|Year : 2020 | Volume
| Issue : 2 | Page : 62-68
An ayurvedic approach to diagnosis and management of psoriatic arthritis on principles of Vatarakta: A review
Yogesh Kumar Pandey, Mansi Grewal
Department of Kayachikitsa, CBP Ayurved Charak Sansthan, New Delhi, India
|Date of Submission||01-May-2021|
|Date of Decision||28-May-2021|
|Date of Acceptance||23-Jul-2021|
|Date of Web Publication||25-Aug-2021|
Dr. Mansi Grewal
Department of Kayachikitsa, CBP Ayurved Charak Sansthan, Khera Dabar, New Delhi - 110 073
Source of Support: None, Conflict of Interest: None
Psoriatic arthritis (PsA) is inflammatory arthritis usually occurring in patients with psoriasis. Even though skin disease and joint involvement are linked in PsA, they can occur irrespective of each other. An equivalent entity in Ayurvedic literature, Vatarakta is a disabling illness occurring due to the concurrent aggravation of Vata and Rakta. Its Moolasthana (~primary site) of manifestation is joints of hands and feet. With this article, we aim to develop a clinical approach to PsA on the principles of Vatarakta. Relevant information from authentic texts of Ayurveda and contemporary medical literature is gathered, and facts are analyzed to find similarities and dissimilarities between PsA and Vatarakta's etiology, pathogenesis, clinical features, prognosis, and management principles. It was seen that PsA bears similarity to Vatarakta on grounds of etiology, pathogenesis, and clinical features. The few differences seen are not found to be conceptually contradictory. Concepts of Vatarakta can explain the vascular, dermal, musculoskeletal, and systemic changes seen in PsA. The differential of Asthimajjagata Kushtha, Kushtha Updrava, and Aamvata is mandatory to rule out any diagnostic dilemma. Often the patients with psoriasis and/or PsA have hyperuricemia, which has been long viewed and treated on principles of Vatarakta. Hence, Vatarakta may be seen as an umbrella term for immune-mediated or inflammatory musculoskeletal disorders with dermal and systemic manifestations. Clinically, PsA can be understood and managed on principles of Vatarakta.
Keywords: Inflammatory arthritis, psoriasis, psoriatic arthritis, Vatarakta
|How to cite this article:|
Pandey YK, Grewal M. An ayurvedic approach to diagnosis and management of psoriatic arthritis on principles of Vatarakta: A review. AYUHOM 2020;7:62-8
|How to cite this URL:|
Pandey YK, Grewal M. An ayurvedic approach to diagnosis and management of psoriatic arthritis on principles of Vatarakta: A review. AYUHOM [serial online] 2020 [cited 2021 Sep 20];7:62-8. Available from: http://www.ayuhom.com/text.asp?2020/7/2/62/324635
| Introduction|| |
Psoriatic arthritis (PsA) is a chronic inflammatory musculoskeletal disease with systemic manifestations usually in individuals with psoriasis, mainly plaque psoriasis variant. Severe arthritis is considered to be associated with pustular psoriasis. Besides joint involvement, PsA also affects tendons and ligaments leading to dactylitis or enthesitis. It also affects nails causing pitting and onycholysis. Although the true incidence and prevalence of PsA are underestimated, it is reported in <1% of the worldwide general population, with a range of 7% to 42% in patients with psoriasis. In 60%–70% of cases of PsA, psoriasis precedes joint disease. In 15%–20% of cases, both appear within 1 year of each other. In about 15%–20% of cases, arthritis precedes the manifestation of psoriasis. So even though the skin and joint involvement are linked, they can occur irrespective of each other, as seen in PsA sine psoriasis which occurs in 20% PsA cases. There are about 166 skin diseases in Ayurveda and prime importance is given to classifications of Kushtha. Vatarakta is another clinical entity that has dermal, musculoskeletal, and systemic manifestations causing severe, debilitating Vedana (~discomfort).
