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A review on hyperuricaemia – A metabolic disease and its homoeopathic management
*Corresponding author: Dr. Divya Verma, Research Officer, Central Research Institute (Homoeopathy), Lucknow, Uttar Pradesh, India. vdivya1526@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Verma D, Agarwal N. A review on hyperuricaemia – A metabolic disease and its homoeopathic management. J Intgr Stand Homoeopathy. 2024;7:144-53. doi: 10.25259/JISH_45_2024
Abstract
Hyperuricaemia is a common health issue encountered in the daily clinical practice of a physician. The gradual increase in the incidence of hyperuricaemia across the world adds to the existing disease burden. The increased uric acid level for a prolonged period is linked to the development of various systemic and metabolic diseases such as hypertension, cardiovascular disorders, chronic renal disease, gout and nephrolithiasis. The conventional treatment of hyperuricaemia is based on urate-lowering therapy. Various studies have been done to understand the role of uric acid in the pathogenesis of such diseases. Studies conducted in the field of homoeopathy show the positive role of homoeopathic medicines in treating hyperuricaemia, which can be cost-effective and free from side effects. This article aims to focus on the pathogenesis of hyperuricaemia and the current trends regarding hyperuricaemia and its homoeopathic approach.
Keywords
Hyperuricaemia
Uric acid
Gout
Uric acid diathesis
Gouty diathesis
Uric acid stones
INTRODUCTION
Hyperuricaemia refers to the increase in the concentration of uric acid in blood above the normally accepted range, which is considered above 7.0 mg/dL in males and above 6.0 mg/dL in females.[1] Hyperuricaemia is a common condition that may affect patients of all age and gender. The increased levels may be attributed to either increased production, decreased excretion of uric acid, or both. Increased levels of uric acid may persist in a person for a long period without any complaints, known as asymptomatic hyperuricaemia.[2] It does not specifically require any treatment. On the contrary, serum uric acid above saturation level may commonly manifest itself in the form of gouty arthritis or nephrolithiasis. It also increases the risk for cardiovascular diseases, metabolic syndrome and neurodegenerative disorders.[3]
METHODS
A comprehensive search of the literature was conducted using PubMed, Cochrane database and general search terms such as hyperuricaemia, epidemiology, risk factors, pathophysiology, clinical manifestation, associated diseases, dietary management and its prevalence in India in particular were reviewed. Potential articles of interest were identified by title and abstract, and citation lists of articles of interest were used to identify additional literature. This review article is based on previously conducted studies and does not contain any studies with animals performed by any of the authors.
BACKGROUND
Uric acid was identified as a distinct substance for a long, along with the discovery of its role in the pathophysiology of Gout. In the year 1776, Carl Wilhelm Scheele, a Swedish chemist was the first one to discover uric acid in urine and kidney stone.[4] In the same year, this discovery was backed up by Bergman, who found a bladder stone composed of the same substance.[5]
Further, Murray Forbes, a Scottish physician, described in his work ‘A Treatise upon Gravel and Gout’ that if urine contains uric acid, the blood might have it too, thereby explaining the precipitation of uric acid in body parts resulting in the formation of tophi.[6] Based on this hypothesis, Wollaston, in 1797, isolated uric acid from a gouty tophus and urinary concretions. Following this, Alfred Baring Garrod conducted research at the University of London demonstrating increased uric acid levels in the blood of persons suffering from gout.[7]
Another contribution was made by Fischer, who demonstrated uric acid as a purine compound.[8] Folin and Denis further added to this research by describing a colorimetric method for detecting levels of uric acid in blood.[9]
EPIDEMIOLOGY
Hyperuricaemia is emerging as a major health issue globally and in India. In a population-based prevalence review, hyperuricaemia occupied the 13th position contributing to the global disease burden.[10] The overall global prevalence of asymptomatic hyperuricaemia is about 21% of the general population and 25% of hospitalised patients.[11]
