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What such cultural analyses can do is to think through the material-semiotic—the meaningful enfleshment—of bodies, histories, and meanings called human and non-human animal. Echocardiography and pulmonary function Possible role of imatinib in clinical pulmon- [52] de Montpreville V, Dulmet E, Fadel E, as screening tests for pulmonary arterial ary veno-occlusive disease. Peggy Kamuf New York: Currently, complication of CTD, cannot be confidently excluded in some of transplantation lung or combined heart-lung is deemed the these studies. Routledge,

Anne Carson writes, The wolf is a conventional symbol of marginality in Greek poetry. The wolf is an outlaw. Can refigurations of the relationship between wolves and humans have an effect on—transform and refigure—the species, race and sex nexus in which this relationship is knotted up? And what might this have to do with wolves? The wolf, like the racialized other of a white European cultural imagination, connotes sexual potency, vigor, a carnality that supplements—with sexualized embodiedness—civilization.

Modern revisionist and sometimes feminist narratives of this species merger popular film and TV adaptations, especially of Red Riding Hood seem usually to reinscribe racialism by linking werewolfism to genetics. The process involves unlearning collectivity and solidarity, unlearning the Deleuzian pack or swarm in favor of the oedipalized individual. Wolves live in packs, in collectivities, and a feminist Deleuzian becoming-wolf that refuses masculinist heroic or demonic individualism might offer a line of flight for both women and wolves.

This essay began by addressing wolves and humans, their similarities, their proximities within the naturecultures where they co-exist, their mutual relations, their difficult entanglements, and their cultural histories. What such cultural analyses can do is to think through the material-semiotic—the meaningful enfleshment—of bodies, histories, and meanings called human and non-human animal.

Wolves, even, perhaps especially the ones with which humans now choose to repopulate the wilderness, are, for human culture, spectral. The spectral wolf, which includes a long line, a genelycology, a multiplicity of wolves brutally and deliberately exterminated over centuries and centuries of human culture, haunts human myths, human stories, human psyches, and continues to haunt the figure of the human-as-animal in literature, political theory, and popular culture.

Routledge, , Peggy Kamuf New York: Routledge, Originally published as Spectres de Marx Paris: Haunting and the Sociological Imagination Minneapolis: University of Minnesota Press, , Duke University Press, , Brian K. Warner Brothers Pictures , television. Is it a domestic racial threat? Freccero 16 9 For an interesting discussion of aristocratic enclosure of forest land and the privatization of hunting rights, see Matt Cartmill, A View to a Death in the Morning: Harvard University Press, repr.

Animals, Humans, and the Study of History, ed. Dorothee Brantz Charlottesville and London: The Boydell Press, , Leah S. Marcus London: Methuen Drama, University of Minnesota Press, See also The Companion Species Manifesto: Dogs, People, and Significant Otherness Chicago: Prickly Paradigm Press, Henry Thomas Riley London: George Bell and Sons, , http: Geoffrey Bennington Chicago and London: University of Chicago Press, Use of engorgement may produce characteristic capillary lesions with movat elastic or orcein stains in order to distinguish between patchy capillary multiplication, leading to a hemangioma-like internal and external elastic laminae can be useful in determin- appearance [49].

By contrast, plexiform lesions, which are ing whether affected vessels are venous or arterial in nature. Dilatation and congestion of tion with parotiditis. Progressive dysphagia, proximal muscle lymphatic vessels and lymphoid follicular hyperplasia is also weakness or classic heliotrope periorbital rash may point to an frequently observed, and so-called vascular transformation of underlying inflammatory myopathy such as polymyositis or the sinus has been described in lymph nodes from affected dermatomyositis, especially if there is a history of associated patients [52].

Interestingly, pathological changes of another rare pulmonary Physical examination should focus on detection of typical signs vascular disease, pulmonary capillary hemangiomatosis PCH , of pulmonary hypertension and may also reveal typical CTD may also be observed in PVOD patients.

