Epidemic dropsy is a form of edema of extremities due to poisoning by Argemone mexicana (Mexican prickly poppy). Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with Argemone mexicana seed oil. Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome. Other major symptoms are bilateral pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness. Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen. Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment. Epidemic dropsy occurs as an epidemic in places where use of mustard oil from the seeds of Brassica juncea, commonly known as Indian mustard, as a cooking medium is common.
Argemone mexicana (family Papaveraceae), a native of West Indies and naturalized in India, is known as “Shailkanta” in Bengal and “Bharbhanda” in Uttar Pradesh. It is also popularly known as “Pivladhatura” or “Satyanashi”, meaning devastating. The plant grows wildly in mustard and other fields. Its seeds are black in colour and are similar to the dark coloured mustards seeds (Brassica juncea) in shape and size. Adulteration of argemone seeds in light yellow colored mustard seeds (Brassica compestris) can easily be detected, but these seeds are rather difficult to visualize when mixed with dark coloured mustard seeds.
Argemone seeds yield approximately 35% oil. Alkaloid content in argemone oil varies from 0.44% to 0.50%. Argemone seeds find use as a substitute because of the easy availability, low cost and their complete miscibility of their oil with mustard oil.
Mortality is usually due to heart failure, pneumonia, respiratory distress syndrome or renal failure and is around 5%. Long-term follow-up studies are scanty so the long-term effects of argemone oil toxicity have not been documented. It has been reported that 25% of cases will have edema beyond 2 months and 10% beyond 5 months. Pigmentation of skin and excessive loss of hair, which lasted 4–5 months following the disease. The majority of patients completely recover in about 3 months.
Reactive oxygen species and oxidative stress: Studies of the blood of dropsy patients has revealed that there is extensive reactive oxygen species (ROS) production (singlet oxygen and hydrogen peroxide) in the argemone oil intoxication leading to depletion of total antioxidants in the body and especially lipid-soluble antioxidants such as vitamin E and A (tocopherol and retinol). There is an extensive damage to the anti-oxidant (AO) defense system (anti-oxidant enzymes and anti-oxidants) of blood. Prior in vitro studies have shown that ROS are involved in AO induced toxicity causing peroxidative damage of lipids in various hepatic sub-cellular fractions including microsomes and mitochondria of rats. The damage in hepatic microsomal membrane causes loss of activity of cytochrome P-450 and other membrane bound enzymes responsible for xenobiotic metabolism which leads to delayed bioelimination of sanguinarine and enhances its cumulative toxicity. Several lines of evidence have been shown to explain the mechanism of toxicity of argemone oil/alkaloid. The toxicity of sanguinarine has been shown to be dependent on the reactivity of its iminium bond with nucleophilic sites like thiol groups, present at the active sites of the enzymes and other vital proteins and thus suggesting the electrophilic nature of the alkaloid.
Pulmonary Toxicity: The decrease in glycogen levels following argemone oil intoxication could be due to enhanced glycogenolysis leading to the formation of glucose-1-phosphate, which enters the glycolytic pathway resulting in accumulation of pyruvate in the blood of experimental animals and dropsy patients. The enhancement of glycogenolysis can further be supported by the interference of sanguinarine in the uptake of glucose through blocking of sodium pump via Na+-K+-ATPase and thereby inhibiting the active transport of glucose across the intestinal barrier. It is well established that increased pyruvate concentration in blood uncouples oxidative phosphorylation, and this may be responsible for thickening of interalveolar septa and disorganized alveolar spaces in lungs of argemone oil-fed rats and the breathlessness as has been observed in human victims.
Cardiac Failure: The inhibition of Na+-K+-ATPase activity of heart by sanguinarine is due to interaction with the cardiac glycoside receptor site of the enzyme, which may be responsible for producing degenerative changes in cardiac muscle fibers in the auricular wall of rats fed argemone oil and could be related to tachycardia and cardiac failure in epidemic dropsy patients.
Delayed clearance: Destruction of hepatic cytochrome P450 significantly affects the metabolic clearance by liver. The retention of sanguinarine in the gastrointestinal (GI) tract, liver, lung, kidney, heart and serum even after 96 hrs of exposure indicates these as the likely target sites of argemone oil toxicity.
Nitric acid test and paper chromatography test are used in the detection of argemone oil. The paper chromatography test is the most sensitive test.