According to the studies, the overall prevalence of hyperuricaemia in India is about 25.8%.[12] Further, male (20.1%) and female (21.5%) are seen to be around equally burdened with the disease with an increase in incidence with age amongst females.[13] In males, the incidence seems to remain consistent or decline with age. According to a study, the Indian rural population shows a 9% higher level of serum uric acid than the urban population.[14] A study revealed the prevalence of hyperuricaemia in around 26.02% of children with a predominance in male and older children as compared to female children. Some common disorders found in hyperuricaemic children were gastroenteritis (23.98%), respiratory infections (23.14%) and asthma (15.45%).[15] Many epidemiological studies reported that the modern lifestyle leads to an increase in the prevalence of hyperuricaemia and gouty arthritis in Asians.[16]
RISK FACTORS
Various factors are known to play a role in increased levels of uric acid in blood. Amongst these are age, gender, alcohol consumption, increased body mass index (BMI) > 30 and use of diuretics that contribute to hyperuricaemia. The incidence of hyperuricaemia has a positive relationship with increasing age among females. A study shows higher levels of uric acid in natural menopausal and surgical menopausal women as compared to premenopausal women. This is supposed to be due to the role of premenopausal oestrogen in increasing renal efficiency in handling uric acid.[17]
An Indian study shows a significant relationship between obesity and hyperuricaemia with an increase in the prevalence of hyperuricaemia with an increasing BMI. Around 34% population with hyperuricaemia was observed with a BMI range of 28–35 kg/m2 and 47% with a BMI >35 kg/m2.[18]
Alcohol consumption shows a variation in levels of uric acid depending upon the type of beverage consumed. In men, an increase in serum uric acid by 0.001 mg/dL for every additional gram of alcohol consumed in a week is noted.[19] Depending upon the type of alcohol used, a cross-sectional study in Americans shows a greater increase in uric acid levels by consumption of beer as compared to liquor with almost no increase by moderate wine intake.[20] The mechanism may be attributed to an increased amount of lactate in the blood due to the consumption of ethanol that facilitates the reabsorption of uric acid in renal tubules, thus decreasing its excretion and causing hyperuricaemia.
PATHOPHYSIOLOGY
Uric acid is a weak acid that is produced as a catabolic product of purine metabolism.[2] The endogenous sources contribute to the major quantity of uric acid produced daily (approx. 500–600 mg), whereas the exogenous purine intake through diet is around 100–200 mg per day.[21] The major amount of uric acid is in the form of urate at the normal physiological pH of 7.4. Around 70% of uric acid is excreted through the renal system, while the remaining 30% is excreted through stool after its breakdown in the intestine, maintaining daily production and excretion under normal conditions.[22]
Increased serum uric acid may be attributed to the accelerated production of urate through purine-rich diets, increased cellular breakdown or overproduction of endogenous purine. These factors are responsible for a minority of cases of hyperuricaemia. The majority of cases (90%) are due to under-excretion as kidneys are mainly responsible for urate handling. Impaired renal function due to any acute and chronic condition may lead to hyperuricaemia.[23]
CLINICAL MANIFESTATIONS
Hyperuricaemia itself does not directly indicate a specific disease. Increased levels of uric acid can remain in a person for a variable period without causing any crystallisation internally or outward symptoms. This type is known as asymptomatic hyperuricaemia, which does not necessarily require any treatment. On the other hand, uric acid levels in blood above saturation level may most commonly present themselves in the form of gout or uric acid nephrolithiasis.
Gout is one of the most common presentations of hyperuricaemia. It is characterised as the deposition of monosodium urate crystals in the soft body tissues, especially around joints, resulting in the inflammation of the affected joints. Uric acid levels can remain elevated in a person before manifesting as gouty arthritis.
