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SCIENTIFIC EXPLANATION OF MODE OF ACTION OF SUTSHEKHAR RAS IN AMLAPITTA WITH SPECIAL REFERENCE TO ACID PEPTIC DISORDERS: A REVIEW

Authors:
  • Government Postgraduate Ayurveda College And Hospital, Varanasi
  • Government Ayurveda College and Hospital, Varanasi, India

Abstract and Figures

Amlapitta or hyperacidity is a very common disease in present era and not only present but also since past era. It is very troublesome disease and can give rise to many serious problems if not treated in time. Signs and symptoms of Amlapitta are very similar to gastritis or hyperacidity. The main cause of hyperacidity is the aggravation of Pitta Dosha in the body. Pitta is an Ayurvedic humor that symbolizes heat or fire. There are many causes for the aggravation of Pitta, main among them are: Eating foods that do not suit the constitution or foods that should not be taken together (milk and fish, milk and salt), excessively sour or spicy foods and liquids. Hyperacidity is known as Amlapitta in Ayurveda. Hyperacidity therefore is a condition characterized by an increase of sourness and heat in the body. The aggravated Pitta impairs the digestive fire, leading to improper digestion of food and production of Ama. Sutshekhar Ras is an important medicine used in Amlapitta. In this review article, we are trying to explain the mechanism of action of this drug on scientific basis.
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SCIENTIFIC EXPLANATION OF MODE OF ACTION OF SUTSHEKHAR RAS IN AMLAPITTA
WITH SPECIAL REFERENCE TO ACID PEPTIC DISORDERS: A REVIEW
Ajay Kumar 1*, Tina Singhal 2
1Lecturer, Dept. of Kayachikitsa & Panchkarma, Government Post Graduate Ayurveda College and Hospital, Varanasi,
Uttar Pradesh, India
2Lecturer, Dept. of Rachana Sharir, Government Post Graduate Ayurveda College and Hospital, Varanasi,
Uttar Pradesh, India
Received on: 15/07/18 Accepted on: 15/09/18
*Corresponding author
E-mail: drajay2000@gmail.com
DOI: 10.7897/2277-4343.095154
ABSTRACT
Amlapitta or hyperacidity is a very common disease in present era and not only present but also since past era. It is very troublesome disease and can
give rise to many serious problems if not treated in time. Signs and symptoms of Amlapitta are very similar to gastritis or hyperacidity. The main cause
of hyperacidity is the aggravation of Pitta Dosha in the body. Pitta is an Ayurvedic humor that symbolizes heat or fire. There are many causes for the
aggravation of Pitta, main among them are: Eating foods that do not suit the constitution or foods that should not be taken together (milk and fish, milk
and salt), excessively sour or spicy foods and liquids. Hyperacidity is known as Amlapitta in Ayurveda. Hyperacidity therefore is a condition
characterized by an increase of sourness and heat in the body. The aggravated Pitta impairs the digestive fire, leading to improper digestion of food and
production of Ama. Sutshekhar Ras is an important medicine used in Amlapitta. In this review article, we are trying to explain the mechanism of action
of this drug on scientific basis.
Keywords: Amlapitta, Hyperacidity, Acid peptic disorder, Sutshekhar Ras.
INTRODUCTION
Amlapitta is a disease of gastro-intestinal tract, especially
mentioned in Kashyap Samhita1, Madhava Nidana2, Bhava
Prakasha, Kashyap Samhita3 and Chakradatta. This disease is not
separately described in Charaka Samhita, Sushruta Samhita and
Ashtang Hriday or Ashtang Samgraha. Amlapitta is mentioned in
these Brihatrayi as a symptoms or complication of many
disorders.
Excess production of acids in stomach is termed as the
hyperacidity. There are varieties of reasons which cause excess
acid production. Heartburn and hyperacidity4 are primarily
lifestyle or age related. While there are various health conditions
and circumstances that could cause hyperacidity and heartburn,
for the most part, the condition results from unhealthy lifestyle
choices. Sutshekhar Ras is an important medicine used in
Amlapitta and it is need of today to explain the mechanism of
action of this drug on scientific basis.