As per Ayurvedic literature, Vatarakta, a clinical diagnostic entity, is caused by concurrent aggravation of both Vata and Rakta, by their respective causative factors, which fuels the pathogenesis of Vatarakta, making it difficult to cure with its quick progression, akin to combination of wind and fire. It results in severe, debilitating Vedana (pain), manifested in small joints of hands and feet, which later on progress to other joints and deeper tissues.
The present article is an attempt to find similarities and dissimilarities between etiology, pathogenesis, clinical features, prognosis, and management of PsA and Vatarakta. It also attempts to find if PsA can be managed on principles of Vatarakta.
| Materials and Methods|| |
Ayurveda ancient texts referred are Brihattrayee, Laghutrayee, Yogratnakar, Chakradutta, and Bhaishajya Ratnavali.
Contemporary modern texts referred are Harrison's principle of internal medicine 20th edition, Kelley and Firestein's Textbook of Rheumatology 10th edition, Oxford textbook of PsA.
Previous work done on PsA as Vatarakta was assessed through Google scholar using keywords PsA and Vatarakta and it showed two relevant works., The conceptual and clinical analysis of facts is done to find the relation between PsA and Vatarakta.
| Results|| |
While exact etiology of PsA remains unknown, contribution of genetic factors, environmental and immunologic influences such as cytokines, the role of infection, and trauma in the development and progression of disease are hinted at.
Various factors are responsible for Vata and Rakta vitiations for the development of Vatarakta. The dominance of element of Agni and character of Tikshnata (~sharpness) and Dravata (~fluidity) in the causative factors of Vatarakta is likely to disturb the physiological properties of Raga and Dravata in Rakta. Change in Raga which is due to Agni element and Dravata due to Jala element is visible in patients of Vatarakta in the form of Vaivarnya, Shotha, Daha. Sthaulya (~obesity), Madya (~alcohol), and Vyayama (~exercise) are also mentioned as etiological factors of Vatarakta.
Anatomical sites prone for the development of Vatarakta are hands, feet, fingers including toes and later on all joints. In the beginning, hands and feet are affected. Later on, it spreads to other parts of the body due to subtle pervasive nature of Vata and Rakta. Sequential events in pathological cascade of Vatarakta are depicted in [Figure 1].
PsA can affect synovial membrane, entheses, juxta articular bone, tendon sheaths along with extra articular systemic manifestations. There is increased vascularity in fibrous part of enthesis, subentheseal bone, etc. Altered bone remodeling is a key feature which is the combined effect of bone formation and resorption by osteoclasts evidenced by marked increase in osteoclast precursors in blood of PsA afflicted individuals. Moll and Wright classified clinical patterns of PsA into 5 subsets of asymmetrical oligoarthritis, symmetrical polyarthritis, distal interphalangeal arthritis, arthritis mutilans, and predominant spondyloarthritis. Nail pitting, horizontal ridging, onycholysis, yellowish discoloration of nail margins, dystrophic hyperkeratosis, and combinations of all these are seen in PsA.
Vatarakta manifests in the form of three distinct clinical conditions, Uttana (~superficial seated) in Tvaka (~skin) and Mamsa (~muscles), Gambhira (~deep seated) in Meda (~adipose), Asthi (~bone), Majja (~marrow), Shukra (~regenerative tissue), and Ubhayashrita (~involving both seats).
Classification criterion for psoriatic arthritis (CASPAR) is widely accepted and well validated with sensitivity of 0.914 and specificity of 0.987 even in early PsA patients.
Diagnostic and prognostic criteria are proposed for Vatarakta in [Table 1].
|Table 1: Clinical staging of Vatarakta - Diagnostic and prognostic Ayurvedic approach|
Click here to view
Treatment recommendations for PsA are as per European league against rheumatism (EULAR) guidelines. Nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, interleukin 12/13 or 17 inhibitors, phosphodiesterase 4 inhibitors are used. Initial response to therapy is evaluated at 3–6-month time period.