Uric acid-associated nephrolithiasis is another common presentation of hyperuricaemia due to the renal handling of uric acid. The persistence of continuous acidic urine for a prolonged period can lead to the formation of renal stones. It accounts for around 5–10% of all renal stones.[24]
ASSOCIATED DISEASES
High uric levels are widely associated with the development of several chronic diseases in humans such as gout, renal stones, cardiovascular disorders, chronic kidney disease, hypertension and metabolic syndrome which are observed both in children and adults.
Cardiovascular disorders
Hyperuricaemia is frequently linked as a risk factor for cardiovascular disorders. The exact role of hyperuricaemia leading to cardiac diseases remains controversial. The high levels of uric acid in cardiac disorders may be attributed to a combined effect of reduced glomerular filtration rate, renal vasoconstriction, tissue ischaemia and increased oxidative stress.[25,26] In other studies, elevated uric acid is proved as an independent risk factor for the incidence and mortality of cardiovascular diseases. The presence of hyperuricaemia is seen to increase the risk of coronary artery disease more in females as compared to males.[27] Further, hyperuricaemia is positively associated with an increase in the incidence of hypertension in adults. This is more accurately linked with an increase in diastolic rather than systolic blood pressure.[23] The incidence is seen to decrease with increasing age as it is absent in older age.
Chronic kidney disease
Chronic kidney disease is a condition of impaired renal function over time. It is a common and life-threatening condition affecting millions of people around the world. Several factors such as obesity, hypertension and other vascular disorders can independently or in combination lead to decreased renal function resulting in total loss. Several recent studies have reviewed the positive role of uric acid in the development and progression of chronic kidney disease.[28,29] Increased levels of serum urate can trigger an inflammatory response in renal tissue leading to the production of pro-inflammatory cytokines and chemokines that are responsible for renal tubular damage and interstitial fibrosis. In addition to its inflammatory effects on renal tubules uric acid may also affect the renal vasculature by impairing the endothelial function and promoting oxidative stress, resulting in vasoconstriction, glomerular hypertension, reduced renal blood flow and a decline in kidney function.[30] As a result, there is disturbed waste excretion and accumulation of body toxins leading to the development of chronic kidney disease.
DIETARY MANAGEMENT
Dietary patterns seem to play a significant role in maintaining the levels of uric acid in blood. A change in the everyday lifestyle and diet of a person can help in reducing the risk of hyperuricaemia and also help in lowering the existing levels in the blood. Dietary consumption of foods having a high content of purines and acids is correlated with high uric acid levels.[31] Amongst these purines, adenine and hypoxanthine are more urogenic as compared to guanine and xanthine. A low purine diet along with an alkaline diet affects the uric acid levels as it facilitates the rapid elimination of the compound with urine.[32]
A moderate reduction in the intake of high-protein food, mainly of animal origin is recommended. The effect of plant proteins on uric acid levels depends upon the amount of dietary intake.[33] A protein-rich, low-fat dairy products are seen to reduce the existing high levels of uric acid and subsequent development of gout. Thus, a total dietary fat of not more than 30% is recommended.[32]
The amount of animal fat intake reduction with the replacement of plant-derived fats such as vegetable oil is recommended due to the beneficial effects of mono and polyunsaturated fatty acids on the cardiovascular risk associated with hyperuricaemia.[32] In addition to these, a limitation on alcohol consumption can help in keeping uric acid levels in check and decrease the risk of gouty attacks.[33,34] Further, a high fructose content in non-alcoholic beverages is associated with hyperuricaemia.[35] Therefore, excessive consumption of carbonated beverages and juices should be limited.