REVIEW OF DISEASE
Etymologically the word Amlapitta comprises of two components
i.e. Amla & pitta. Chakrapani5 in his commentary on Charak
Samhita defines “Amlapittam Cheti amlagunoundriktam pittam
means the augmented or increased amla guna of pitta is known as
Amlapitta. Whereas Shrikanthadutta in his Madhukosha
vyakhya6 of Madhav Nidan defines Vidahadhyamla
gunaoundrikta pittam amlapittam” i.e. the pitta becomes vidagdha
because of excessive increase of amla guna of pitta & Amlam
vidagdham cha tat pittam amlapittam the pitta which attains
amla guna & vidagdhata is called as Amlapitta. Indulgence of
foods which are incompatible combinations, spoiled, very sour,
causes increase of pitta and produces Amlapitta.
The Samprapti i.e. pathogenesis of Amlapitta involves three
important factors7 i.e.
1. Agnimandya,
2. Ama
3. Annavaha Srotodushti.
Along with these factors, the vitiation of pitta leading to
quantitative & qualitative increase of its Ama & Drava Guna
gives rise to Amlapitta. The main sign and symptoms as
mentioned in Madhav Nidan are described under two types.
[Table 1]
1. Adhoga Amlapitta
Thirst, burning sensation, fainting, giddiness, delusion, rashes on
skin, poor digestion are the main symptoms of this type of
Amlapitta.
2. Urdhwaga Amlapitta
Vomiting of green, yellow, black, bright red coloured sour
material, resembling mutton wash, belching, burning sensation in
throat, chest and upper abdomen, headache, loss of appetite,
fever, appearance of rashes are the main symptoms of this type of
Amlapitta.
Table 1: Classification of Amlapitta
Type
Direction
Symptoms
Adhoga
Amlapitta
Downward
Thirst, Burning sensation,
fainting, rashes on skin etc
Urdhwaga
Amlapitta
Upward
Vomiting, Headache, Burning
sensation, Loss
of appetite
The biggest contributing factor towards heartburn and
hyperacidity is bad eating habits. Eating large meals and foods
that are high in unhealthy fats, starch, sugars, spices and oil can
all lead to heartburn. Eating heavy meals before sleeping also
causes hyperacidity, as you are not giving your body adequate
Ajay%Kumar%&%Tina%Singhal%/%Int.%J.%Res.%Ayurveda%Pharm.%9%(5),%2018%
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48!
time to digest the food properly. When you sleep soon after
eating, the reclined position also makes it easier for acid reflux to
occur. Keeping long gaps between meals and skipping meals can
also cause acids to build up in the stomach and lead to heartburn
and acidity. Bad eating habits put extra stress on the digestive
system making it work overtime to try and function normally.
Acid peptic disorders are the result of distinctive, but overlapping
pathogenic mechanisms leading to either excessive acid secretion
or diminished mucosal defence. They are common entities
present in daily clinical practice that, owing to their chronicity,
represent a significant cost to healthcare.
PHYSIOLOGY OF ACID SECRETION8
The stomach consists of two primary functional zones i.e., the
oxyntic gland area, representing approximately 80% of the organ,
and the pyloric gland area representing the remaining 20%.
Parietal cells secrete hydrochloric acid and intrinsic factor which
are predominantly present in the oxyntic glands. Chief cells
secrets the digestive enzyme precursor pepsinogen9. The
histamine, gastrin and acetylcholine released from postganglionic
enteric neurons10 are the principal stimulants for acid secretion
from gastric mucosa.
Basal acid secretion is modulated by acetylcholine from
parasympathetic vagal efferent. It directly stimulates acid
secretion by binding to muscarinic receptors on parietal cells.
Indirectly, acetylcholine also stimulates acid secretion through
activation of M2 and M4 receptors on D cells11.
Antacids work instantaneously and give rapid relief from
hyperacidity. The primary effect of antacids is partial
neutralization of gastric hydrochloric acid and inhibition of the
proteolytic enzyme pepsin12. These all antacids are administered
orally, and their potency is measured by the amount of acid
neutralized by a given dose of the antacid.
