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PubMed1991

In vivo antiaggregatory action of platelet-activating factor in beagle dogs: role for prostacyclin.

The effects of platelet-activating factor (PAF) on in vivo platelet aggregation were studied in anaesthetized beagle dogs by using the extracorporeal filter-loop technique. Intraarterial administration of PAF caused an immediate increase in filter pressure, indicating enhanced in vivo platelet aggregation. Intravenous administration of PAF (3-100 ng kg-1) resulted in a transient dose-dependent inhibition of spontaneous platelet aggregation on the filter with concomitant elevation in plasma 6-keto-PGF1 alpha levels. These changes were significantly attenuated by pretreatment of the animals either with BN 52021 (4 mg kg-1), a specific PAF receptor antagonist or with acetylsalicylic acid (25 mg kg-1). Intraarterial infusion of exogenous prostacyclin at concentrations similar to those observed following intravenous PAF administration, resulted in a transient inhibition of the spontaneous platelet aggregation. These data provide evidence for prostacyclin release in response to PAF, and suggest that prostacyclin may mediate the in vivo anti-aggregatory action of PAF in anaesthetized dogs.

6-Ketoprostaglandin F1 alpha↗

PubMed1997

Influence of the alpha-adrenoreceptor naftopidil and doxazosin, on adrenaline-induced serotonin platelets: comparison with the antagonists, collagen and efflux by human effects of nifedipine.

Collagen (5 microg/ml) stimulation of washed platelets increased endogenous serotonin (5-HT) release to the medium from 13.88 1.39 to 188.67 26.37 pmol/108 platelets ( P < 0.001). Adrenaline (16 microM) also increased 5-HT release, from 11.0 1.46 to 110.6 29.9 pmol/108 platelets ( P < 0.02). Naftopidil enhanced collagen-induced 5-HT efflux; significant increases occurred with 2 microM (+71.6%, P < 0.01), 10 microM (+89.1%, P < 0.01) and 40 microM (+69.7%, P < 0.01). With 0.4 muM and 2 microM naftopidil, adrenaline-induced 5-HT release was enhanced, albeit non-significantly, whilst with 10 microM and 40 muM naftopidil release was reduced (40 microM,-58.5%, P < 0.05). Doxazosin increased collagen-induced 5-HT release, significant increases being recorded with 7.5 microM (+81.7%, P < 0.05) and 30 microM (+78.4%, P < 0.05). Adrenaline-induced 5-HT release was also increased by doxazosin, but not significantly. Collagen-stimulated 5-HT release was inhibited by nifedipine (7 microM,-38.8%, P < 0.05; 28 microM, -61.2%, P < 0.001). These data suggest that the-antagonists, naftopidil and doxazosin, and the Ca2+ channel blocker, nifedipine, influence agonist-induced platelet 5-HT release through different mechanisms. Thus naftopidil and doxazosin may possess 5-HT transporter-blocking activity. The observation that naftopidil inhibited, adrenaline-induced 5-HT release may indicate that naftopidil also inhibits adrenaline uptake and exchange with dense granular 5-HT, with consequent inhibition of 5-HT release and platelet aggregation. The data obtained with nifedipine are consistent with 5-HT release being reduced as a result of its inhibitory action on platelet Ca2+ mobilisation.

Journal Article↗

PubMed2006

Professional liability payments in obstetrics and gynecology.

OBJECTIVE: The purpose of this study was to test the hypothesis that the percentage of subspecialists in obstetrics and gynecology who made payments on professional liability claims was less than the percentage of general obstetrician-gynecologists who made payments. METHODS: Professional liability payment data from the Massachusetts Board of Registration in Medicine was used. RESULTS: During the 10 years preceding August 2005, 38.6% of obstetrician-gynecologists and 32.2% of gynecologists made at least 1 professional liability payment. During the same time period, the percentage of subspecialists who made a payment was significantly less than obstetrician-gynecologists: gynecologic oncologists 10.0% (P = .012), maternal-fetal medicine 3.7% (P = .002), and reproductive endocrinologists 11.9% (P = .016). Using aggregate payment data for the period 1994-2003, the average payment per claim for specialists in maternal-fetal medicine ($1,950,000) and gynecologic oncology ($1,014,006) were above the average payment per claim for obstetrician-gynecologists ($447,983) or gynecologists ($400,338). Reproductive endocrinologists had an average payment per claim of $454,047. CONCLUSION: All specialists in the field of obstetrics and gynecology have major professional liability risks. Among subspecialists in obstetrics and gynecology, the favorable trend toward fewer physicians making payments is counterbalanced by greater payments per lost claim. LEVEL OF EVIDENCE: II-2.