HOMOEOPATHIC APPROACH
The homoeopathic principle is based on the law of ‘similia similibus curantur.’[36] The homoeopathic approach towards a disease condition takes into account a complete totality of the patient including the mental and physical plane rather than only considering pathological symptoms. Dr. Hahnemann has described miasm as the fundamental cause of all chronic diseases.[37] With this context, hyperuricaemia falls under the sycotic miasm. Further along with the fundamental cause, each person is categorised into a particular type of diathesis that refers to a predisposition to a certain type of disease. Hyperuricaemia falls under the uric acid diathesis also known as gouty or rheumatic diathesis.[38,39]
Homoeopathic research studies
Five research studies were identified and two case reports were included in this paper and details of them are mentioned in Table 1.
| S. No. | Title | Author | Study design | Sample size | Intervention | Assessment/analysis tools | Results/conclusion |
|---|---|---|---|---|---|---|---|
| 1. | IHMs and UUMT in treatment of hyperuricaemia: an open, randomised, pragmatic, pilot trial (October 2020) | Nayak et al.[40] | An open, randomised (1:1:1), 3 parallel arms (IH, UUMT and IH+UUMT), pragmatic, pilot trial | 90 | Group 1: Individualised Homoeopathic Medicine. Group 2: UUMT. Group 3: Individualised Homoeopathic Medicine along with UUMT. |
SUA (primary), GAQ2 (secondary) and MYMOP2 (secondary); all measured at baseline, and after 3 and 6 months. | As per protocol analysis of SUA level revealed a similar trend of significantly higher reduction in the UUMT group than the other two (3 months: P=0.001; 6 months: P=0.007). No significant differences existed in reductions of GAQ2 scores amongst the three groups. Few significant differences were detected in MYMOP scores over 3 months favouring IH against others (symptom 2, P=0.001 and well-being score, P=0.002), and also over 6 months favouring IH+UUMT against others (symptom 1, P<0.001). |
| 2. | Homoeopathic management of hyperuricaemia in primary gout: A randomised single-blind placebo-controlled study | Deep and Kumar[41] | A prospective randomised single-blind placebo-controlled study | 91 | Experimental group: Individualised homoeopathic medicine+Diet and lifestyle measures. Control group: Placebo+Diet and lifestyle measures. |
SUA was analysed at baseline, 3rd, 6th and 9th month in both medicinal and control group. Assessment of VAS score was done for the baseline score and score after 9th month. |
In the population study the mean of SUA level before treatment was 8.61 and after homoeopathic treatment, it was 4.96 in the medicinal group. P value is <0.0001 In control group mean of SUA before treatment was 8.10 and after treatment, it was 7.6. P value is <0.0002. The changes were relatively greater in medicinal group; however, the changes were statistically significant in both groups. |
| 3. | Role of IHM in the treatment of gout - An observational study | Biswas and Mandal[42] | Observational study. | 150 | IHM in centesimal potency. | Assessment of uric acid at baseline and 4 weeks after the amelioration of symptoms. Symptomatic improvement was assessed in 4 categories (marked, moderate, mild and no improvement). |
Significant changes were seen in both uric acid levels and marked improvement in clinical symptoms. Marked- 26 (17.33%) Moderate- 67 (44.67%) Mild- 32 (21.33%) No improvement- 25 (16.67%) |
| 4. | An open-label prospective observational trial for assessing the effect of homoeopathic medicines in patients suffering from gout |
Saha et al.[43] | A prospective, single-arm, non-randomised, open-label, observational trial | 32 | Individualised homoeopathic medicine along with advice on diet and regimen. | Primary outcome: SUA at baseline and 3 months. Secondary outcome: GAQ2 at baseline and 3 months. MYMOP2 at baseline and every month for up to 3 months. |
Mean SUA level# reduced from 7.6±1.4 to 6.0±1.5 (P<0.001) GAQ2 total score (45.0 ± 9.1 vs. 21.0±14.0; mean reduction: 24.0, 95% CI=19.1, 29.0, P<0.001, Student’s t-test) reduced significantly over 3 months. |
