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PubMed1999

Thromboembolic events predispose the brain to widespread cerebral infarction after delayed transient global ischemia in rats.

BACKGROUND AND PURPOSE: Transient distal platelet accumulation after common carotid artery thrombosis (CCAT) leads to hemodynamic, metabolic, and molecular events that may influence the response of the postthrombotic brain to secondary insults. We investigated how a thromboembolic insult would affect histopathological outcome when combined with an ischemic insult induced 24 hours later. METHODS: Three groups of rats underwent either (1) CCAT+10 minutes of normothermic 2-vessel occlusion (n=6), (2) CCAT+sham ischemia procedures (n=6), or (3) sham CCAT procedures+10 minutes of 2-vessel occlusion (n=6). At 7 days, rats were perfused for quantitative histopathological and immunocytochemical analysis. RESULTS: Rats undergoing combined insults (group 1) had significantly larger areas of ischemic injury (P<0.05) within the cerebral cortex, striatum, and thalamus compared with the other, single-injury groups. Increased ischemic damage included selective neuronal necrosis, infarction, and focal hemorrhage. By means of glial fibrillary acidic protein immunocytochemistry and lectin histochemistry, reactive astrocytes and microglia were found to be associated with widespread tissue necrosis. In contrast, infrequent infarction or CA1 hippocampal neuronal necrosis was observed in groups 2 and 3, respectively. CONCLUSIONS: A prior thromboembolic event is a risk factor for widespread cerebral infarction and hemorrhage when combined with a delayed ischemic insult. The understanding of what factors enhance the susceptibility of the postthrombotic brain to secondary insults may aid in the development of neuroprotective strategies to be applied after transient ischemic attacks to prevent the initiation of stroke.

Animals↗
PubMed1979

Experimental arterial thromboembolism in baboons. Mechanism, quantitation, and pharmacologic prevention.

A quantitative primate model of arterial thromboembolism has been characterized with respect to mechanism and usefulness in evaluating modifying variables. The model involved the kinetic measurements of (51)Cr-platelets and (125)I-fibrinogen consumption by femoral arteriovenous cannulae in chaired baboons. Cannula platelet consumption correlated directly with exposed cannular area for irradiated Silastic and polyurethane (correlation coefficients of 0.940 and 0.901, respectively; P < 0.001) and remained steady state for months. Nonirradiated Silastic was only minimally reactive with platelets. Despite increased rates of platelet consumption circulating fibrinogen was not measurably destroyed by any of the cannulae tested. Cannula platelet consumption was independent of cannula flow rate, platelet count, heparin anti-coagulation, and ancrod defibrinogenation.(111)In-platelet imaging of irradiated Silastic cannulae demonstrated luminal accumulation and subsequent embolization of irregular platelet masses. When irradiated Silastic cannulae were inserted as extension segments in the renal arteries of four animals the glomerular vessels became progressively occluded with nonfibrin-containing platelet thromboemboli. Nonirradiated Silastic cannulae in control arteries produced no significant vascular occlusion. Because the survival of platelets from animals with consumptive cannulae was not shortened in normal recipient animals we concluded that platelets were either irreversibly removed through thromboembolic consumption or unaffected in their viability. Oral administration of dipyridamole and sulfinpyrazone decreased cannula platelet consumption in a dose-dependent manner with complete interruption at 20 and 250 mumol/kg body wt per d (in three divided doses), respectively, whereas oral acetylsalicylic acid (10-330 mumol/kg per d) had no measurable effect on cannula platelet consumption. We conclude that this primate model simulates arterial thrombotic processes in man and that this model is suitable for the in vivo evaluation of biomaterials and of drugs that modify platelet behavior.

Animals↗
PubMed1993

Eosinophil cationic granule proteins impair thrombomodulin function. A potential mechanism for thromboembolism in hypereosinophilic heart disease.