Withdrawal of the contaminated cooking oil is the most important initial step. Bed rest with leg elevation and a protein-rich diet are useful. Supplements of calcium, antioxidants (vitamin C and E), and thiamine and other B vitamins are commonly used. Corticosteroids and antihistamines such as promethazine have been advocated by some investigators, but demonstrated efficacy is lacking. Diuretics are used universally but caution must be exercised not to deplete the intravascular volume unless features of frank congestive cardiac failure are present, as edema is mainly due to increased capillary permeability. Cardiac failure is managed by bed rest, salt restriction, digitalis and diuretics. Pneumonia is treated with appropriate antibiotics. Renal failure may need dialysis therapy and complete clinical recovery is seen. Glaucoma may need operative intervention, but generally responds to medical management.
Besides India, widespread epidemics have been reported from Mauritius, Fiji Islands, Northwest Cape districts of South Africa, Madagascar and also from Nepal. Apart from a South African study, where the epidemic occurred through contamination in wheat flour, all the epidemics occurred through the consumption of mustard oil contaminated with argemone oil.
In these cultural populations mustard oil is the prime edible oil.
The earliest reference to argemone oil poisoning was made by Lyon, who reported four cases of poisoning in Calcutta in 1877 from the use of this oil in food.
Since then, epidemic dropsy has been reported from Bengal, Bihar, Orissa, Madhya Pradesh, Haryana, Assam, Jammu and Kashmir, Uttar Pradesh, Gujarat, Delhi and Maharashtra, mainly due to consumption of food cooked in argemone oil mixed with mustard oil or occasionally by body massage with contaminated oil.
The epidemic in 1998 at New Delhi, India is the largest so far, in which over 60 persons lost their lives and more than 3000 victims were hospitalized. Few studies reported the findings in patients affected with this condition.
Even after that the epidemics occurred at alarming frequency in Gwalior (2000), Kannauj (2002) and Lucknow (2005) cities of India. 6 possible cases with 2 deaths were reported in Gundari village in Banaskantha district of Gujarat in India were reported in June 2021.
Ugonjwa wa kuvuja maji ni aina ya uvimbe wa viungo vya mwili unaosababishwa na sumu ya Argemone mexicana (mchwa wa Mexico). Epidemic dropsy ni hali ya kliniki inayotokana na matumizi ya mafuta ya kula yaliyobadilishwa na mafuta ya mbegu ya Argemone mexicana. Sanguinari na dihydrosanguinari ni alkaloids mbili kuu za sumu za mafuta ya argemon, ambayo husababisha kuenea kwa capillary, kuenea na kuongezeka kwa upenyezaji wa capillary. Mafuta ya haradali yanapochanganywa na mafuta ya argamon, proteinuria (kwa mfano, kupoteza albumin) hutokea, na kuibuka kwa edema kama ilivyo katika ugonjwa wa nephrotic. Dalili nyingine kuu ni pitting edema ya pande mbili za viungo, maumivu ya kichwa, kichefuchefu, matumbo huru, erythema, glaucoma na kukosa pumzi. Uvujaji wa sehemu ya plasma yenye protini katika sehemu ya nje ya chembe husababisha kuundwa kwa edema. Matokeo ya hemodynamic ya upanuzi huu wa mishipa na upenyezaji husababisha hali ya hypovolemia ya jamaa na kichocheo cha mara kwa mara kwa ajili ya kuhifadhi kioevu na chumvi na figo. Ugonjwa huanza na dalili za tumbo na kisha hufuatwa na madoa ya ngozi na rangi. Dalili za kupumua kama vile kikohozi, upungufu wa pumzi na orthopnoea, zinazoendelea hadi kushindwa kwa moyo wa kulia wa kulia, huonekana. Anemia ya kiasi kidogo hadi cha wastani, hypoproteinaemia, azotemia ya kiasi kidogo hadi cha wastani ya figo, kutokwa na damu kwa retina, na glaucoma ni dalili za kawaida. Hakuna