| The mean pain intensity score of MYMOP2 (Symptom 1) improved from 5.2 (baseline) to 4.3 (at the 1st month), 3.8 (at the 2nd month), and finally, 3 (at the 3rd month). The mean activity score improved from 4.8 (baseline) to 3.9 (at the 1st month), 3.5 (in the 2nd month) and finally, 2.7 (in the 3rd month) after medication. The mean well-being score of the patients with gout also improved from 5.1 (baseline) to 4.1 (at the 1st month), 3.5 (at the 2nd month), and finally, 2.5 (at the 3rd month). A significant improvement in the mean intensity score of associated symptom in each case (recorded as symptom 2) was changed from 3.9 at baseline to 1.6 after the 3rd month |
|||||||
| 5. | IHMs in Treatment of Hyperuricaemia: Evaluation by Double-Blind, Randomised, Placebo-Controlled Trial | Ghosh et al.[44] | Double-blind, randomised, placebo-controlled, two parallel arms trial | 60 | Group 1: Individualised Homoeopathic medicine+ dietary management. Group 2: Placebo+ dietary management |
Primary outcome: SUA at baseline and every month up to 3 months. Secondary outcome: HUQLQ at baseline and 3 months. MYMOP2 at baseline and every month for up to 3 months. |
Between-group differences in SUA levels (F1, 56¼13.833, P<0.001), HUQLQ scores (F1, 56¼32.982, P<0.001) and MYMOP-2 profile scores (F1, 56¼23.873, P<0.001) were statistically significant, favouring IHMs against placebos, with medium to large effect sizes. |
| 6. | A Clinical Study on the Efficiency of Homoeopathic Medicines in the Treatment of Gout with an evaluation Based on SUA Level | Shibina[45] | A prospective experimental study design without control group. | 30 | Homoeopathic medicines are based on the constitution of patients. | SUA before and after treatment (baseline and after 1 year). Symptomatic improvement (marked, moderate, mild). |
Reduction in total SUA from 262 mg/dL before treatment to 198 mg/dL after treatment. Symptomatic improvement: Marked (n=25) Moderate (n=4) Mild (n=1). |
| 7. | Treatment of hyperuricaemia with homoeopathic medicine | Perveen et al.[47] | Case series | 5 cases | Patients were provided with the medicine Lycopodium clavatum mentioned in the synthesis repertory under the rubric uric acid diathesis, in proper dose and potency by considering only the raised value of SUA level. | Patients with SUA levels above 7 mg/dL will be considered for this case series. | Homoeopathic medicine Lycopodium clavatum was associated with significant alleviation of hyperuricaemia Symptoms along with decrease in SUA levels, enabling the reduction in use of conventional medicine. |
| Lycopodium clavatum: A case series | |||||||
| 8. | An evidence-based homoeopathic case series in the treatment of hyperuricaemia | Halder et al.[46] | Case series | 3 cases | individualised homoeopathic medicine along with diet and lifestyle measures | Primary outcome- SUA. Secondary outcome-SF-36 questionnaire |
Positive changes in both SF 36 scale and SUA levels show the evidence of a curative approach of the homoeopathic system in hyperuricaemia without any adverse effects. |
IHMs: Individualized homoeopathic medicines, UUMT: Urtica urens mother tincture, GAQ2: Gout assessment questionnaire version 2, MYMOP2: Measure yourself medical outcome profile version 2, VAS: Visual Analogue Scale, SUA: Serum uric acid, CI: Confidence interval, HUQLQ: Hyperuricaemia Quality of life, SF: Short-form
A study by Nayak et al. investigated the clinical effectiveness of three treatment regimens in hyperuricaemia - individualised homoeopathy (IH), Urtica urens mother tincture (UUMT) and both (IH + UUMT) along with lifestyle modifications in a sample of 90 patients with hyperuricaemia. Although all three therapies showed similar improvements, the IH + UUMT group had more positive direction of effects than IH or UUMT alone; however, no definite conclusion could be arrived at.[40]
Many studies[41-45] and case series[46,47] showed the positive effect of Individualized homoeopathic medicines (IHMs) medicines against placebo in the management of hyperuricaemia in gout.