Thromboembolism is a prominent but poorly understood feature of eosinophilic, or Loeffler's endocarditis. Eosinophil (EO) specific granule proteins, in particular major basic protein (MBP), accumulate on endocardial surfaces in the course of this disease. We hypothesized that these unusually cationic proteins promote thrombosis by binding to the anionic endothelial protein thrombomodulin (TM) and impairing its anticoagulant activities. We find that MBP potently (IC50 of 1-2 microM) inhibits the capacity of endothelial cell surface TM to generate the natural anticoagulant activated protein C (APC). MBP also inhibits APC generation by purified soluble rabbit TM with an IC50 of 100 nM without altering its apparent Kd for thrombin or Km for protein C. This inhibition is reversed by polyanions such as chondroitin sulfate E and heparin. A TM polypeptide fragment comprising the extracellular domain that includes its naturally occurring anionic glycosaminoglycan (GAG) moiety (TMD-105) is strongly inhibited by MBP, whereas its counterpart lacking the GAG moiety (TMD-75) is not. MBP also curtails the capacity of TMD-105 but not TMD-75 to prolong the thrombin clotting time. Thus, EO cationic proteins potently inhibit anticoagulant activities of the glycosylated form of TM, thereby suggesting a potential mechanism for thromboembolism in hypereosinophilic heart disease.

Aged↗
PubMedDate not supplied

Do different atrial flutter types carry the same thromboembolic risk?

Thromboembolic risk of atrial flutter (AFl) types has not been elucidated sufficiently in previous reports. The authors classified the patients according to surface electrocardiogram and electrophysiologic characteristics as those with typical AFl (37 patients, 78.4% male, mean age 59.8 +/-9.5 years) and atypical AFl (13 patients, 69.2% male, mean age 60.9 +/-6.9 years) and compared them regarding some clinical, echocardiographic, and hematologic parameters. An age- and gender-matched control group composed of 20 individuals without any organic heart disease in sinus rhythm was chosen (80% male, mean age 60.3 +/-7.9 years). Clinical features such as age, gender, organic heart disease, hypertension, diabetes mellitus, AFl duration, and the prevalence of paroxysmal atrial fibrillation were similar in both AFl groups. Echocardiographic parameters such as left ventricular ejection fraction, left atrial (LA) diameter, LA spontaneous echo contrast, and LA appendage emptying velocities were similar in both AFl groups. Fibrinogen, fibrin D-dimer, and thrombin-antithrombin III levels reflecting coagulation system activity were found to be increased in the patients with atypical AFl when compared with those with typical AFl and the control group (p < 0.001). In Pearson's correlation analysis, significant correlation between these hematologic markers and clinical and echocardiographic parameters were not found (p > 0.05). The coagulation system activity was found to be increased in patients with atypical AFl. Thus, anticoagulation due to the increased thromboembolic risk should be considered in patients with atypical AFl.

Age Factors↗
PubMedDate not supplied

Recurrent thrombosis in patients with deep vein thrombosis and/or venous thromboembolism associated with anticardiolipin antibodies.

Anticardiolipin antibodies represent one of the main hypercoagulation states associated with venous thromboembolism. The aim of this work was to evaluate symptomatic recurrent thrombosis in patients with anticardiolipin antibodies and deep vein thrombosis of the lower limbs with or without thromboembolism. Sixty patients who suffered from deep vein thrombosis were observed for a 5-year period, whether they had anticardiolipin antibodies or not. The group was made up of 34 females and 26 males with ages ranging from 13 to 73 years. All were diagnosed with deep vein thrombosis by means of phlebography and were tested for anticardiolipin antibodies by use of the ELISA method. The symptomatic signs of recurrent thrombosis were evaluated during this period. In total, 56.6% of the group were considered above normal for anticardiolipin antibodies, 25% positive, another 31.6% borderline, and 43.4% negative. Patients were tested positive when the anticardiolipin antibody count was >15 units/mL, borderline between 10 and 15 units/mL, and normal when <10 units/mL. The method of relative risk was used for statistical analysis of the results. Four positive patients, 1 borderline, and 1 normal patient had recurrent events of thrombosis. In the statistical analysis the relative risk for recurrent thrombosis in the positive patients was 6.0; CI 95%; 1.2 to 29.5. In conclusion patients with deep vein thrombosis who are positive for anticardiolipin antibodies present a higher risk of recurrent thrombosis.

Adolescent↗
PubMed1976

Incidence of venous thromboembolic disease in nonpregnant women of childbearing age.