Gynecology↗

PubMed1998

Intragenic polymorphisms of the vitamin D receptor gene associated with intervertebral disc degeneration.

STUDY DESIGN: A study in genetic epidemiology of disc degeneration, based on lifetime exposure data, findings on magnetic resonance imaging, and genotyping of intragenic markers. OBJECTIVES: To pursue the potential correlation between common allelic variations in the vitamin D receptor locus and degeneration of the intervertebral disc. SUMMARY OF BACKGROUND DATA: Familial aggregation has been observed in intervertebral disc degeneration, but the relative significance of the genetic component and shared environmental influences is unknown. The identification of relevant candidate genes associated with disc degeneration would specify a genetic component and increase our understanding of the etiopathogenesis of disc degeneration. METHODS: From the population-based Finnish Twin cohort, 85 pairs of male monozygotic twins were selected based on exposure to suspected risk factors for disc degeneration. Interview data were gathered on relevant lifetime exposures, and thoracic and lumbar disc degeneration was determined through quantitative and qualitative assessments of signal intensity on magnetic resonance imaging, and qualitative assessments of disc bulging and disc height narrowing. Possible associations were examined between disc degeneration measures and two polymorphisms of the coding region of the vitamin D receptor locus. RESULTS: Two intragenic polymorphisms of the vitamin D receptor gene revealed an association with disc degeneration. Quantitatively assessed signal intensities of thoracic and lumbar (T6-S1) discs were 12.9% worse in men with the Taql tt genotype and 4.5% worse in men with the Tt genotype, compared with signal intensity in men with the TT genotype (age adjusted P = 0.003). A similar pattern was found between disc signal intensity and Fokl genotypes; men with the ff and Ff genotypes had mean signal intensities that were 9.3% and 4.3% lower, respectively, than those in men with FF genotypes (age-adjusted P = 0.006). The summary scores of qualitatively assessed signal intensity, bulging, and disc height were 4.0% and 6.9% worse in men with Ff and ff genotypes, respectively, when compared with those in men with the FF genotype (age-adjusted P = 0.029). CONCLUSION: Specific vitamin D receptor alleles were associated with intervertebral disc degeneration as measured by T2-weighted signal intensity, demonstrating for the first time, the existence of genetic susceptibility to this progressive, age-related degenerative process.

Adult↗

PubMed1976

The young platelet population in children with cyanotic congenital heart disease.

Some morphological, biochemical and functional parameters of platelet population in children with cyanotic congenital heart disease (CCHD) were studied by making comparisons of the normal platelet population in both CCHD patients and controls. The mean volume of the platelets from cyanotic patients was greater than from normals. The platelet size distribution curves demonstrated a shift towards larger than normal size in the case of CCHD. The mean protein content, as well as the mean PF3 content of platelets was increased in CCHD. Following addition of kaolin, PF3 release was more rapid and of shorter duration with platelets from CCHD patients as compared to normal platelets. They also released more PF3 than did normal platelets. After addition of ADP, collagen, or adrenalin, platelets of CCHD patients were more responsive than similarly treated platelets from normals. Platelets from CCHD showed an increased initial rate of aggregation and greater maximum aggregation. These data suggested that the platelet population of CCHD patients consists of larger, younger and functionally more active platelets than does the platelet population of normals.

Adolescent↗

PubMed1989

Low-density lipoprotein derived from atherosclerotic patients enhances macrophage cholesterol accumulation and in vitro platelet aggregation.

The aims of our study were to assess the differences between plasma lipoproteins separated from five angiographically normal subjects and five patients with proven CHD. The patients with CHD had significantly higher levels of LDL-cholesterol and apo-B, and reduced levels of HDL-cholesterol and apo-Al. The biological characteristics of LDL and HDL from both groups of patients demonstrated that the LDL from the CHD patients enhanced platelet aggregation and increased cholesterol content and cholesterol esterification in MPM compared to the normal patients. HDL had no significant effect on MPM; however, there was an increased platelet aggregation with HDL derived from the CHD patients, while the HDL from the normal group decreased platelet aggregation. The data suggest that lipoproteins isolated from CHD patients are more atherogenic than lipoproteins from normal patients.

Adult↗

PubMed1996

Non-specific pinocytosis by human endothelial cells cultured as multicellular aggregates: uptake of lucifer yellow and horse radish peroxidase.