PCH is distinguished features. An accentuated pulmonic component to the second histologically by abundant but well-circumscribed capillary heart sound is a key finding and indicative of increased pul- proliferation [53]. Lantuejoul et al. The sequelae of such an increase in considerable overlap in the pathologic findings of these two pressure, including a pansystolic murmur of tricuspid regurgita- disorders, such that patients with PVOD frequently also demon- tion, a diastolic murmur of pulmonary regurgitation and a right strate features characteristic of PCH and vice versa [21].

In advanced disease, there of PVOD and PCH are similar, leading these investigators to may also be evidence of right ventricular decompensation speculate that the two disorders may in fact represent variants cyanosis, elevation of the jugular venous pulse, hepatome- of the same disease. Digital clubbing may also be seen in some Clinical presentation patients.

One of the most important physical signs that helps Progressive dyspnoea, fatigue, dizziness, palpitations, and distinguish PVOD from other forms of PAH is the presence of chest discomfort, particularly if worsened by exercise, are ausculatory fine inspiratory crackles that develop in the context the cardinal symptoms of PVOD.

However, these presenting of acute pulmonary oedema, particularly after initiation of clinical features are also characteristic of PAH and are similarly specific PAH therapy see below and if there is no evidence associated with other pulmonary complications of CTDs [27]. However, the Indeed, given its relative rarity, patients are frequently mis- absence of crackles does not exclude the diagnosis.

Pleural diagnosed with and treated for other, more common dis- effusions may also occur and similarly reflect elevated post- orders prior to the diagnosis of PVOD being established.

In tips, calcinosis, telangiectasias, narrowed oral aperture, or the majority of cases, therefore, significant haemodynamic and healed ulcerations , SLE malar rash, livedo reticularis, palpable morphological changes will have already developed within the purpura, or an erythematous rash between the MCP and PIP pulmonary vasculature long before the onset of clinical man- joints and early possible RA symmetrical synovial distension, ifestations.

However, The diagnosis of CTD-associated PVOD requires not only the patients presenting with features suggestive of PVOD and PAH clinical appreciation of the associated symptoms but also the in general should be carefully assessed for a possible under- use of screening tools and the confirmation of the diagnosis by lying CTD.

For example, the presence of new onset or worsening independent diagnostic procedures. We have previously shown that by combining data ulceration, alopecia or previous venous thromboembolic events from a range of routine investigative modalities it is generally should alert the clinician to the possibility of SLE. Arthralgia and possible to make the diagnosis of idiopathic PVOD with reason- synovitis also represent key features of rheumatoid arthritis able certainty [27].

However, these larger vein branches are characterised by a normal intravascular pressure, being distal to the site of venous obstruction and uninvolved in the disease process. Thus, the true value for the pulmonary capil- radiological features with PVOD that can be difficult to diffe- lary pressure is underestimated using the wedge technique in rentiate Box 1.

In particular, distinguishing PVOD from left PVOD cases and does not reflect the important elevation of ventricular dysfunction that complicates CTD can be difficult pressure in the smaller diameter venous tributaries. Even so, making this distinction is of critical ciated PH and post-capillary pulmonary hypertension should importance, since the management approaches for the differ- form part of the differential diagnosis for this patient popula- ent forms of PH that may complicate CTD are dictated by the tion [15].

In particular, diastolic heart failure with preserved left underlying mechanism see below. Furthermore, it is becoming increa- uncommon in patients treated with diuretics. In this regard, singly employed as part of routine screening programs for at- cystalloid fluid challenge performed during right heart cathe- risk groups, particularly SSc patients [15].

Detection of a systolic terisation may unmask co-existent pulmonary hypertension pulmonary artery pressure of greater than 40 mmHg, as esti- that is predominantly post-capillary in origin [55].

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Where mated by the velocity of the regurgitant jet of flow through the suspicion of associated left ventricular disease remains, it tricuspid valve, is suggestive of pulmonary hypertension.

