Introduction
Chronic urticaria (CU) is a debilitating allergic skin disease, which affects 0.5%–1% of the population and is characterized by erythematous, papulous, and itchy lesions of a fluctuating nature that persists for over 6 weeks.[1] It is highly complex in relation to its etiology and treatment is challenging, even for experts.
CU interferes with subjective well-being and daily life; some patient's health status is comparable to that of coronary artery disease and severe asthma patients. It also causes inconvenience in family structures, compromising performance at work, school, and negatively impacting on leisure activities.[23]
Chronic urticaria also has a number of other characteristics:[4]
- -Wheals lasting more than 1 h (unlike simple dermatographic urticaria) and <24–36 h (unlike urticarial vasculitis). Lesions may be indurated and painful
- -The natural course of the disease varies greatly without breaks and remissions that can last from a few months to more than 20 years
- -Major repercussions on quality of life (QoL) that are considered equivalent to those in severe coronary disease[25]
- -No underlying food or drug allergies.
CU is divided into inducible urticaria (triggered by specific physical stimuli) and spontaneous (or idiopathic) urticaria.[6] In at least one-third of idiopathic presentations, the etiology is autoimmune and could be associated with thyroid autoimmunity, with or without clinical hypothyroidism.[7] As well as presenting antithyroid antibodies more frequently than the general population,[7] CU patients may have IgG antibodies targeting circulating immunoglobulin E (IgE) or (much more often) a subunit of the IgE high-affinity receptor (FcεRI).[8] These antibodies may be present in other autoimmune processes such as lupus or dermatomyositis, although in autoimmune CU, they correspond to the IgG1 or IgG3 subclass, which is capable of activating complement and generating anaphylatoxins such as C5a. In other words, they are functional, a characteristic that is considered to be specific of autoimmune CU.[9]
In a very small number of patients, severe, debilitating urticaria, associated possibly with airway angioedema, bronchospasm, and hypotension, persists despite treatment with high-dose H1 anti-histamines; H2 anti-histamines and/orLTRA; corticosteroids; and, perhaps, dietary interventions. These patients usually have autoimmune urticaria.
In terms of etiology, autoimmune urticaria is a subset of immunologic urticarias. In 1983, Leznoff and Sussman[10] first reported on the association between CU and autoimmune thyroid disease.
In allopathy, so many clinical trials are available on CAU management, but patients who had taken oral or parenteral corticosteroids, methotrexate, cyclosporine, or other immunosuppressant medications during the 4 weeks before screening were excluded in these studies. In Ayurveda also, many clinical trials has been conducted on urticaria, but none of them is specific to this type of CAU case which is steroid resistant and nonresponsive to cyclosporine. Hence, this case study is unique where this type of patient responded well to vamana therapy and oral Ayurvedic medicines without any side effect.
Case Report
A 38-year-old female working in a pharmaceutical company visited the pañcakarma Outpatient Department (OPD) in CBPACS, New Delhi, on March 6, 2017. The patient was already taking medicines from AIIMS, New Delhi (UNID-102270027), where it was diagnosed as autoimmune urticaria with tinea cruris. It was also known case of autoimmune thyroiditis. The patient was complaining of the following symptoms:
- Urticarial erythematous, edematous wheals over trunk and bilateral upper and lower extremities without leaving behind pigmentation for 9 years
- Wheals associated with burning sensation for 1 month
- Wheals lasting for more than 24 h for 3 months
- Annular erythematous lesions on bilateral thighs and buttocks for 4 months
- Weight gain for 4 months
- Occasional oral ulcers for 2 years.
There was a history of raised blood pressure after starting tablet cyclosporine. There was no history of fever or angioedema. The frequency of episodes was initially 1 month every year, but persistent episodes of wheals were for the last 1 year. It was side effects of allopathic medicines;[11] the patient was getting rather than relief which forced her to give a chance to Ayurvedic therapy. The patient was diagnosed as udardda (Urticaria) and advised for vamana karma (therapeutic emesis) considering requirement of biopurification as steroids and cyclosporine were not working at all.