Most Commonly we use sodium bicarbonate, calcium carbonate,
magnesium hydroxide and aluminium hydroxide as antacids. For
example, calcium carbonate is sparingly soluble and it reacts with
HCl and generates soluble calcium chloride, which is converted
back to calcium carbonate in the alkaline conditions of the small
intestine. Other used antacids are the insoluble aluminium
hydroxide and magnesium hydroxide. Aluminium and calcium-
containing products generally cause constipation therefore these
agents are often combined with magnesium hydroxide, which can
cause diarrhoea and loose stools when administered alone.
SUTSHEKHAR RAS
Sutshekhar Ras is an important medicine used in Ayurveda,
which acts on Pitta Dosha and reduces symptoms like heartburn,
nausea, vomiting, abdominal pain, epigastric tenderness, hiccup,
fever, breathing troubles, headache etc. The main ingredients are
given in Table 2.
Table 2: Ingredients of Sutshekhar Ras (Siddha Yoga Samgraha)
S.N.
Contents
Parts
S.N.
Parts
1
Parad
1
2
1
3
Raupya Bhasm
1
4
1
5
Marich
1
6
1
7
Dhatura
1
8
1
9
Tamra Bhasm
1
10
1
11
Tejpatra
1
12
1
13
Nagkeshar
1
14
1
15
Bilwa
1
16
1
17
Bhringraj Kwath
Bhawana Dravya
MODE OF ACTION OF DIFFERENT INGREDIENTS
DHATURA
Datura stramonium is a main ingredient of Sutshekhar Ras. It is
a widespread annual plant, containing atropine, hyoscyamine, and
scopolamine, which can produce poisoning with a severe
anticholinergic syndrome13. Atropine, scopolamine, and
hyoscyamine/daturine (the l-enantiomer of atropine) are the
primary active constituents in all dhatura species. The three
primary alkaloids in dhatura are antimuscarinic anticholinergics,
which means they competitively antagonize (block) the
muscarinic acetylcholine receptors.
As this is a potent anticholinergic drug, it inhibits the action of
Acetylcholine. Previously we said that Acetylcholine from
parasympathetic vagal efferent modulates basal acid secretion
and stimulate acid secretion indirectly by inhibiting the release of
somatostatin, so ultimately by blocking the acetylcholine,
Dhatura inhibits acid(HCl) production in gastric mucosa and
relieves hyperacidity.
SHANKH BHASM
The other component of Sutshekhar Ras is Shankh Bhasm. This
is a Calcium carbonate compound. This directly reacts with
gastric HCl and neutralise them, so this acts as potent antacid.
CaCO3 + HCl = H2O + CO2 + CaCl2
LAUHA BHASM
Another compound Lauha Bhasm also directly neutralises HCl as
Fe + 2HCl = FeCl2 + H2
HCl is strong acid and FeCl2 is soluble ionic compound. Both
have ions as major species in their solution.
TANKAN
Another ingredients Tankan (Borax) reacts with HCl and
neutralise it as following.
Na2B4O710H2O+2HCl4H3BO3+2NaCl+5H2O
DISCUSSION
Amlapitta is caused by aggravated pitta due to excessive intake
of pungent and sour food items, alcoholic preparations, salt, hot
and sharp stuff. This aggravated pitta cause burning sensations.
To pacify the pitta, anger, fear, excessive exposure to sun and fire,
intake of dry vegetables and alkalis, irregularity in taking food,
and all pitta prakopak factors should be avoided14. Various drugs
are described for treatment of Amlapitta. Among these
Avipattikar Churna, Leela Vilas Ras, Amla-Pittantak Lauha,
Triphala Mandur, Kushmand Khand, Prawaal Panchamrit,
Shankh Bhasm, Prawaal Pishti, Mukta Pishti, and Yavakshar are
the main drugs. Sutshekhar Ras is used very commonly used in
Amlapitta. But due to lack of scientific explanation, nobody
wants to believe that it is as useful as allopathy drugs. After
scientific explanation of its mechanism everyone has proud on the
concepts of Ayurveda that it is also very scientific.
Ajay%Kumar%&%Tina%Singhal%/%Int.%J.%Res.%Ayurveda%Pharm.%9%(5),%2018%
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49!