How- may be necessary to perform left heart catheterisation so that ever, echocardiography is neither specific nor sensitive enough LVEDP can be directly measured. In particular, finding of an elevated systolic acute vasodilator testing with short acting vasodilators such PAP cannot be considered as confirmatory of PAH, and it is as inhaled nitric oxide NO , intravenous epoprostenol or ade- important to stress that therapeutic decisions should not be nosine during right heart catheterization in order to identify made on the basis of echocardiographic findings in isolation.

In a recent study from the French National Pulmonary Hyper- Invasive hemodynamic assessment tension Reference Centre, positive acute vasodilator responses As is the case for all forms of suspected pulmonary hyperten- rates for idiopathic- and CTD-associated PAH were comparable sion, investigation for possible PVOD requires invasive hemo- [56].

PVOD mostly affects small pulmonary veins, leading to an elevation of pressure in this region Pv , as well as to an elevation in true pulmonary capillary pressure Pc and pre- capillary pulmonary arterial pressure Pa. Larger pulmonary veins are usually not affected by PVOD, though it is in fact the pressure in these vessels that is reflected by Ppcw.

The static column of blood hatched occluded by pulmonary arterial catheter wedging after balloon inflation in a pulmonary arterial branch balloon 1 reflects the pressure in a vein of similar diameter balloon 2. However, these veins are usually of a larger size than those vessels affected by PVOD.

Therefore, this measurement technique does not reflect the important elevation of pressure in the smaller diameter vessels associated with PVOD Source: Reproduced with permission from: Montani et al. Eur Respir J ; However, these improvement after 3—4 months and NYHA functional class I or II classically described findings are not universal and the chest after 1 year of therapy.

Frank pulmonary oedema may who demonstrated a long-term response, and discontinuation be apparent in the setting of acute clinical deterioration, parti- of CCBs was deemed necessary for nearly all CTD patients due to cularly after introduction of specific PAH therapy see below. The triad of mediastinal lymph responders and all such patients treated with CCBs developed node enlargement, septal thickening and diffuse ground-glass at least mild pulmonary oedema during follow up [56].

Given opacities, particularly in a centrilobular distribution, is classically these observations, we consider use of CCBs to be contra- described figure 3.

It is important to Moreover, one quarter of pathologically confirmed PVOD cases stress that even though there were no episodes of acute have one or none of these tomographical features [27]. Thus, pulmonary oedema during acute vasodilator testing in our the absence of typical radiological abnormalities does not study group, its absence during testing does not exclude a exclude the diagnosis.

In general, for CTD-associated PAH patients cardial effusions, diffuse pulmonary nodules, and other fea- there appears to be little merit in systemically performing acute tures common to all forms of PAH central pulmonary arterial vasodilator testing even though it appears safe, since an acute enlargement, right ventricular hypertrophy and dilatation and response is not predictive of a favourable outcome with long- bowing of the interventricular septum.

Pleural effusions have term CCB treatment. This is especially the case particularly where been reported but are uncommon. In typical cases, the plain chest radio- HRCT is also an important investigation to help exclude other graph demonstrates pulmonary arterial enlargement and fea- more common pulmonary complications of CTD and disorders tures consistent with post-capillary congestion Kerley B lines and that may mimic PVOD Box 1.

Figure 3 High resolution computed tomography demonstrating typical features of pulmonary veno-occlusive disease. Extensive ground-glass opacities in a centrilobular distribution, poorly defined nodular opacities and septal lines.

Contrast-enhanced scan demonstrating mediastinal lymph node enlargement arrows hallmarks of interstitial lung disease early fibrosis with or alveolar hemorrhage may develop in CTD patients in the without honeycombing or bronchiolitis obliterans air trapping absence of this complication [62]. No study has been under- and bronchial wall thickening is of equal diagnostic relevance. Contrast-enhanced chest CT is an important tool for the tion. However, mosaic perfusion patterns associated value and is associated with a high rate of complications [42].

There are no large series specifically reporting the obstructive pattern may occasionally be demonstrated [27,63]. In contrast, measure- HRCT findings appear broadly similar to those commonly iden- ments of the single-breath diffusing capacity for carbon mono- tified in PVOD that is idiopathic in nature [58].