We have analyzed the pattern of time-dependent and concentration-dependent incorporation of Lucifer Yellow CH (LY) and Horseradish Peroxidase (HRP) by human umbilical vein endothelial cells cultured on a non-adhesive substratum, where they they become organized into stable, multicellular aggregates. The data were compared with those previously obtained from low-density cultures of non-growing endothelial cells adherent to plastic. While the linear trend of the incorporation kinetics is preserved, the rate of uptake with both time and concentrations is highly dependent on the culture conditions, namely typology of cell-cell and cell-substrate interactions. An at least two-fold increase of the rate of uptake was observed with both markers in the aggregated cells. The extracellular concentration of LY required to saturate the binding capacity of the cell surface shifts from approximately 0.25 mg/ml, with the adherent cells, to approximately 0.5 mg/ml in the aggregated cells; the rate of uptake of three different forms of HRP shows, besides a sharp quantitative increase, also qualitative variations, testified by differential changes of their incorporation rates. These results are entirely consistent with the assumption that the association of the endothelial cells into multicellular aggregates increases the rate of pinocytic uptake by modifying the physicochemical properties of the cell surface, thereby increasing its differential affinity for the extracellular markers.

Biological Transport↗

PubMed2003

Colonoscopy: practice variation among 69 hospital-based endoscopists.

BACKGROUND: The medical profession, payers, and patients are interested increasingly in the quality of endoscopic procedures, including colonoscopy. The American Society for Gastrointestinal Endoscopy has recommended "report cards" by which endoscopists may keep track of certain key elements of their practice including indications, findings, duration, technical end points, complications, and patient satisfaction. METHODS: The GI-Trac endoscopy reporting database includes many of the data points recommended by ASGE for report cards. Seven hospital centers in North America have been collecting data prospectively for varying periods since 1994. These data were aggregated and analyzed by individual endoscopist. A total of 69 endoscopists performed 17,868 colonoscopies. RESULTS: Twelve percent of the endoscopists reported that more than 20% of procedures they performed were completely normal. The average time taken by 27% of endoscopists was more than 40 minutes (without trainees involved), and only 55% achieved a cecal intubation rate of over 90%; for 9% the rate was less than 80%. Complication rates were too low for individual comparisons. CONCLUSION: These data provide an idea of colonoscopy performance by individual endoscopists in mainly academic centers. Incorporating all recommended data elements in future reporting databases will contribute to meaningful bench marking and to quality improvement efforts.

Aged↗

PubMedDate not supplied

Local venomotor response to intravenous infusion of substance P and glyceryl trinitrate in systemic sclerosis.

Endothelial injury has been shown in ultrastructural studies in systemic sclerosis (SSc). In the present study, we tested the functional response of the endothelium in the early phase of the disease and at a more advanced stage. Substance P (SP) (25 and 50 ng) and glyceryl trinitrate (GT) (100 and 200 ng) were infused intravenously in 6 control subjects and in 6 female patients affected with early systemic sclerosis (SSc) to verify whether or not a lack of endothelial function could be detected. Venous compliance was assessed with a linear variable differential technique. Endothelial injury was evaluated by the von Willebrand Factor Antigen (vWF:Ag) plasma level and platelet aggregation by the platelet aggregate ratio (PAR). Endothelial-mediated response to SP was deficient in SSc patients in comparison with controls, whereas endothelium independent vasodilation was detected after the infusion of GT both in patients and controls. All vWF:Ag levels were in the normal range while in vivo platelet aggregation was increased as demonstrated by the PAR levels in the SSc subjects. The experiment was repeated in the same patients when the clinical status worsened and the levels of vWF:Ag were noted to rise: the endothelium dependent vasodilatory response to SP was still deficient as before and a decrease in vasodilatory response to GT was noted. vWF:Ag levels were significantly increased and the PAR still demonstrated an increased platelet aggregation. These data clearly indicate that an early functional deficit of the endothelial function is present before the onset of extensive visceral and skin involvement. The mechanism that provokes the impairment of the endothelial function need further investigation.

Female↗

PubMed2001

Production and characterization of saratin, an inhibitor of von Willebrand factor-dependent platelet adhesion to collagen.