CONCLUSION
Sutshekhar Ras is a very commonly used drug in Amlapitta and
it helps not only in reducing the symptoms but also maintains the
health. The specially prepared lifestyle chart containing Ahara
and Vihara helps in reducing the symptoms and maintaining the
healthy lifestyle. This drug is very beneficial in this disease due
to multiple actions such as anticholinergic and directly acting
antacid.
REFERENCES
1. Tewari P V, Kashyap Samhita of Vriddha Jivakiya Tantra,
Reprint edition, Chapter 16/1-30, p.630-38, Chaukhambha
Vishvabharati, Varanasi, 2008.
2. Tripathi Brahmanand, Madhav Nidaan Madhukosha
commentary, Reprint edition, Part 2, Chapter 51, p.225,
Chaukhambha Surabharati Prakashan, Varanasi; 2002
3. Laxmipati Shastri, Yogaratnakara Vidyotini Hindi
Commentary, Edition-2, verse 1-3; Chaukhambha Sanskrit
Series, Varanasi. 2012
4. Gaddam Srinivas, Sharma Prateek, Shedding light on the
epidemiology of GERD in India a big step forward, Indian
J. Gastroenterol, May-June 2011; 30(3): 105-107
5. Priyavrat Sharma, Chakradutta hindi commentary, Chapter
52/17, Chaukhambha orientalia, Delhi, 2007
6. Yadunandana upadhyaya, Madhava Nidana, Madhukosha
hindi commentary, reprint edition, chapter 51/ 2.
Chaukhambha Sanskrit Series, Varanasi;2013
7. Shivappa Pujari, Shreevathsa, Bharathi B. Hiremath, Dileep
kumar KJ. Gastritis (Amlapitta) A Case Study. J of
Ayurveda and Hol Med (JAHM).2014;2(9):59-60
8. Mejia A, Kraft WK. Acid peptic diseases: pharmacological
approach to treatment. Expert review of clinical
pharmacology. 2009;2(3):295-314
9. Hirschowitz BI, Keeling D, Lewin M, Okabe S, Parsons M,
Sewing K, Wallmark B, Sachs G, Pharmacological aspects of
acid secretion, Dig Dis Sci. 1995 Feb; 40:3S-23S
10. Schubert ML, Peura DA, Control of gastric acid secretion in
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11. Schubert ML, Peura DA, Control of gastric acid secretion in
health and disease. Gastroenterology. 2008 Jun; 134(7):1842-
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12. Maton PN, Burton ME. Antacids revisited: a review of their
clinical pharmacology and recommended therapeutic use.
Drugs. 1999; 57:855870
13. Trancă SD, Szabo R, Cociş M. Acute poisoning due to
ingestion of Datura stramonium a case report. Romanian
Journal of Anaesthesia and Intensive Care. 2017;24(1):65-68
14. Vikas Saroch, Jajbir Singh. A Review on Ayurvedic
Medicines for Amlapitta (Hyperacidity), AAMJ 2015; 1 (2):
40-2
Cite this article as:
Ajay Kumar and Tina Singhal. Scientific explanation of mode of
action of sutshekhar ras in amlapitta with special reference to acid
peptic disorders: A review. Int. J. Res. Ayurveda Pharm.
2018;9(5):47-49 http://dx.doi.org/10.7897/2277-4343.095154
Source of support: Nil, Conflict of interest: None Declared
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Acid peptic disorders are the result of distinctive, but overlapping pathogenic mechanisms leading to either excessive acid secretion or diminished mucosal defense. They are common entities present in daily clinical practice that, owing to their chronicity, represent a significant cost to healthcare. Key elements in the success of controlling these entities have been the development of potent and safe drugs based on physiological targets. The histamine-2 receptor antagonists revolutionized the treatment of acid peptic disorders owing to their safety and efficacy profile. The proton-pump inhibitors (PPIs) represent a further therapeutic advance due to more potent inhibition of acid secretion. Ample data from clinical trials and observational experience have confirmed the utility of these agents in the treatment of acid peptic diseases, with differential efficacy and safety characteristics between and within drug classes. Paradigms in their speed and duration of action have underscored the need for new chemical entities that, from a single dose, would provide reliable duration of acid control, particularly at night. Moreover, PPIs reduce, but do not eliminate, the risk of ulcers in patients taking NSAIDs, reflecting untargeted physiopathologic pathways and a breach in the ability to sustain an intragastric pH of more than 4. This review provides an assessment of the current understanding of the physiology of acid production, a discussion of medications targeting gastric acid production and a review of efficacy in specific acid peptic diseases, as well as current challenges and future directions in the treatment of acid-mediated diseases.