tiba hususa. Kuondoa mafuta ya udanganyifu na matibabu ya dalili za kushindwa kwa moyo na dalili za kupumua, pamoja na utoaji wa antioxidants na multivitamins, bado ni msingi wa matibabu. Ugonjwa wa dropsy hutokea kama janga katika maeneo ambapo matumizi ya mafuta ya haradali kutoka kwa mbegu za Brassica juncea, inayojulikana kama haradali ya India, kama njia ya kupika ni ya kawaida. Argemone mexicana (familia Papaveraceae), mzaliwa wa West Indies na asili katika India, inajulikana kama <unk>Shailkanta<unk> katika Bengal na <unk>Bharbhanda<unk> katika Uttar Pradesh. Pia inajulikana kama <unk>Pivladhatura<unk> au <unk>Satyanashi<unk>, ikimaanisha kuharibu. Mti huo hukua kwa wingi katika mashamba ya haradali na mashamba mengine. Mbegu zake ni nyeusi katika rangi na ni sawa na giza rangi mustard mbegu (Brassica juncea) katika umbo na ukubwa. Uharibifu wa mbegu za argemon katika mbegu za haradali (Brassica compestris) za rangi ya manjano ya mwanga unaweza kugunduliwa kwa urahisi, lakini mbegu hizi ni ngumu kuona wakati zimechanganywa na mbegu za haradali zenye rangi nyeusi. Mbegu za argemon hutoa mafuta ya asilimia 35 hivi. Kiasi cha alkaloids katika mafuta ya argemon ni 0.44% hadi 0.50%. Mbegu za Argan ni mbadala wa mafuta ya haradali kwa sababu ya upatikanaji wake rahisi, bei ya chini na uwezo wao kamili wa kuchanganya mafuta yao na mafuta ya haradali. Ugonjwa huu unaathiri kwa kiasi kikubwa moyo, moyo, moyo, moyo, na moyo, na kwa kawaida huathiri asilimia 5 ya watu. Mafunzo ya kufuatilia ya muda mrefu ni machache kwa hivyo athari za muda mrefu za sumu ya mafuta ya argemone hazijaandikwa. Inaripotiwa kuwa asilimia 25 ya watu wana ugonjwa wa edema baada ya miezi miwili na asilimia 10 baada ya miezi mitano. Pigmentation ya ngozi na kupoteza nywele kupita kiasi, ambayo ilidumu miezi 4 hadi 5 baada ya ugonjwa. Wagonjwa wengi hupona kabisa baada ya miezi mitatu. Utafiti wa damu ya wagonjwa wa dropsy umeonyesha kuwa kuna uzalishaji mkubwa wa aina za oksijeni (ROS) katika sumu ya mafuta ya argamon, na kusababisha kupungua kwa antioxidants katika mwili, hasa antioxidants lipid-soluble kama vile vitamini E na A (tocopherol na retinol). Ugonjwa huu unaathiri mfumo wa ulinzi wa antioxidant (antioxidant enzymes) katika damu. Utafiti wa awali wa in vitro umeonyesha kuwa ROS inahusika katika sumu ya AO inayosababisha uharibifu wa peroxidative wa lipids katika sehemu mbalimbali za chini ya seli za ini, ikiwa ni pamoja na microsomes na mitochondria ya panya. Uharibifu katika utando wa microsomal ya ini husababisha kupoteza shughuli ya cytochrome P450 na enzymes nyingine zinazohusishwa na utando zinazohusika na kimetaboliki ya xenobiotic, ambayo husababisha bio-elimination ya sanguinarine na kuongeza sumu yake ya jumla. Mistari kadhaa ya ushahidi imeonyeshwa kuelezea utaratibu wa sumu ya mafuta ya argemone / alkaloid. Ugonjwa wa sanguinarin umeonyeshwa kuwa unategemea athari ya uhusiano wake wa iminium na maeneo ya nucleophilic kama vikundi vya thiol, zilizopo katika maeneo ya kazi ya enzymes na protini nyingine muhimu na hivyo zinaonyesha asili ya electrophilic ya alkaloid. Kuongezeka kwa viwango vya glycogen baada ya sumu ya mafuta ya arginine inaweza kuwa kutokana na kuongezeka kwa glycogenolysis inayoongoza kwa malezi ya glucose-1-phosphate, ambayo huingia kwenye njia ya glycolytic na kusababisha mkusanyiko wa pyruvate katika damu ya wanyama wa majaribio na wagonjwa wa dropsy. Kuongeza kwa glycogenolysis inaweza kuungwa mkono zaidi na kuingiliwa kwa sanguinary katika upimaji wa glukosi kupitia kuzuia pampu ya sodiamu kupitia Na + K + ATPase na hivyo kuzuia usafirishaji wa glukosi kupitia kizuizi cha matumbo. Kwa kweli, kuongezeka kwa mkusanyiko wa pyruvate katika damu kunasababisha