Rheumatoid Arthritis in Catalonia: Diagnostic and Therapeutic Delayed and the Role of Medical Equipment

Haitham Hassan Khalil^*

Department of Medicine, Vanderbilt University Medical Center, Nashville, United States

Abstract

Objective

Diagnosis and therapy of patients with early onset rheumatoid arthritis (RA) is influenced by accessibility to specialized care devices. We attempted to analyze the impact of their availability.

Methods

We analyzed time related to diagnosis delay measuring: (1) Time from first clinical symptoms to the first visit with the rheumatologist; (2) Time from referral to the first visit of rheumatology; (3) Time between first symptom until final diagnosis; (4) Time between first symptom until the initiation of the first disease-modifying antirheumatic drug (DMARD). The presence of these 6 rheumatology devices was defined: (1) Early arthritis monographic clinics, (2) RA monographic clinics, (3) mechanisms for fast programming, (4) algorithms for referral from primary care (PC), (5) rheumatology consultation services in PC and (6) consulting services in PC.

Results

The mean time from onset of symptoms to diagnosis or the establishment of a DMARD in RA patients in Catalonia is very long (11 months). Patients seen in rheumatology devices such as RA monographic clinics, rheumatology consultation in PC and specially in early arthritis clinics are treated early with DMARDs.

Conclusion

The existence of monographic clinics or consulting in primary care centers is essential to improve early care of RA patients.

Keywords

Discoid lupus erythematosus • Cutaneous lupus erythematosus • Connective tissue diseases • Delphi method • classification criteria • World congress of dermatology

Introduction

The bracket of pulmonary hypertension (PH) has gone through a series of changes since the first bracket was proposed in 1973 at a transnational conference on primary PH (PPH) championed by the World Health Organization. The original bracket designated only 2 orders, PPH or secondary PH, depending on the presence or absence of identifiable causes or threat factors. Twentyfive times latterly, the 2nd World Symposium on Pulmonary Arterial Hypertension (PAH) was held in Evian, France. The “Evian bracket” tried to produce orders of PH that participated pathologic and clinical features as well as analogous remedial options. This was a much broader, more encompassing bracket, with 5 major orders; it allowed investigators to conduct clinical trials in a well- defined group of cases with a participated underpinning pathogenesis. This has led to multiple clinical trials and the blessing of 8 different specifics worldwide for the treatment of PAH [1].

The 3rd World Symposium on PAH was held in Venice, Italy, 5 times after the Evian conference. At this conference, the impact and utility of the “Evian bracket” was reviewed, and modest changes were made. The most notable change was to abandon the term PPH in favor of idiopathic pulmonary arterial hypertension (IPAH); domestic PAH if there's a family history of PAH; or associated PAH if another cause, similar as connective towel complaint or mortal immunodeficiency contagion (HIV), is present. Although the term PPH had come well hardwired in the literature after Dresdale first used it in 1951 it had come clear that the pathologic changes and response to remedy were analogous in several other conditions or conditions. The term “secondary PH” had been abandoned at the Evian meeting because it was confusing and didn't help with opinion or in directing treatment. The other prominent change made at the Venice meeting was to move pulmonary veno- occlusive complaint (PVOD) and pulmonary capillary hemangiomatosis (PCH) from separate orders into a single subcategory of PAH. These 2 realities have numerous parallels with each other, which will be bandied latterly in this composition, as well as some parallels with PAH. The 2008 4th World Symposium on PH held in Dana Point, California, handed the occasion to slightly modify the former clinical groups [2].

Materials and Method

Aminorex, fenfluramine derivations, and poisonous rapeseed oil painting represent the only linked “definite” threat factors for PAH. A recent retrospective analysis of further than 100 cases of PAH associated with fenfluramine exposure showed that this order shares clinical, functional, hemodynamic, and inheritable features with IPAH, suggesting that fenfluramine exposure represents a implicit detector for PAH without impacting its clinical course. The most recent surveillance study of PH, Surveillance of Pulmonary Hypertension in America (SOPHIA), enrolled 1,335 subjects at tertiary PH centers in theU.S. Between 1998 and 2001(17) [3]. This study verified the association of fenfluramine and dexfenfluramine input with the development of PAH. The average yearly number of IPAH cases didn't change during the study, which was, still, conducted after fenfluramine and its derivates had been withdrawn from theU.S. Request. A new finding was that St. John's Wort( odds rate( OR)3.6,vs. thromboembolic PH) and untoward antiobesity agents containing phenylpropanolamine( OR5.2,vs. thromboembolic PH) also increased the threat of developing IPAH. The SOPHIA study examined input of a variety of unselective monoamine reuptake impediments, picky serotonin reuptake impediments, antidepressants, and anxiolytics, and set up no increased threat for developing PAH( 17). still, a recent case- control study of picky serotonin reuptake asset use in pregnant women after 20 weeks of gravidity showed an increased threat( OR6.1) in the seed of developing patient PH of the invigorated, a form of PAH( 18). Grounded on this study, picky serotonin reuptake impediments may play a part in the development of PH, at least in association with gestation, and thus they've been reclassified in the “possible” order [4].