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Amlapitta is a very common disease in present era. It is very troublesome disease and can give rise to many serious problems if not treated in time. Signs and symptoms of Amlapitta are very similar to gastritis or hyperacidity. According to conventional medical science the most common causes of gastritis are H. pylori infections and prolonged use of Non-Steroidal Anti Inflammatory Drugs (NSAIDS). The incidence of gastritis in India is approximately 3 in 869 that is about 12,25,614 people suffering from gastritis out of the total 1,06,50,70,607 population. Hence there is a need to understand the concepts and first line treatments
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The secretion of gastric acid is regulated both centrally and peripherally. The finding that H2-receptor antagonists are able to reduce or abolish acid secretion due to vagal, gastrinergic, and histaminergic stimulation shows that histamine plays a pivotal role in stimulation of the parietal cell. In the rat, the fundic histamine is released from the ECL cell, in response to gastrin, acetylcholine, or epinephrine, and histamine release is inhibited by somatostatin or by the H3-receptor ligand, R-alpha-methyl histamine. The parietal cell has a muscarinic, M3, receptor responsible for [Ca]i regulation. Blockade of muscarinic receptors by atropine can be as effective as H2-receptor blockade in controlling acid secretion. However, general effects on muscarinic receptors elsewhere produce significant side effects. The different receptor pathways converge to stimulate the gastric H+,K(+)-ATPase, the pump responsible for acid secretion by the stomach. This enzyme is an alpha,beta heterodimer, present in cytoplasmic membrane vesicles of the resting cell and in the canaliculus of the stimulated cell. It has been shown that acid secretion by the pump depends on provision of K+Cl- efflux pathway becoming associated with the pump. As secretion occurs only in the canaliculus, this K+Cl- pathway is activated only when the pump inserts into the canalicular membrane. Transport by the enzyme involves reciprocal conformational changes in the cytoplasmic and extracytoplasmic domain. These result in changes in sidedness and affinity for H3O+ and K+, enabling active H+ for K+ exchange. The acid pump inhibitors of the substituted benzimidazole class, such as omeprazole, are concentrated in the canaliculus of the secreting parietal cell and are activated there to form sulfenamides. The omeprazole sulfenamide, for example, reacts covalently with two cysteines in the extracytoplasmic loops between the fifth and sixth transmembrane and the seventh and eighth transmembrane segments of the alpha subunit of the H+,K(+)-ATPase, forming disulfide derivatives. This inhibits ATP hydrolysis and H+ transport, resulting in effective, long-lasting regulation of acid secretion. Therefore, this class of acid pump inhibitor is significantly more effective and faster acting than the H2 receptor antagonists. K+ competitive antagonists bind to the M1 and M2 transmembrane segments of the alpha subunit of the acid pump and also abolish ATPase activity. These drugs should also be able to reduce acid secretion more effectively than receptor antagonists and provide shorter acting but complete inhibition of acid secretion.
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Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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Recent milestones in the understanding of gastric acid secretion and treatment of acid-peptic disorders include the (1) discovery of histamine H(2)-receptors and development of histamine H(2)-receptor antagonists, (2) identification of H(+)K(+)-ATPase as the parietal cell proton pump and development of proton pump inhibitors, and (3) identification of Helicobacter pylori as the major cause of duodenal ulcer and development of effective eradication regimens. This review emphasizes the importance and relevance of gastric acid secretion and its regulation in health and disease. We review the physiology and pathophysiology of acid secretion as well as evidence regarding its inhibition in the management of acid-related clinical conditions.
  • Tripathi Brahmanand
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Gaddam Srinivas, Sharma Prateek, Shedding light on the epidemiology of GERD in India -a big step forward, Indian J. Gastroenterol, May-June 2011; 30(3): 105-107
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Yadunandana upadhyaya, Madhava Nidana, Madhukosha hindi commentary, reprint edition, chapter 51/ 2. Chaukhambha Sanskrit Series, Varanasi;2013