Site of involvement and intensity of Dosha Prakopa (~vitiation) form the basis of treatment for Vatarakta. As obstruction in pathway of Vata is one of the pathological hallmarks of Vatarakta, bloodletting is done to remove it. Vata predominant Vatarakta patient can also be planned for Mridu Virechana (~ mild, induced purgation) of Ruksha (~dry) or Ishat snigdha (~ with mild oleation) nature. If patient has dryness in his body, Virechana (~induced purgation) should be done after sufficient oleation. Basti (~medicated enema) is the treatment of choice in Vatarakta. Therefore, it is repeatedly given to the patient., In case of deep-seated Vatarakta, Rakta is under strong influence of Vata. Hence, the physician is first required to manage the imbalanced Vata using treatment described for Vatavyadhi. Thereafter, the treatment of Vatarakta is started.
PsA has several similarities with Vatarakta as mentioned in [Table 2]. There are a few differences as well between the two diseases as mentioned in [Table 3].
| Discussion|| |
At present, there is no widely accepted Ayurvedic correlation for PsA. Psoriasis is commonly correlated to Kushtha, but there are differences of opinion on which type of Kushtha better explains psoriasis. Psoriasis is often diagnosed clinically as Kitibha, Ekkushtha, Sidhma, Mandal kushtha, where the latter has totally different Dosha dominance than others. These clinical diagnoses are also insufficient to cover the subtypes of psoriasis such as pustular and erythrodermic variant. Hence, although psoriasis has been long viewed and treated as Kushtha, it remains to be seen whether its various subtypes can also be viewed through the lens of Uttana Vatarakta with variable Dosha dominance because most medications given in Vatarakta are also effective in treating Kushtha and vice versa.
Concepts of Vatarakta can explain the vascular, dermal, musculoskeletal, and systemic changes seen in PsA. The differential of Asthimajjagata Kushtha, Kushtha Updrava, and Aamvata is mandatory to rule out any diagnostic dilemma. PsA is a manageable condition and therefore cannot be viewed as Gambhirdhatu gata Kushtha, which is Asadhya. They are also different because the severity of pain associated with inflammatory arthritis is not seen in patients with AsthiMajjagata Kushtha whereas Atyartha Dusaha Vedana (~excessive pain) is a feature of Vatarakta. Only supraclavicular involvement is mentioned in AsthiMajjagata Kushtha which does not explain the most common subtype of peripheral arthritis in PsA. It is not merely Kushtha Updrava because in 15%–20% patients, PsA occurs before skin involvement which contradicts the concept of Updrava. In Kushtha Updrava, disease progression is linked to excess Kleda predisposing to the involvement of Krimi which damages the tissues and results in deformity, whereas the deformities of PsA are due to bone remodeling and inflammation which can be explained through Vatarakta. PsA is not similar to Aamavata because of the absence of dermal manifestations and discoloration in patients with Aamvata Psoriatic skin lesions are indurated papule to plaque with prominent erythema and desquamation which bleeds on removal of scale. There is tendency to develop new lesions on area of trauma. Skin lesions are seen in prodrome, superficial, and mixed variety of Vatarakta due to involvement of Tvaka. Pidika and Mandalotpatti as indurations of Uttana Shotha with violaceous or erythematous base, along with altered hidrosis and itching, indicate the lodging of Vata, Rakta, and Kapha in tissues. Scaling can be considered a Vata dominant Vedana due to unchecked division of skin as epidermal hyperplasia. Resultant Ruksha, Parusha, and Sphutita desquamation with underlying Raktata and Snigdhta as shiny erythematous base with bleeders closely mimics Vata Rakta dominant and associated Kapha vitiation in Tvaka and superficial tissues. Erythrodermic and pustular psoriasis indicate dominance of Vata, Rakta, and Pitta. Often the patients with psoriasis and/or PsA have hyperuricemia, which has been long viewed and treated on principles of Vatarakta.
Even if Kushtha is primary diagnosis of psoriasis, PsA can still be understood as Vatarakta. Because debility due to any prolonged and uncontrolled illness is said to aggravate Vata. This aggravated Vata can be vitiated further by direct causative factors of Vatarakta. Pathological state of Rakta is preexisting in patients of Kushtha, it can get vitiated further by direct causes of Rakta Dushti in Vatarakta. The pathological cascade of a disease is unbiased because the entire body is its potential host where it can modify, change course, and pave way for other diseases in its course of illness. Vyadhi sankara can occur at any state irrespective of the type of disease. Moreover, the presence of Vyadhi sankara does not negate the potential of a disease to occur independently.