Data from 12 Cincinnati hospitals were examined to determine the incidence of venous thromboembolic disease in nonpregnant women of reproductive age. The incidence of superficial and deep vein thromboembolic disease in women age 15 to 44 was 1.09 cases per 1,000 women per year; for women age 20 to 44 the incidence was 1.3 cases for 1,000 women per year. These figures include idiopathic and non-idiopathic cases and thus are representative of the general population of nonpregnant women of reproductive age. The incidence of pulmonary embolism was approximately 1 case per 5,000 women age 20 to 44. There were two deaths from pulmonary embolism, giving a mortality rate of 11.3 deaths per million women age 15 to 44.

Adolescent↗
PubMedDate not supplied

Safety and efficacy of picotamide, a dual anti-thromboxane agent, in patients with thrombocytosis and a previous thromboembolic event: a 1-year observational study.

Patients with chronic myeloproliferative disease are at increased risk of both thromboembolic and haemorrhagic complications. Cerebral thrombosis is a common cause of death in myeloproliferative disease patients. Picotamide is a new anti-platelet drug sharing a dual anti-thromboxane activity: inhibition of thromboxane A2 synthase and thromboxane A2 receptor antagonism. Picotamide inhibits in vitro and ex vivo platelet aggregation induced by different agonists. Interestingly, in vitro studies show that picotamide is able to increase prostacycline biosynthesis. In the clinical setting, picotamide treatment induces only a slight prolongation of bleeding time. The safety and efficacy of picotamide long-term treatment in 15 patients with essential thrombocytosis and a positive history of previous thromboembolic events was evaluated. After 12-month treatment with picotamide no patients suffered from thrombotic events and only one minor and transient bleeding episode was observed. This observational long-term trial shows that picotamide treatment in patients with thrombocytosis at high risk of thrombotic events is safe and well tolerated. Picotamide did not increase the risk of bleeding in these patients, while at the same time, no thrombotic events were observed during the 1-year treatment.

Adult↗
PubMedDate not supplied

Safety and efficacy of enoxaparin treatment in venous thromboembolic disease during acute leukemia.

BACKGROUND: Venous thromboembolism (VTE) is a quite common complication in acute leukemia, although its real incidence is unknown. The best treatment of this complication is still a matter of debate due to the very high risk of hemorrhage in this group of patients. PATIENTS AND METHODS: From December 2000 to December 2002 four Caucasian patients with acute leukemia developed VTE complications. The patients were three men and one woman, mean age 55.7 years (range, 27-77). Two patients with acute lymphoid leukemia (L1 and L2 according to the FAB classification) developed deep venous thrombosis during the administration of chemotherapy; one patient with acute myeloid leukemia (AML, M2 according to the FAB classification) had pulmonary thromboembolism at diagnosis, while another AML patient (M4 according to FAB) showed deep venous thrombosis as the first symptom of leukemia. The clinical diagnosis of symptomatic VTE was confirmed by objective imaging procedures including lower limb venous color Doppler imaging in all cases and a ventilation-perfusion lung scan in one case. All patients were treated with enoxaparin 100 IU/kg subcutaneously twice daily for one month, followed by 150 IU/kg once daily for at least five months. When the platelet count was below 20,000 x 10(9)/L, the dose was reduced by 50%. RESULTS: During antithrombotic treatment neither VTE recurrences nor hemorrhagic complications or heparin-induced thrombocytopenia occurred. The platelet count at the beginning of enoxaparin treatment was very low (mean, 55,750 x 109/L; range, 12,000-121,000 x 10(9)/L) and treatment did not affect platelet recovery. CONCLUSIONS: Enoxaparin proved to be efficacious and safe in the management of deep venous thrombosis with or without pulmonary embolism in patients affected by acute leukemia. Enoxaparin cured acute venous thrombosis, prevented recurrences and did not cause any hemorrhagic complications despite prolonged severe thrombocytopenia.

Adult↗
PubMed2002

Is family history sufficient to identify women with risk of venous thromboembolism before commencing the contraceptive pill?

Oral contraceptives (OGs) increase risk of venous thromboembolic disease (VTE). The incidence of thomboembolic disease in healthy young women who are not taking OCs is 0.4-0.8/10,000, and in healthy young women using OCs, it is 3-4/10,000. To assess whether a family history of thromboembolism is a suitable tool to identify women who should not be given OCs, 50 women who suffered a VTE while taking OCs were studied. Only 16% of these women had family history which is why in our opinion, it is not a sufficient safeguard to recommending the use of OCs.