Clinical findings
The following were findings on physical examination:
General
- Pulse rate: 86/min, regular, normal sinus rhythm, blood pressure 150/100 mmHg
- Temperature: Afebrile, respiratory rate: 17/min
- No pallor/icterus/cyanosis/clubbing/pedal edema/palpable lymphadenopathy.
Systemic
No abnormality was noticed in any systemic examination.
Sounds were present.
Ayurvedic examination
Ayurvedic examination was done as per the [Table 1] and the findings are recorded in the Table. (Ideally table can be positioned here itself).
Table 1: Ayurvedic examination
Timeline
A detail of the case study and follow-up is given in [Table 2] (language used is the same as described in available prescriptions of AIIMS).
Table 2: Timeline
Diagnostic assessment
The case was already diagnosed as autoimmune urticaria in AIIMS, New Delhi. It was confirmed by ASST which was positive. Antithyroid peroxidase and anti-T4 antibodies were positive which confirmed association between chronic autoimmune urticaria and autoimmune thyroiditis [Table 3].
Table 3: Investigations of CAU patient
The available investigations were as follows
All symptoms of śītapitta-udardda-koṭhaare are described in Ayurveda[12] and can be summarized as below:
- varaṭīdaṣṭasamsthānaḥ śotha (edema-rash like an insect bite)
- kan[Latin Small Letter d with dot below]ūbahula (severe itching)
- toda bahula (excessive pricking pain)
- chardi (vomiting)
- jvara (fever)
- vidāha (burning sensation)
- bahūni (spreading all over the body).
So udardda was concluded to be Ayurvedic diagnosis. It has similar symptomatology, but only difference is “doṣika” dominancy, i.e., “śītapitta” has “vātika” dominancy, while “udardda” has “kaphaja” dominancy.
Therapeutic intervention
Considering the bahudoṣāvasthā (excessive toxins) of the disease, the patient was advised for vamana therapy to detoxify the body as kapha pitta doṣa were aggravated and vamana is considered best therapy for this condition. Fearing of consequences of cyclosporine, the patient got convinced for vamana immediately. Hence, citrakādi vaṭi[13] 500 mg was given for 3 days for dīpan-pācan purpose. snehapān (oral intake of ghrta) with pañcatikta ghrta guggulu 25 ml was started from March 9. Then, the dose was increased to 25 ml daily. On 7th day (March 15), 175 ml pañca was consumed. After observing samyak snehana (adequate oleation) symptoms, the patient was admitted on March 15. sarvāṅga abhyaṅga (massage all over body) with maricyādi tail[14] and sarvāṅga bāṣpa svedana (moist heat all over body) was performed on March 16 and 17. This oil gives immediate but temporary relief to the patient from symptoms such as itching and rashes. The patient was advised to take kaphotkleśaka (heavy diet) such as curd, halwa, or kheer on 16th evening. On March 17, vamana with madanaphala (Randia dumetorum) was performed empty stomach early in the morning as per classics.[15] Then, samsarjanakrama (specific diet regimen after vamana)[16]was followed for 7 days. Then, she was advised to continue oral medicines [Table 4] for 3 months and visit OPD monthly for follow-up.
Table 4: Oral Ayurvedic medicines given to case of chronic autoimmune urticaria
Follow-up and outcomes
On March 6, 2017, the patient's condition was assessed on UAS7 score,[17] CU-Q2oL score,[18]and Dermatology Life Quality Index score[19] which were 42, 110, and 30, respectively. After vamana, it reduced to 36, 108, and 28. Date wise scoring detail is given in [Table 5]. After 3 months, medication UAS7 score was 0, CU-Q2oL was 24, and DLQL score was 1. The patient skipped all allopathic medicines after vamana therapy, only tablet Allegra 180 mg s. o. s. she continued. Now, she could tolerate the urticarial attacks as it was less itchy and without burning sensation. After 3 months of treatment, the patient was stable only with Ayurvedic medicines. Urticarial wheals were without erythema or edema. Frequency was once in 15 days lasting for 2 h only. Tinea cruris was also cured. Weight reduced from 73 kg to 64 kg. Now, routine life was not hampering due to horrible urticarial lesions. Constipation was relieved. Oral ulcers were cleared. Sleep, appetite, and digestion also improved. Blood pressure also started remaining in the normal range, again. All investigations were within normal limits. Treatment was well tolerated by the patient and no side effect was noted during this duration.