In PsA, damage to joint structures due to proinflammatory states is primarily due to tortuous hypervascularity in synovium. The chronic inflammatory state is also associated with uncoupling in osteoblast-osteoclast homeostasis leading to faulty bone remodeling.
The vascular phenomenon can be correlated with actions of vitiated Rakta and the erosive/tissue destructive state/faulty remodeling can be correlated with actions of vitiated Vata which occurs primarily on Asthi (~bone) due to negative Ashraya-Ashrayi bhava (~unique concept of interdependency between bodily tissues and humors) between the two. Asthi is a physiologic abode of Vata. Any increase in action of imbalanced Vata decreases the normal functioning of Asthi and vice versa Therefore, imbalanced Vata leading to Asthi kshaya (~decreased bone tissue) and pain in Sandhi, Asthi, and Majja in Vatarakta can be understood as unchecked osteoclastogenesis due to differentiation of monocytes into osteoclasts by signals like RANKL (receptor activator of nuclear factor kappa B ligand). In PsA, there is marked upregulation of RANKL which can be understood as a vitiated Vata phenomenon. The phenomenon of pro-inflammation and osteoclast-blast uncoupling have codependent role in disease pathogenesis, similar to involvement of Rakta and Vata.
Involvement of Pittadi in illness can be explained by affected synovium/synovial fluid which can be correlated with Sleshmadhara kala (~membrane secreting synovial fluid) and Sleshaka Kapha (~synovial humor), respectively. Lasika (~tissue fluid) and Rakta (~blood) are sites of Pitta; therefore, tissue fluid accumulation after extravasation of intravascular volume due to inflammation can be considered a Pittaja phenomenon. Joints are primary site of manifestation of Vatarakta and PsA due to their normal anatomic Vakrata at gross level and pathological Vakrata in joint vasculature (~tortuous hypervascularity) due to dysregulated angiogenesis. The tortuosity affects physiological flow of blood. Peripheral arthritis characteristically occurs early in PsA disease course, similar to Hasta Pada involvement in Vatarakta.
Differences that we found are not contradictory to the conceptual analysis. Even when genetic component of PsA is not directly mentioned in chapters of Vatarakta, concept of Aadibala pravritta Vyadhi stands true for all genetic disorders. There are different opinions on Moha as the complication of Vatarakta. As per Ayurvedadipika commentary on the matter, some Acharya mention Meha in place of Moha. Comorbidities of metabolic syndrome are seen in PsA and can be viewed under light of Meha. Nail involvement in PsA makes Vata involvement apparent because Nakhbheda is a disease caused by Vata.
| Conclusion|| |
PsA shows many similarities to Vatarakta, but they are not the same. There are differences in Vatarakta and PsA as well but these are not conceptually contradicting. And after taking all the aspects into consideration, it is safe and seems logical to say that Vatarakta can be seen as an umbrella term for several joint disorders that have both dermal (local or generalized) and systemic manifestations. Integrative approach of concepts of contemporary and Ayurvedic sciences has clinical relevance. In Ayurveda, Chikitsa is said to be one which subsides the current disease without breeding another illness. Hence, management through disease-modifying immunosuppressive therapies is not wholesome. Whereas treatment of PsA on principles of Vatarakta seems a promising area of research.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jameson JL, Kasper DL, Longo DL, Fauci AS, Hauser SL, Loscalzo J, et al. The spondyloarthritides. In: D Taurog, J(eds.) Harrison's Principles Of Internal Medicine. New York: Mc-Graw Hill Education; 2018. p. 2571.
Gladmann DD, Antoni C, Mease P, Clegg DO, Nash P. Psoriatic arthritis: Epidemiology, clinical features, course, and outcome. Ann Rheum Dis 2005;64 Suppl 2:ii, 14-7.