Contraceptives, Oral↗
PubMed2006

Thromboembolism in cancer patients: pathogenesis and treatment.

In this review we summarize the causes of cancer related thrombosis as well as modern treatment approaches. Malignancy as a risk factor for thromboembolism is becoming increasingly recognized by clinicians caring for these patients. The probability of thrombosis occurring in an individual patient is dependent on several factors, including accompanying medical problems, the type of cancer, the clinical stage, performance status, and the treatment modalities employed. Thrombophilia with a history of thromboembolism is important as well. The overall risk of thrombosis is sevenfold that of noncancer patients. Though much has been learned about the pathogenesis of cancer-related thrombosis, we are in fact just beginning to understand the cross-talk between cancer cells and their related microenvironment, and such investigations are likely to increase our knowledge of cancer-related thrombosis mechanisms. Research in these areas may also suggest new strategies for cancer prevention, metastasis suppression, and new treatments. Drugs used in cancer therapy are increasingly recognized to directly contribute to the thrombotic tendency. Few studies provide data on the optimal management of cancer patients with thrombosis. It has been learned that retreating with the same drug can be very hazardous. In general the approach to prevention of thrombosis is the same as for noncancer patients, recognizing that specific cancer types and stage can place a patient in a high-risk category. Initial coumadin therapy fails in a significant number of patients with cancer. Recognition of the cancer patients at highest risk for coumadin failure is challenging. Low-molecular-weight heparins appear to be more effective in such situations where coumadin is likely to fail or has failed, but these drugs are thought to be costlier. Newer agents such as Factor Xa inhibitors and TF inhibitors are currently under investigation and may be found useful in the management of cancer-related thrombosis.

Anticoagulants↗
PubMedDate not supplied

The potential risk for upper extremity thromboembolism in patients with occluded axillofemoral bypass grafts: two case reports.

Axillofemoral bypass grafts (AxFG) are widely used in the management of poor-risk patients with aortoiliac occlusive disease. On the other hand, AxFGs are associated with a variety complications to the upper extremity (UE). UE thromboembolism represents a significant and specific complication of occluded AxFGs in our series (2.6% of patients, 33.3% of occluded grafts). This article describes two cases of late axillary artery thrombosis caused by the occlusion of externally-supported AxFGs. The two patients were treated by graft disconnection, a distal embolectomy, and patch angioplasty of the axillary artery. Their postoperative courses were uneventful. Based on the authors' experience and a review of the literature, they suggest that an occluded AxFG represents a high risk for use of a donor artery and that such patients must therefore be very carefully followed. To prevent late UE thromboembolism in patients with occluded grafts, the authors strongly advise that such patients undergo a surgical operation with careful follow-up after surgery.

Aged↗
PubMed2005

Acquired risk factors for venous thromboembolism in medical patients.

Acute venous thromboembolism (VTE) is a serious and potentially fatal disorder, which often complicates the course of hospitalized patients, but may also affect ambulatory and otherwise healthy people. While the introduction of thromboprophylactic measures is expected to have reduced the occurrence of postoperative VTE, there is an increasing awareness of the importance of medical conditions in determining thromboembolic events. Among the conditions that predispose patients to VTE are increasing age, cancer and its treatment, prolonged immobility, stroke or paralysis, previous VTE, congestive heart failure, acute infection, pregnancy or puerperium, dehydration, hormonal treatment, varicose veins, long air travel, acute inflammatory bowel disease, rheumatologic disease, and nephrotic syndrome. Other factors that have recently been associated with an increased risk of VTE disorders include persistent elevation of D-dimer and atherosclerotic disease. Recognition of the incidence and clinical importance of thrombosis will most likely encourage more widespread use of antithrombotic prophylaxis in medical patients.

Acute Disease↗
PubMed2002

The incidence of venous thromboembolism in thrombophilic children: a prospective cohort study.