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In the setting of CTD, scans are either normal or non-specifically abnormal. However, however, the finding of a reduced DLCO may be multifactorial as is observed in idiopathic PAH, multiple mismatched perfu- interstitial or pleural disease, neuromuscular involvement, sion defects may also be observed, which may lead to diag- anaemia etc.

In addition, values for DLCO in Where diagnostic uncertainty remains, pulmonary angiography the normal range do not exclude the diagnosis, as overestima- should be performed in order to exclude CTEPH and is tions may occur in the context of occult alveolar haemorrhage. Nonetheless, a decrease in DLCO that is significantly out of proportion to any degree of restrictive or obstructive abnor- Bronchoalveolar lavage mality should alert clinicians to the possibility of PVOD.

A study by Rabiller and lower SpO2 during 6 min walk test. Whether the same et al. Biomarkers have also been clinical trial data, their application is biologically plausible in this evaluated as a means of predicting risk of developing PAH in patient population and thus broadly advocated [68].

Avoidance SSc. In one prospective study involving SSc patients without of strenuous exercise to reduce the risk of syncope, particularly evidence of PAH at baseline, quantification of the NT-proBNP in in those with advanced disease, is important.

The utility of deterioration and even death. Female patients of childbearing such a predictive tool specifically in CTD-associated PVOD has age should therefore be advised on effective contraceptive not yet been explored. Measurement of exercise capacity by measures. Cardio- also confer symptomatic improvement. Annual pneumococcal pulmonary exercise testing is less frequently used, as it is time and influenza vaccinations should be encouraged. As Reduction of right ventricular preload with the use of loop in all cases, the work-up of suspected or confirmed pulmonary diuretics, aldosterone antagonists or both is warranted for hypertension should additionally include other elements to those with symptomatic volume overload.

Indeed, in our exclude other treatable causes as outlined in recent guidelines, experience, high-dose diuretics are generally necessary be- even in those with a known CTD [1,2]. However, a recent study tion with vitamin K antagonist therapy improves prognosis in by Hachulla et al suggests that PAH in fact develops within five idiopathic PAH through prevention of in situ thrombosis and years of the first non-Raynaud phenomenon symptom in venous thromboembolism.

In this setting, an international roughly half of SSc patients [65]. Although there are no specific data to support this relatively poor prognosis, there is increasing interest in earlier strategy in PVOD, the therapeutic rationale is the same.

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A identification of the disease. Earlier detection and introduction higher target INR is appropriate in patients with known asso- of treatment, it is hoped, would in turn lead to improved ciated antiphospholipid syndrome, particularly in the context of outcomes [66].

As most patients with a known CTD are fol- recurrent thromboembolic events. However, anticoagulants lowed-up at regular intervals, the opportunity therefore exists should be administered with caution in CTD-associated PVOD for clinicians to routinely assess patients that have no respira- given the significant risk of occult alveolar haemorrhage [61]. Particular care should be taken when considering diography, performed annually in at-risk populations. However, anticoagulation in cases of angiodysplasia.

In addition, screening bleeding events.

Nonetheless, where screening programs detect cases of The last two decades have witnessed remarkable progress with pulmonary hypertension in this population, it is important to respect to the therapeutic options available for the treatment of consider PVOD as a differential diagnosis.

PAH [69]. Regulatory approval has now been granted for a Management approaches number of drug therapies that produce meaningful and sus- tained clinical improvements as a result of associated pulmon- Supportive measures and therapies ary-specific vasodilatory and antiproliferative activities.

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In A number of general lifestyle modifications, therapeutic inter- contrast, there is a distinct lack of prospective clinical trial data ventions and relatively simple precautions are generally ad- in support of these various treatments options in the context of vocated for all PVOD patients. As a result, there is no established transplantation is rarely proposed in these patients due to medical treatment recommended for the disease [1,2].