Olivieri I, Padula A, D'angelo SA, Cutro MS. Psoriatic arthritis sine psoriasis. J Rheumatol Suppl 2009;83:28-9.
Pandey YK, Meena A, Gaur MB, Sabharwal P. Dermatological manifestations in Ayurveda : A review. EJPMR, 2019;6:277-93.
Shruthi S, M Kumar A, Lohith B A, M Shankar U, Mishra G. Ayurvedic management of psoriatic arthritis: A case study. Int J Appl Ayurveda Res 2017;2:1472-7.
Dhone P, Jadhav M, Psoriatic arthritis and Vatarakta
: A comparative literary review. IJRAP 2017;8:8-10.
De Vlam K. Overview of psoriatic arthritis pathogenesis. In: Fitzgerald O, Gladmann D, editors. Oxford Textbook of Psoriatic Arthritis. Great Calrendon Street, Oxford, United Kindgom: Oxford University Press; 2018. p. 21-30.
De Vlam, K. Overview of psoriatic arthritis pathogenesis. In: Fitzgerald, O, Gladmann, D (eds.) Oxford Textbook Of Psoriatic Arthritis. Great Calrendon Street, Oxford, United Kindgom: Oxford University Press; 2018. p. 25.
Laloux L, Voisin MC, Allain J, Martin N, Kerboull L, Chevalier X, et al. Immunohistological study of entheses in spondyloarthropathies: comparison in rheumatoid arthritis and osteoarthritis. Ann Rheum Dis. 2001;60(4):316-21.
Colucci S, Brunetti G, Cantatore FP, Oranger A, Mori G, Quarta L, et al. Lymphocytes and synovial fibroblasts support osteoclastogenesis through RANKL, TNFalpha, and IL-7 in an in vitro
model derived from human psoriatic arthritis. J Pathol 2007;212:47-55.
Moll JM, Wright V. Familial occurrence of psoriatic arthritis. Ann Rheum Dis1973;22:181-95.
Jameson JL, Kasper DL, Longo DL, Fauci AS, Hauser SL, Loscalzo J, et al.
The spondyloarthritides. In: D Taurog, J(eds.) Harrison's Principles Of Internal Medicine. New York: Mc-Graw Hill Education; 2018. p. 2572.
Tillett W, Costa L, Jaden D, Wallis D, Cavill C, McHugh J, et al
. The Classification for Psoratic Arthritis (CASPAR) criteria-a retrospective feasibility, sensitivity, and specificity study. J Rheumatol 2012;39:154-6.
Gossec L, Smolen JS, Gaujoux-Viala C, Ash Z, Marzo-Ortega H, Van der Heijde D, et al
. European league against rheumatism recommendations for the management of psoriatic arthritis with pharmacological therapies. Ann Rheum Dis 2012;71:4-12.
Tsuruta N, Imafuku S, Narisawa Y. Hyperuricemia is an independent risk factor for psoriatic arthritis in psoriatic patients. J Dermatol 2017;44:1349-52.
De Vlam K. Overview of psoriatic arthritis pathogenesis. In: Fitzgerald, O, Gladmann, D (eds.) Oxford Textbook Of Psoriatic Arthritis. Great Calrendon Street, Oxford, United Kindgom: Oxford University Press; 2018. p. 28.
Acharya Vagbhatta. Doshadivigyaneeya 11/26-28. In: Gupta AK (ed.) Ashtangahridayam, Sutrasthana. Varanasi: Chaukhambha Prakashan; 2018. p. 117.
De Vlam, K. Overview of psoriatic arthritis pathogenesis. In: Fitzgerald, O, Gladmann, D (eds.) Oxford Textbook Of Psoriatic Arthritis. Great Calrendon Street, Oxford, United Kindgom: Oxford University Press; 2018. p. 28,86.
Acharya Vagbhatta. Doshabhediya.12/02 In: Gupta AK (ed.) Ashtangahridayam, Sutrasthana.Varanasi: Chaukhambha Prakashan; 2018. p.120.
[Table 1], [Table 2], [Table 3]