kufutwa kwa phosphorylation ya oxidative, na hii inaweza kuwa na jukumu la kupanua septa ya interalveolar na nafasi za alveolar zisizo na utaratibu katika mapafu ya panya waliolishwa mafuta ya argamon na kukosa pumzi kama ilivyoonekana kwa watu. Ugonjwa wa moyo: Kuzuia utendaji wa Na + K + ATPase ya moyo na sanguinarium ni kwa sababu ya mwingiliano na tovuti ya receptor ya glycoside ya moyo, ambayo inaweza kuwa na jukumu la kuzalisha mabadiliko ya degenerative katika nyuzi za misuli ya moyo katika ukuta wa auricular wa panya waliolishwa mafuta ya argamon na inaweza kuhusiana na tachycardia na kushindwa kwa moyo katika wagonjwa wa dropsy. Uharibifu wa cytochrome P450 ya ini huathiri kwa kiasi kikubwa uondoaji wa metabolic na ini. Kuhifadhi kwa sanguinarine katika mfumo wa gastrointestinal (GI), ini, mapafu, figo, moyo na seramu hata baada ya masaa 96 ya mfiduo inaonyesha hizi kama maeneo ya uwezekano wa sumu ya mafuta ya argamon. Jaribio la asidi nitriki na jaribio la chromatography ya karatasi hutumiwa katika kugundua mafuta ya argemone. Jaribio la chromatography ya karatasi ni jaribio nyeti zaidi. Kuondoa mafuta ya kupikia yaliyochafuliwa ndiyo hatua muhimu zaidi ya kwanza. Kupumzika kitandani na kuinua miguu na kula vyakula vyenye protini ni muhimu. Dawa za kuongeza kalsiamu, vioksidishaji (vitamini C na E), na thiamine na vitamini vingine vya kikundi cha B hutumiwa kwa kawaida. Kortikosteroidi na antihistamines kama vile promethazine zimetetewa na baadhi ya wachunguzi, lakini ufanisi ulioonyeshwa haupo. Diuretics hutumiwa ulimwenguni kote, lakini tahadhari lazima ionyeshwe ili kutopunguza kiasi cha intravascular isipokuwa dalili za kushindwa kwa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo wa moyo. Kushindwa kwa moyo kudhibitiwa kwa kupumzika kitandani, kupunguza chumvi, digitalis na diuretics. Ugonjwa wa mapafu hupatiwa dawa za kuua viini zinazofaa. Kushindwa kwa figo kunaweza kuhitaji tiba ya dialysis na kupona kamili kwa kliniki kunaonekana. Huenda glaukoma ikahitaji upasuaji, lakini kwa kawaida hupona kwa matibabu. Mbali na India, magonjwa ya kuambukiza yameandikwa kutoka Mauritius, Visiwa vya Fiji, wilaya za Kaskazini Magharibi mwa Cape za Afrika Kusini, Madagascar na pia kutoka Nepal. Kwa mfano, katika utafiti wa Afrika Kusini, ambapo ugonjwa huo ulisababishwa na unga wa ngano, magonjwa yote yalitokea kutokana na matumizi ya mafuta ya haradali yaliyochafuliwa na mafuta ya argamon. Katika tamaduni hizo, mafuta ya haradali ndiyo mafuta bora ya kula. "Kutokana na uchunguzi wa utafiti wa utafiti wa ""Argemone"" na utafiti wa utafiti wa ""Argemone"" na utafiti wa ""Argemone"" na utafiti wa ""Argemone"" na utafiti wa ""Argemone"" na utafiti wa ""Argemone"" na utafiti wa ""Argemone"" na ""Argemone"" na utafiti wa ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone"" na ""Argemone.""" Tangu wakati huo, ugonjwa wa dropsy umeripotiwa kutoka Bengal, Bihar, Orissa, Madhya Pradesh, Haryana, Assam, Jammu na Kashmir, Uttar Pradesh, Gujarat, Delhi na Maharashtra, hasa kutokana na matumizi ya chakula kilichopikwa katika mafuta ya argamon iliyochanganywa na mafuta ya haradali au mara kwa mara kwa massage ya mwili na mafuta ya uchafuzi. Janga la Corona la mwaka 1998 huko New Delhi, India, lilikuwa la kwanza duniani, na watu zaidi ya 60 walipoteza maisha yao na zaidi ya watu 3000 walipelekwa hospitalini. Uchunguzi wachache uliripoti matokeo katika wagonjwa walioathiriwa na hali hii. Hata baada ya hapo, magonjwa hayo yalitokea kwa wingi katika miji ya Gwalior (2000), Kannauj (2002) na Lucknow (2005) nchini India. Katika miezi ya mwisho ya mwezi Juni, watu 6 waliugua na wengine 2 wakafa katika kijiji cha Gundari katika wilaya ya Banaskantha, Gujarat nchini India.