Further- the high rate of associated comorbidites. Lastly, and perhaps more, given its rarity, it is highly unlikely that randomised most importantly, there are no published data, even from studies of existing or novel agents will ever be realised. Instead, retrospective series, that support this strategy in CTD patients treatment decisions are therefore based on clinical experience, that develop PVOD.

It is also important therapies that demonstrate both vasodilatory and antiproli- to note that pathological confirmation is rare and treatment ferative properties have become available for use in PAH of decisions are usually based on clinico-radiologic grounds alone. However, there is limited clinical experi- Idiopathic PAH patients treated by chronic intravenous epo- ence with the use of such agents in the setting of PVOD.

Isolated prostenol therapy show improvements in symptoms, exercise incidences of clinical improvements following introduction of capacity, quality of life, pulmonary haemodynamics and survi- the non-selective endothelin antagonist bosentan [76] and the val. Recently published data suggest that in SSc- phosphodiesterase type-5 inhibitor sildenafil have been pub- associated PAH, long-term continuous epoprostenol therapy lished [77,78]. In contrast, other investigators have reported may confer a survival advantage [72].

There is also in vitro that treatment with bosentan confers no benefit in SSC-asso- evidence that this agent may reverse increased vasomotor tone ciated PVOD [58]. Use of inhaled iloprost has also been success- in pulmonary venules [73]. However, exposure to pulmonary fully attempted, suggesting a potential application in advanced vasodilators, including epoprostenol, may result in severe and disease [79]. Beneficial effects with the tyrosine kinase inhi- even fatal acute pulmonary oedema in PVOD [27,74].

In one bitor imatinib were reported in one patient with PVOD refrac- series, nearly half of patients studied developed this complica- tory to other therapies, though this approach is also highly tion after initiation of vasodilators, with epoprostenol the most experimental and not recommended [80]. It is important to commonly used agent [27]. Indeed, the development of acute emphasize that there is no data to support the use of long-term dyspnoea and hypoxemia after initiation of specific PAH ther- calcium antagonist therapy in CTD-associated PVOD, even apy for presumed CTD associated-PAH is one of the classic among those who demonstrate a positive acute vasodilator modes of presentation of PVOD.

The likely mechanism is a response, and given the risk of pulmonary oedema, we con- selective dilatation of the small pulmonary arteries without sider such an approach to be contraindicated [27,56]. There have poorer therapeutic responses than do their idiopathic PAH are no clinical or hemodynamic characteristics that are pre- counterparts [81—83]. One possible explanation for this dis- dictive of this complication. Overbeek et al. In one retrospective study of 12 patients with associated PAH patients to tissue samples from 11 patients advanced idiopathic PVOD listed for lung transplantation, con- deemed to have the idiopathic form the disease [84].

Inter- tinuous intravenous epoprostenol conferred significant im- estingly, the investigators observed evidence of remodeling of provements in NYHA functional class and haemodynamic both the arterial and venous pulmonary microvasculature in all indices in most patients after 3—4 months of therapy [75].

SSc cases and a typical pattern of PVOD in half of these Treatment was well tolerated, and mild pulmonary oedema individuals. By contrast, venous involvement was present in was observed in only one patient. However, in comparison to less than a third of the idiopathic PAH group. This high rate of the standard approach adopted for idiopathic PAH patients, a post-capillary involvement in CTD-associated PAH was also slower dose augmentation strategy was undertaken and target documented by Dorfmuller et al.

In addition, high doses of and pre-septal venules in six out of eight CTD patients diuretic therapy were co-administered. Firstly, durable treatment PAH that do not meet therapeutic targets with monotherapy effects with epoprostenol are unusual and eventual clinical [85,86]. A supervised setting is necessary in order to closely nurses and paramedical health staff as appropriate.

Serial monitor for the development of worsening oxygenation or evaluations e. In our centre, patients with PVOD exam, 6 min walk test, chest radiograph, blood testing, pul- commencing vasodilator therapy are routinely hospitalized in monary function testing and echocardiography is advisable. Recognizes a new development on university campuses: He was Simon, due to the fact that Amir would need death certificates of his parents Hassan and Farzana.

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