Platelets tether to collagen in both a von Willebrand factor (vWF)-dependent and a vWF-independent manner. We have recently characterized a recombinant protein, saratin, isolated from the saliva of the leech Hirudo medicinalis, expressed it in Hansenula polymorpha, and studied its effect on direct and indirect platelet-collagen interactions. Saratin dose dependently inhibited the binding of purified human vWF to human type I and III collagens (IC(50)= 0.23 +/- 0.004 and 0.81 +/- 0.04 microg mL(-1), respectively) and to calf skin collagen (IC(50)= 0.44 +/- 0.008 microg mL(-1)). Furthermore, saratin showed a similar inhibitory potency against the binding of human, rodent, and porcine plasma vWF to these collagens. In a flow chamber under conditions of elevated shear (2700 s(-1)), saratin dose dependently and potently inhibited platelet aggregate formation on a collagen-coated surface (IC(50)= 0.96 +/- 0.25 microg mL(-1)), but at reduced shear (1300 s(-1)) a rightward shift in the dose-response curve was noted (IC(50)= 5.2 +/- 1.4 microg mL(-1)). Surface plasmon resonance analysis revealed both high and low affinity binding sites for saratin on human collagen type III (K(d) 5 x 10(-8) M and 2 x 10(-6) M, respectively). Although low concentrations of saratin, which inhibited platelet adhesion under increased shear (i.e., saturation of high-affinity binding sites), had no effect on vWF-independent collagen-induced platelet aggregation, high concentrations (i.e., saturation of low-affinity binding sites) were found to inhibit platelet aggregation. These data demonstrate that saratin is a potent inhibitor of vWF-dependent platelet adhesion to collagen and hence may have therapeutic potential as an antithrombotic agent.

Animals↗

PubMed1994

Binding and state of aggregation of spin-labeled cecropin AD in phospholipid bilayers: effects of surface charge and fatty acyl chain length.

The binding and state of aggregation of cecropin in large unilamellar vesicles of different surface potential and varying acyl chain length were examined using a Cys-33 spin-labeled derivative of cecropin AD (CAD). Association isotherms of the peptide were measured for vesicles of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) containing 5, 15, and 30 mol % 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylglycerol (POPG). The isotherms display a concentration-dependent positive cooperativity indicating the possible formation of cecropin aggregates in the lipid phase. The critical aqueous concentration for aggregation was dependent on the fraction of POPG, suggesting the involvement of acidic lipids in the formation and stabilization of the putative aggregate. Our data also indicate that cooperativity depends on the state of side-chain ionization of an acidic residue that titrates between pH 7 and 4.4. The binding of spin-labeled Cys-33 CAD was found to be influenced by the acyl chain length of the host lipid. The association isotherm of the peptide for dilaureoyl-sn-glycero-3-phosphatidylcholine vesicles containing 30 mol % dilauroyl-sn-glycero-3-phosphatidylglycerol (DLPG) differed significantly from that in POPC/POPG and could be interpreted in terms of a monomer-monomer partitioning between the aqueous and lipid phases. ESR line-shape analysis was consistent with peptide aggregation in dioleoyl-sn-glycero-3-phosphatidylglycerol vesicles but not in DLPG vesicles.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMedDate not supplied

Predictive value of normal sperm morphology: a structured literature review.

The aim of the study was to conduct a structured review of the literature published on the use of normal sperm morphology, as an indicator of male fertility potential in the in-vitro fertilization (IVF) situation, and to establish the universal predictive value of this semen parameter. Published literature in which normal sperm morphology was used to predict fertilization and pregnancy, during the period 1978-1996, was reviewed. A total of 216 articles were identified by the sourcing methodology, but only 49 provided data that could be tabulated and analysed. Of these, only 18 provided sufficient data for statistical analysis. Fifteen studies used the strict criteria to evaluate sperm morphology, two used World Health Organization (WHO) guidelines and one used both the strict criteria and the WHO guidelines. All the studies (n = 10) using the 5 and 14% normal sperm morphology thresholds (strict criteria) produced positive predictive values for IVF success. In the prediction of pregnancy, 82% (9/11) and 75% (6/8) of the studies produced positive predictive values when using the 5% and 14% thresholds respectively. Aggregating the data produced around the 5% normal sperm morphology threshold (strict criteria), the overall fertilization rates were 59.3% (1979/3337; per oocyte) for the < or = 4% group and 77.6% (10345/13327; per oocyte) for the >4% group, and the overall pregnancy rates were 15.2% (60/395; per cycle) and 26.0% (355/1368; per cycle) respectively. The no-transfer rates across the 5% threshold were 24.0% (86/359; per cycle) in the < or = 4% group compared to 7.4% (80/1088; per cycle) in the >4% group. The inclusion of an accurately evaluated normal sperm morphology count as an integral part of the standard semen analysis makes this analysis still the most cost-effective means of evaluating the male factor.