Antithrombin and protein C and S defects, factor V Leiden mutation, and G20210A prothrombin gene mutation are well-recognized risk factors for venous thromboembolism (VTE) in adults, especially during circumstantial situations such as trauma, immobilization, surgery, or oral contraceptive treatment. The relevance of these defects in predisposing children to VTE is still undefined. In a prospective cohort study we assessed the incidence of spontaneous and risk period-related VTE in asymptomatic children (aged 1-14 years), who were family members of a proband with an objectively diagnosed venous thromboembolic event and a documented single thrombophilic abnormality. We enrolled 143 children from 63 families. Of them, 81 (56.6%) were carriers of an inherited defect, whereas the remaining 62 were free from known genetic or acquired causes of thrombophilia. The mean observation period was 5 years (range, 1-8 years) in each group. Thirty-one risk periods occurred in the carriers group and 20 in noncarriers. Neither spontaneous nor risk period-related VTE occurred in either group during 395 and 296 observation years, respectively. However, circumstances where most of the pediatric thromboses occur (insertion of central venous lines, cancer, and cardiovascular surgery) were not encountered. In conclusion, the thrombotic risk in otherwise healthy children with a single identified thrombophilic defect appears to be very low. Common triggering conditions for VTE in thrombophilic adults do not seem to increase the thrombotic risk in children carrying the same inherited defect. Accordingly, screening for thrombophilia in otherwise healthy children younger than 15 years who belong to families with inherited defects predisposing to thrombosis seems unjustified.

Adolescent↗
PubMed2006

The efficacy of bosentan in inoperable chronic thromboembolic pulmonary hypertension: a 1-year follow-up study.

The treatment of choice for chronic thromboembolic pulmonary hypertension (CTEPH) is pulmonary endarterectomy (PEA). However, many patients develop a severe progressive small vessel pulmonary arteriopathy that is inaccessible to surgical intervention and is associated with poor survival. The purpose of the present study was to evaluate the medium-term efficacy and safety of the dual endothelin receptor antagonist, bosentan, in inoperable CTEPH. Forty-seven patients with inoperable CTEPH (distal disease or persistent pulmonary hypertension following PEA) underwent evaluation after 1 yr of bosentan therapy. Outcomes included assessment of 6-min walk test (6MWT), haemodynamics and World Health Organization functional classification. Monitoring of serious adverse effects and changes in therapy was undertaken. Patients showed sustained improvements in 6MWT (49+/-8 m), functional classification, cardiac index (+0.2+/-0.07 L.min(-1).m(-2)) and total pulmonary resistance (-139+/-42 dyn.s.cm(-5)). Those patients with persisting pulmonary hypertension following PEA showed the greatest improvement. One-yr survival was 96%, and bosentan was well tolerated with only one patient developing deranged liver function. Although all patients with chronic thromboembolic pulmonary hypertension should be considered for pulmonary endarterectomy, bosentan provides an alternative medical therapy to improve function and delay the progression of this devastating disease in those in whom surgery is not suitable.

Adult↗
PubMed1997

Chronic thromboembolic pulmonary hypertension and vascular transformation of the lymph node sinuses.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease often not recognized until it is far advanced. Medical management does not reverse the effects of the disease, nor does it prevent its progression. Pulmonary thromboendarterectomy is the preferred treatment. We present the case of a patient in whom CTEPH was mistaken for an interstitial lung disease with mediastinal lymph node enlargement. The mediastinal lymph node enlargement was due to vascular transformation of the lymph node sinuses (VTS). This is an unusual case of chronic thromboembolic pulmonary hypertension with vascular transformation of the lymph node sinuses.

Adult↗
PubMed2001

Prevention and diagnosis of venous thromboembolism in critically ill patients: a Canadian survey.