Table 5: Assessment of a case of CAU on various scores
Discussion
CAU seriously compromises the health-related quality of life of patients due to debilitating and uncomfortable symptoms that may last for years. In addition to classic symptoms, such as pruritus and papules, other factors are more relevant for patients with CU, such as unpredictability of flares, sleep disorders, fatigue, drug-related side effects, and physical appearance. Thus, merely evaluating urticaria progress by counting lesions and measuring pruritus intensity is insufficient. A holistic evaluation of the patient is required for a better understanding of disease impact. Unfortunately, patients with CAU often have severe disease and are poorly responsive to antihistamines, even in high off-label dosages. Cyclosporine has been seen to be effective in selected patients who were ASST positive.[20] Other immunomodulators that have been reported effective in selected patients with CAU include intravenous immunoglobulin and plasmapheresis.[21] The presence of autoantibodies may be important clinically in a small group of severely affected, treatment-resistant patients, where immunomodulatory treatments may be helpful. The general line of treatment for udarddawastaken is taken into consideration for the case. The patient was treated with vamana along with a combination of drugs as discussed above with satisfactory clinical outcomes.
The autoimmune nature of disease along with kaphaduṣṭi initially started as itchy lesion. Hence, the primary doṣa is kapha when it involves the rasa dhātu and causes kan[Latin Small Letter d with dot below]ū (kaphaduṣṭi). Association of raktadhātu leads to erythematous wheals. vamana is said to be useful in the treatment of “śītapitta udardda kotha”[22] as udbhavasthāna is āmāśaya and svabhāva is āśukāri. Hence, vamana was planned as the first line of treatment for CAU and autoimmune thyroiditis for śodhana (cleansing of microcirculatory channels) purpose.
pañcatikta ghrta guggulu[23] is indicated in cytotoxicity, gan[Latin Small Letter d with dot below]amālā (Goiter), and gambhīrdhātugatakuṣṭha (group of various skin diseases which are deep root sited).goghrta pacifies the vikāras (symptoms) manifested due to vāta and pitta, beneficial for rasa, immunity, and hence shows effects on the skin causing a decrease in itching. Kamadudhā Ras[24] was given to pacify pitta doṣa with toxic conditions. Gudūchighanvati[25] is used as rasāyana (rejuvenation), so it was advised as an immunomodulator. gandhakarasāyana[26] is helpful in skin disorders especially associated with toxicity. haridrākhan[Latin Small Letter d with dot below]a[27] is indicated in śītapitta, udardda, and dadru (fungal infection) and effective in allergic conditions. ārogyavardhinīvaṭi[28] is malašuddhikari (helps in releasing toxins from body) and improves liver functions. khadirāriṣṭa[29] relieves itching and cures so many skin diseases. After vamana, the prescribed medicines helped in speedy recovery. It clearly proved better for prevention of the relapse of CAU.
Conclusion
In this study, the mean UAS decreased to 0, mean rescue medication use declined. Overall therapeutic response and QoL improved. This study shows that Ayurvedic drugs along with Vamana can be used safely for the treatment of tortuous CAU instead of hazardous steroids and cyclosporine.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Patient perspective
The patient, her family members, and relatives were fully satisfied with clinical outcome that it was without any side effects.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Acknowledgment
We are thankful to all technicians and attendants of pañcakarma department for providing all therapies to the patient with full dedication.
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