Confidence Intervals↗

PubMed1997

Stimulation of calcium influx and platelet activation by canatoxin: methoxyverapamil inhibition and downregulation by cGMP.

Canatoxin (CNTX), a toxic protein isolated from seeds of Canavalia ensiformis, induces Ca2+ influx across the platelet plasma membrane, mobilization of arachidonic acid mediated by phospholipase A2, ATP secretion, and platelet aggregation. All these events depend on the presence of extracellular Ca2+ and are blocked by methoxyverapamil, a calcium-channel blocker. CNTX does not activate phospholipase C, and the intracellular calcium mobilization mediated by IP3 does not play a role in platelet activation by this toxin. Preincubation of rabbit platelets with 8-Br-cGMP inhibited the CNTX-evoked calcium influx, arachidonate release, ATP secretion, and cell aggregation. Our data suggest that the calcium influx is a prior step on platelet activation by CNTX, being modulated by cGMP.

Animals↗

PubMed1993

Is there a valid association between skin tags and colonic polyps: insights from a quantitative and methodologic analysis of the literature.

OBJECTIVE: To assess the reported association between skin tags and colonic polyps and to evaluate the methodologic rigor of the studies. DESIGN AND DATA IDENTIFICATION: English-language literature search using MEDLINE, Index Medicus, and bibliographic reviews of texts and all pertinent articles to perform a quantitative and methodologic analysis of all studies from 1983 (the original publication) assessing the association under study. Eligible studies were independently assessed using explicit methodologic guidelines for validity and generalizability of observational research. Two appraisers independently performed tests for heterogeneity and used meta-analytic methods in an attempt to provide summary estimates of the overall strength of association. MEASUREMENTS AND MAIN RESULTS: Significant statistical heterogeneity across studies indicated sharp differences in the direction and magnitude of the odds ratios for the association between skin tags and colonic polyps (chi-square test of homogeneity = 37.42, 9 degrees of freedom; p < 0.005). This marked disparity prevented meaningful pooling of the individual data. The degree of statistical heterogeneity was not significantly reduced after an analysis of specific subgroups of studies. Limitations potentially responsible for the varying outcomes included lack of blinded ascertainment of clinical information, noncomparability of subjects, differing diagnostic evaluations of the colon, and uncontrolled confounding. In addition, all but one study were performed in a tertiary care setting, seriously limiting the results to the "average" subject seen in primary care settings. CONCLUSION: Methodologic limitations and inconsistencies in study outcomes preclude the aggregation of data necessary to compute a valid and meaningful summary estimate of association. Sufficient variability prevents any consensus regarding the association between skin tags and colonic polyps. In addition, the applicability of the results is limited primarily to subjects seen in tertiary care centers, limiting the overall clinical usefulness of skin tags as "biomarkers" of colonic polyps. Recommendations for further research are provided.

Adult↗

PubMed2000

Pharmacological profile of recombinant, human activated protein C (LY203638) in a canine model of coronary artery thrombosis.

The antithrombotic activity of recombinant, human activated protein C (rh-APC, LY203638) was examined in a model of canine coronary artery thrombosis. Three doses of rh-APC (0.5, 1.0, and 2.0 mg/kg/h) were administered intravenously for 2 h. Whole blood clotting times (thrombin time, activated partial thromboplastin time), ex vivo platelet aggregation, and template bleeding times were determined. Activated partial thromboplastin time significantly increased 2- and 3.7-fold during the 2-h infusion of rh-APC (1.0 and 2.0 mg/kg/h, respectively); thrombin time did not change. Intravenous infusions of rh-APC (1.0 and 2.0 mg/kg/h) produced significant prolongations to occlusion, 186 +/- 21 and 190 +/- 22 min, respectively, compared with the vehicle and the 0.5 mg/kg/h group (86 +/- 12 and 93 +/- 17 min, respectively). Vessel patency was better at the end of the experiment in the intermediate- and high-dose groups (3 of 6 and 3 of 5 vessels, 1.0 and 2.0 mg/kg/h, respectively) compared with the vehicle and 0.5 mg/kg/h groups (0/5 and 0/6, respectively). Only the 1.0 mg/kg/h group was found to have significantly elevated template bleeding times, with peak increases seen 60 min into the drug infusion. All groups had returned to baseline values by the end of the study. There was no observed inhibition of platelet aggregation. These data demonstrate that recombinant, human activated protein C is an effective anticoagulant and antithrombotic agent in the dog.