BACKGROUND: Venous thromboembolism (VTE) confers considerable morbidity and mortality in hospitalized patients, although few studies have focused on the critically ill population. The objective of this study was to understand current approaches to the prevention and diagnosis of deep venous thrombosis (DVT) and pulmonary embolism (PE) among patients in the intensive care unit (ICU). DESIGN: Mailed self-administered survey of ICU Directors in Canadian university affiliated hospitals. RESULTS: Of 29 ICU Directors approached, 29 (100%) participated, representing 44 ICUs and 681 ICU beds across Canada. VTE prophylaxis is primarily determined by individual ICU clinicians (20/29, 69.0%) or with a hematology consultation for challenging patients (9/29, 31.0%). Decisions are usually made on a case-by-case basis (18/29, 62.1%) rather than by preprinted orders (5/29, 17.2%), institutional policies (6/29, 20.7%) or formal practice guidelines (2/29, 6.9%). Unfractionated heparin is the predominant VTE prophylactic strategy (29/29, 100.0%) whereas low molecular weight heparin is used less often, primarily for trauma and orthopedic patients. Use of pneumatic compression devices and thromboembolic stockings is variable. Systematic screening for DVT with lower limb ultrasound once or twice weekly was reported by some ICU Directors (7/29, 24.1%) for specific populations. Ultrasound is the most common diagnostic test for DVT; the reference standard of venography is rarely used. Spiral computed tomography chest scans and ventilation-perfusion scans are used more often than pulmonary angiograms for the diagnosis of PE. ICU Directors recommend further studies in the critically ill population to determine the test properties and risk:benefit ratio of VTE investigations, and the most cost-effective methods of prophylaxis in medical-surgical ICU patients. INTERPRETATION: Unfractionated subcutaneous heparin is the predominant VTE prophylaxis strategy for critically ill patients, although low molecular weight heparin is prescribed for trauma and orthopedic patients. DVT is most often diagnosed by lower limb ultrasound; however, several different tests are used to diagnose PE. Fundamental research in critically ill patients is needed to help make practice evidence-based.

Anticoagulants↗
PubMed2003

Thromboembolism in paediatric lupus patients.

Paediatric patients with systemic lupus erythematosus (SLE) and antiphospholipid antibodies (aPL), specifically lupus anticoagulants (LAC) are at high risk of developing thromboembolic events (TE). Our objectives were to determine the prevalence of TE in paediatric SLE patients with LAC and to determine if anticoagulation was effective to decrease morbidity, and prevent recurrent TE. We reviewed data on 149 paediatric SLE patients treated over 10 years. In all, 24 patients (16%) were LAC positive, and 21 TE occurred in 13 of these LAC positive patients (54% incidence of TE in LAC positive patients). The events were cerebral venous thrombosis (9), arterial stroke (3), deep venous thrombosis (4), pulmonary embolism (2), other venous event (1) and other arterial events (2). The median duration between SLE diagnosis and first TE was 15.2 months (range 0-62), and the median age at first TE was 15.1 years (range 11.4-18.4). Long-term anticoagulation was prescribed, and eight patients (62%) were transferred to adult care on lifelong oral warfarin; four (31%) remain under our care on lifelong warfarin, and one patient died of causes unrelated to her TE. No patient has been identified with deficiencies of protein C, protein S or antithrombin III. One patient is heterozygous for Factor V Leiden, and one is heterozygous for both the Prothrombin 20210A mutation and the MTHFR (methylene tetrahydrofolate reductase) mutation. Four patients had recurrent TE (31%), and three were not anticoagulated at the time of their second event. One patient had two recurrences on therapeutic anticoagulation. Thromboembolic events are prevalent in the LAC positive paediatric SLE population, and consideration for lifelong anticoagulation must occur after an initial TE.

Adolescent↗
PubMed2006

Specificities of platelet autoantibodies and platelet activation in lupus anticoagulant patients: a relation to their history of thromboembolic disease.

Lupus anticoagulants (LA) prolong in vitro phospholipid-dependent coagulation tests, but are associated with thromboembolic disease (TE). However, a subgroup of individuals with LA has no TE, and it is therefore desirable to distinguish those at risk for TE from those without. Whether platelets have a primary role in the development of TE is not clear yet. We determined platelet autoantibodies to identify a specific platelet target which is associated with platelet activation in 97 patients with a long history of detectable LA, 65 patients with TE (LA/TE+), and 32 individuals without TE (LA/TE-). Thrombocytopenia was more common in the LA/TE- than in the LA/TE+ group (P < 0.05). Both groups had platelet antibodies, but the frequency of antibodies was lower in LA/TE+ than LA/TE- patients (P < 0.01), who had higher antibody titres against glycoprotein IIb/IIIa and glycoprotein Ib/IX (P < 0.05). Also, their platelets were more activated, as determined by PAC-1 binding (P < 0.01). These differences were also noted if patients with arterial thrombosis were evaluated separately. These findings in LA/TE- individuals were similar to those in patients with chronic autoimmune thrombocytopenia. However, there was no autoantibody target identifiable to distinguish between LA/TE- from LA-TE+ individuals. We therefore conclude that the presence of platelet antibodies, even if associated with platelet activation, is not sufficient to dispose LA patients to thromboembolic disease.

Adolescent↗