Rubrics mentioned in various repertories related to uric acid and gout
Synthesis repertory
Urine - Casts, containing – Urate: Benz-ac., berb., chinin-s., coc-c., Kali-c., kali-pic., lith-c., Lyc., sars., Senn., Sep., urt-u.
Kidneys - Uric acid increased: Chel.
Urine - Acid - Uric acid increased: Cortico., cortiso., maland.[48]
Murphy Repertory
Constitutions - Gouty, constitutions - uric acid diathesis: Benz-ac., Colch., form., Lith-C., LYC.
Diseases - Uric acid diathesis: Benz-AC., berb., chinin-s., coc-c., COLCH., Lyc., nat-s., sep., thlas., thuj., URT-U.
Kidneys - Uric acid diathesis: Benz-AC., berb., chinin-s., coc-c., COLCH., Lyc., nat-s., sep., thlas., thuj., URT-U.
Urine - Sediment, urinary - uric, acid: Arg-n., thymol., Urt-u.
Urine - Uric acid: Benz-ac., thyr.[49]
Boger Boeninghausen’s Characteristics and Repertory
Conditions of aggravation and amelioration in general - Uric acid, diathesis: Colch., coloc., gins., led., Lyc., sang., sars., Sep., sulph., Ter.[50]
Boericke Repertory
Urinary system - Urine - Sediment, type - Lithic acid, uric acid, gravel, brick dust: Arg-n., arn., Aspar., Bar-m., baros., bell., Benz-ac., Berb., cal-ren., Calc., cann-s., Canth., caust., chel., Chin., Chinin-s.,Coc-c.,cocc-s., coch., colch., coloc., dig.,dios., Epig., ery-a., Eup-a., Eup-pur., fab., ferr-m., gali., graph., Hed., Hydrang., Kali-c., kali-i., kreos., Lith-be., Lith-c., lob., Lyc., merc-c., nat-m., nat-s., Nit-ac., nit-m-ac., Nux-v., Oci., pareir., pariet., ph-ac., phos., phys., pipe., plb-i., puls., Sars., sel., senn., Sep., skook., Solid., stigm., Thlas., tritic., Urt-u., vesi.[51]
Complete Repertory
BLOOD - URIC acid diathesis, lithaemia: adren., agn., agri., alco., ant-c., ap-g., APIS, aran., arg-n., arn., aspar., BAR-M., bell., BENZ-AC., berb., berb-a., bry., calc., calc-m., CALC-P., CANTH., CAPS., CARBN-S., caust., CHAM., chel., chim., chin., chinin-s., chlf., cimic., clem., coc-c., coff-t., colch., coloc., cortico., cortiso., CROT-H., dig., dulc., EPIG., ERIC-VG., fab., form., gins., guaj., hedeo., kali-c., kali-i., kali-m., kalm., led., lith-be., lith-c., lob., LYC., MAG-C., med., MENY., mez., mit., nat-m., nat-s., nit-ac., nux-v., OCI., ONON., oxyg., PAREIR, phase., phos., phyt., pic-ac, pipe., plb., PULS., RHOD., rhus-t., sabin., samb-e., sang., sars., sep., skook., solid., spirae., sulph., ter., thlas., thuj., thymol., thyr., URT-U., vinc.[52]
COMMON HOMOEOPATHIC MEDICINES FOR HYPERURICAEMIA
Ammonium Phosphoricum
A remedy for chronic gouty patients uric acid diathesis indicated in bronchitis and nodosities of the joints of the fingers and back of the hand. Pain in shoulder joint.
Baryta Muriaticum
Increased level of uric acid with cracking of joints. Tearing and shooting pain in the limbs with swelling of hands and feet. Haemorrhagic extravasations in knee-joint. Great increase in uric acid, diminution of chlorides.