Amphetamine use represents a “likely” threat factor for PAH, although they're infrequently taken as a single agent and are constantly used in combination with fenfluramine. A recent comprehensive retrospective study suggested a strong relationship with the use of methamphetamine (gobbled, smoked, oral, or intravenous) and the circumstance of IPAH. Grounded primarily on the results of this study, methamphetamine use is now considered a “veritably likely” threat factor for the development of PAH. Fresh changes in medicine- and poison- convinced PAH will be bandied latterly. With the exception of heritable haemorrhagic telangiectasia associated with PAH, the first 3 subcategories of Group 1, idiopathic, inheritable, and medicine- and poisonconvinced PAH, are all associated with the development of insulated pulmonary arterial conditions [5].

PAH associated with connective towel conditions

PAH associated with connective towel conditions represents an important clinical group. The frequence of PAH has been well established only for systemic sclerosis. Two recent prospective studies using echocardiography as a webbing system and right heart catheterization for evidence set up a frequence of PAH of between 7 and 12( 20, 21). Several long- term studies suggest that the outgrowth of cases with PAH associated with systemic sclerosis is markedly worse than that of cases with IPAH, despite the use of ultramodern curatives [6].

Importantly, PAH doesn't represent the only cause of PH in systemic sclerosis. Pulmonary hypertension owing to lung fibrosis is also frequent (22), and diastolic left heart dysfunction isn't uncommon (23). There's also primary cardiac involvement in the complaint process (24). These compliances emphasize the significance of a complete evaluation when PH is suspected in cases with systemic sclerosis and the need for right heart catheterization to confirm the opinion of PH and to directly classify its etiology to determine applicable treatment [7].

In systemic lupus erythematosus and mixed connective towel complaint the frequence of PAH remains unknown but likely occurs less constantly than in systemic sclerosis. In the absence of fibrotic lung complaint, PAH has been reported rarely in other connective towel conditions similar as Sjögren pattern polymyositis or rheumatoid arthritis.

HIV infection

Pulmonary arterial hypertension is a rare but wellestablished complication of HIV infection. Epidemiologic data in the early 1990s, a time when remedy with largely active antiretroviral remedy wasn't yet available, indicated a frequence of0.5 (95 confidence interval0.10 to0.50)( 34). The frequence of HIV- associated PAH was estimated more lately and showed a stable frequence of 0.46 (95 confidence interval0.32 to0.64) [8]. Mortal immunodeficiency contagion- associated PAH has clinical, hemodynamic, and histologic characteristics analogous to those seen in IPAH. The medium for the development of PH remains unclear. Because neither the contagion nor viral DNA has been set up in pulmonary endothelial cells, an circular action of contagion through secondary couriers similar as cytokines, growth factors, endothelia, or viral proteins is explosively suspected. Unbridled studies suggest that cases with severe HIVassociated PAH could profit from baseman or long- term infusion of epoprostenol. Interestingly, in a substantial number of cases, normalization of pulmonary vascular hemodynamic can be attained with remedy indicated for PAH; this is veritably infrequently seen in IPAH [9].

Portopulmonary hypertension

The development of PAH in association with elevated pressure in the portal rotation is known as portopulmonary hypertension (POPH). Portal hypertension, rather than the presence of underpinning liver complaint, is the main determining threat factor for the development of POPH. Prospective hemodynamic studies have shown that 2 to 6 of cases with portal hypertension have PH. Right heart catheterization is absolutely obligatory for the definitive opinion of POPH because several factors may increase pulmonary arterial pressure (PAP) in the setting of advanced liver complaint (e.g., high inflow associated with the hyperdynamic circulatory state and increased pulmonary capillary wedge pressure owing to fluid load and/ or diastolic dysfunction). Pulmonary vascular resistance (PVR) is generally normal in these cases. Pathologic changes in the small highways appear identical to those seen in IPAH. A recent multicenter casecontrol study linked 2 threat factors for the development of POPH womanish coitus and autoimmune hepatitis. Interestingly, hepatitis C infection was associated with a dropped threat. A recent, large cohort study of POPH showed that long- term prognostic was related to the presence and inflexibility of cirrhosis and to cardiac function [10].