Animals↗

PubMed1989

Triwaglerin: a potent platelet aggregation inducer purified from Trimeresurus wagleri snake venom.

Trimeresurus wagleri venom is the most potent inducer of platelet aggregation among the seven Trimeresurus snake venoms tested. By means of CM-Sephadex C-50 column chromatography, T. wagleri venom was separated into 19 fractions. Fraction XVI possessed the strongest aggregating activity and was further purified by Sephadex G-75 and on heparin-agarose columns, and finally Triwaglerin, with a molecular weight of 68000, was obtained. Its aggregating and ATP-releasing activity was dose-dependent and 10-times more potent than the crude venom. Triwaglerin was devoid of any of the enzymatic activities possessed by the crude venom. Triwaglerin-induced aggregation was not affected by indomethacin, creatine phosphate/creatine phosphokinase (CP/CPK), platelet-activating factor (PAF) antagonists, verapamil or heparin, but was inhibited completely by mepacrine, imipramine and forskolin and markedly by tetracaine and sodium nitroprusside. Thromboxane B2 formation caused by Triwaglerin was suppressed by mepacrine, imipramine and indomethacin. R59022 and TMB-8 caused a synergistic inhibitory effect against Triwaglerin-induced aggregation. These data suggest that Triwaglerin activates platelets in a unique action which is independent of formation of thromboxane A2 and PAF, or release of ADP.

Animals↗

PubMed2005

Shiga toxin 2 and lipopolysaccharide cause monocytic THP-1 cells to release factors which activate platelet function.

Platelet and monocyte activation may contribute to hemolytic anemia, thrombocytopenia and renal failure associated with the hemolytic uremic syndrome (HUS) caused by Escherichia coli O157:H7. Since Shiga toxins (Stxs) and lipopolysaccharide (LPS) from this bacterium are implicated in the pathogenesis of HUS, we examined whether stimulation of THP-1 human monocytic cells by Shiga toxin 2 (Stx2) and LPS can lead to the activation of platelet function. We now show that Stx2 causedTHP-1 cells to release the chemokines IL-8, MDC, and RANTES and that the presence of LPS further stimulated this release. IL-8 was produced in greatest amount and was an effective co-agonist for inducing platelet aggregation. Primary human monocytes also released large amounts of IL-8 in response to LPS and Stx2. Factors released byTHP-1 cells exposed to Stx2 and LPS activated platelet function as evidenced by increased aggregation, serotonin secretion, P-selectin exposure and by the formation of stable platelet-monocyte aggregates. Our data therefore show that monocytes exposed to E.coli-derived Stx2 and LPS release factors which activate platelet function.

Blood Platelets↗

PubMed1986

The immunohistology of the persistent generalized lymphadenopathy syndrome (PGL).

The authors employed a large panel of monoclonal antibodies to characterize and quantitate lymphoid subpopulations within the paracortex, mantle, and germinal centers of frozen sections of lymph nodes from 18 patients with the persistent generalized lymphadenopathy (PGL) syndrome and five heterosexual controls. The authors' data indicate that Leu-3+ phenotypic T-helper cells (TH) are reduced within all three compartments, while T-cytotoxic-suppressor cells (Tcs) are increased. Using the antibody 9.3, which allows dissection of the Leu-2+ Tcs subset into 9.3+ cytotoxic cells (Tc) and 9.3- suppressor cells (Ts), the authors found that the Ts subset is increased in the lymph nodes of these patients. In contrast to acquired immune deficiency syndrome (AIDS) patients, paracortical total T-cells and Leu-8+ cells appear to be preserved in patients with PGL. Study of TH and Tcs subpopulations in peripheral blood in 12 of these patients revealed inverted ratios (mean, 0.59), which did not correlate with those seen in the lymph nodes. Although the paracortical TH/Tcs ratios were significantly reduced (mean, 1.44) they were not inverted, in contrast to some other reported series. In aggregate, these data suggest that, relative to AIDS, there is preservation of the paracortical T-cell microenvironment in PGL. Clinically, this correlates with more intact cell-mediated immunity and the absence of opportunistic infections and Kaposi's sarcoma in this patient group. Follicle lysis was present in 11 patients. Increased HLA-DR+ paracortical cells, aggregates of Leu-6+ dendritic cells, decreased TAC+ cells, increased OKT-10+ plasma cells, and increased interstitial immunoglobulin were among the other features observed in these patients.

AIDS-Related Complex↗