Benzoic Acid
It produces and cures symptoms of a uric acid diathesis, with urine highly coloured and very offensive and gouty symptoms. Antisycotic. Gouty and asthmatic. It is often an excellent palliating remedy in old gouty constitutions. Gouty concretions. Gouty deposits in both wrists between metacarpal bones; swelling of elbow joints. Rheumatic gout; nodes very painful. Gouty deposits pain and swelling in the knees. Tearing pain in the great toe.[51,53,54]
Chininum Sulph
Acute articular rheumatism. Polyarticular gout. Great sensitiveness of the dorsal vertebrae; pain on pressure. Last cervical sensitivity. Oedematous swelling of the feet. A small amount of urea and phosphoric acid with excess uric acid and an abundance of chlorides, accompanied by subnormal temperature.
Coccus Cacti
Urging to urinate; brick red sediment. Urinary calculi, haematuria, urates and uric acid; lancinating pains from kidney to bladder.
Colchicum
Acute rheumatism and uric acid diathesis; rheumatic complaints in general, with swelling and without swelling. Colchicum is best known as a remedy for gout and rheumatism. It corresponds to gouty diathesis uric acid diathesis. There is the irritability and aversion to touch so common in gout; pain in small joints, and especially the great toes.
Epigaea Repens
Uric acid deposit, gravel, renal calculi. Fine sand in urine of a brown colour.
Fabiana Imbricata
Useful in uric acid diathesis with very excoriating urine and urinary calculi.
Ferrum Phosphoricum
Rheumatism of knee joint with fever. Gouty affection of joints. Stiffness of lower limbs and feet. Swollen joints, upper limbs, forearm, hands, feet.
Franciscea Uniflora
Rheumatic pain in feet and lower part of legs. Urine contains uric acid.
Ichthyolum
Polyarthritis, chronic rheumatism, uric acid diathesis. Lameness in the right shoulder and right lower Uric acid deposits. Gouty joints have also been benefited. Ichthyol appears to act by virtue of its power of allaying pain and inflammation.
Lithium Benzoicum
Had a great effect in diminishing uric acid deposits and increasing the free hippuric acid in urine. ‘It acts upon urine before it leaves the blood.’
Lithium Carbonicum
Rheumatic nodes. Uric acid diathesis. Gout and tophi. Rheumatic pain throughout the shoulder joint, arm and fingers and small joints generally. Swelling and tenderness of fingers and toe joints; better hot water. Nodular swelling in joints.
Lycopodium
Chronic gout, with chalky deposits in joints. Tearing in shoulder and elbow joint.
Ocimum Canum
Uric acid diathesis. Red sand in the urine is its chief characteristic and is frequently verified. The symptom of renal calculus is pronounced high acidity formation of spike crystals of uric acid. Turbid, thick, purulent, bloody; brick-dust red or yellow sediment. Odour of musk.
Thalapsi Bursa Pastoris
This is an anti-haemorrhagic and anti-uric-acid remedy. Pain in the left shoulder was so great he thought his neck and shoulder would break.
U. Urens
Gout and uric acid diathesis. Pain in acute gout deltoid; pain in ankles, wrist. Rheumatism associated with urticarial-like eruptions.
CONCLUSION
Hyperuricaemia causes inflammation of the joints, which can cause redness, heat, swelling and pain. There is a large and increasing number of asymptomatic hyperuricaemia cases in the population. Hyperuricaemia is an easily tested and treated condition; therefore, we should urge the importance of routine screening of uric acid in middle-aged men or women without oestrogen or other diseases leading to high uric acid levels because hyperuricaemia may threaten our health and cause cardiovascular diseases and renal diseases. Homoeopathic literature shows a wide group of remedies affecting uric acid levels and hence can be used in conditions such as hyperuricaemia and gout. Research studies also give a positive impact of homoeopathy in the management of hyperuricaemia; however, randomised controlled trials with larger sample sizes should be conducted to investigate further the evidenced-based effect of Homoeopathy in the treatment of hyperuricaemia.
Ethical approval
Institutional Review Board approval is not required.
Declaration of patient consent
Patient’s consent is not required as there are no patients in this study.
Conflicts of interest
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship
Nil.
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