED BY ANTICARDIOLIPIN ANTIBODIES

The effect on thrombin-induced release of prostacyclin fromhuman umbilical vein endothelial cells of preincubation withboth serum and serum derived from platelet-poor plasma (PDS)from patients with systemic lupus erythematosus (SLE), systemicsclerosis, the antiphospholipid syndrome (APS) and normal controlswas examined. Although no significant differences in thrombin-inducedprostacyclin release were found in any of the patient groups,further analysis revealed that PDS from patients with SLE andAPS that contained IgG anticardiolipin antibodies produced significantinhibition of prostacyclin release when compared with controls(P = 0.02). The effect was maximal with samples that containedboth IgG and IgM anticardiolipin antibodies (P<0·01)and which had a significantly higher titre of IgG antibodiesthan samples which contained solely IgG antibodies (P<0·05).The absence of any corresponding inhibition of prostacyclinrelease by serum samples that contained anticardiolipin antibodies,possibly due to the release of masking stimulatory factors byplatelets during coagulation, provides an explanation for theconflicting nature of previous reports. KEY WORDS: Endothelium, Prostacyclin, Anticardiolipin antibodies, Systemic lupus erythematosis, Systemic sclerosis, Antiphospholipid syndrome