Discussion

Occlusion of the microvasculature by metastatic excrescence emboli represents another rare cause of fleetly progressive PH. The original laboratory evaluation shows hypoxemia, frequently severe, with a clear lung field. Reckoned tomography scanning doesn't show proximal thrombi but frequently shows thickening of septa. In discrepancy, the V/ Q lung checkup is generally abnormal with multiple subsegmental perfusion blights. Pulmonary microvascular cytology slice through a pulmonary roadway catheter in the wedge position is an important individual tool. The maturity of reported cases does in association with bone, lung, or gastric lymphomas.

Cases with mediastinal fibrosis may present with severe PH owing to contraction of both pulmonary highways and modes (138, 139). V/ Q checkup, reckoned tomography, and pulmonary angiography are veritably useful for accurate opinion, but findings can mimic proximal thrombotic inhibition. The predominant etiology is histoplasmosis, although mediastinal fibrosis has been reported with other fungal organisms, with tuberculosis, and in cases with sarcoidosis.

Incipiently, PH has been reported in cases with endstage renal complaint (ESRD) maintained on long- term hemodialysis. Grounded on echocardiographic studies, the frequence of PH in this patient population is estimated at over to. There are several implicit explanations for the development of PH in cases with ESRD. Hormonal and metabolic derangement associated with ESRD might lead to pulmonary vascular condensation. The PAP may also be increased by high cardiac affair (performing from the arteriovenous access itself and frequently attendant anemia) as well as fluid load. In addition, diastolic and systolic left heart dysfunctions are frequent in this setting.

Conclusions

In streamlining the bracket of PH, we incorporated recent findings and sought to clarify areas of nebulosity. We believe that this interpretation is both further comprehensive and more scrutable and hope that it'll also be more useful to clinicians, pending farther exploration into this different complaint.

Conflicts of Interest

None

References

1. Mitchell KL, Pisetsky DS.  Early rheumatoid arthritis. Curr Opin Rheumatol. 19,278-283 (2007).

Indexed at, Google Scholar, Crossref

2. Haraoui B. Assessment and management of rheumatoid arthritis. J Rheumatol Suppl. 82, 2-10 (2009).

Indexed at, Google Scholar, Crossref

3. Bahadori B, Uitz E, Thonhofer R et al. omega-3 Fatty acids infusions as adjuvant therapy in rheumatoid arthritis.  J Parenter Enteral Nutr. 34,151-155 (2010).

Indexed at, Google Scholar, Crossref

4. O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J. 350, 2591-602 (2004).

Indexed at, Google Scholar, Crossref

5. Birch JT, Bhattacharya S. Emerging trends in diagnosis and treatment of rheumatoid arthritis. Prim Care. 37,779-92 (2010).

Indexed at, Google Scholar, Crossref

6. Smolen J, Aletaha D. The burden of rheumatoid arthritis and access to treatment, a medical overview. Eur J Health Econ. 2, 39-47 (2008).

Indexed at, Google Scholar, Crossref

7. Seidel W, Pierer M, Häntzschel H et al. Internist's therapy of rheumatoid arthritis. Internist (Berl). 45,693-705 (2004).

Indexed at, Google Scholar, Crossref

8. Mangkorntongsakul V, Phan K, Smith SD et al. Pemphigus and rheumatoid arthritis, A systematic review and meta-analysis. Dermatol Ther. 34, 14845 (2021).

Indexed at, Google Scholar, Crossref

9. March L, Lapsley H. What are the costs to society and the potential benefits from the effective management of early rheumatoid arthritis?  Best Pract Res Clin Rheumatol. 15,171-85 (2001).

Indexed at, Google Scholar, Crossref

10. Akkoc N, Akar S. Standardization is essential for a more rigorous comparison of rates, comment on the reply by Gilgil, Kacar, and Tuncer. Clin Rheumatol. 26,136 (2007).

Indexed at, Google Scholar, Crossref