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CASE REPORT |
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Year : 2014 | Volume
: 60
| Issue : 1 | Page : 72-74 |
Luffa echinata: Healer plant or potential killer?
S Giri, CR Lokesh, S Sahu, N Gupta
Department of Medicine, University College of Medical Sciences and Guru Tegh Bahadur Hospital, Delhi, India
Date of Submission | 03-Jan-2013 |
Date of Decision | 05-Sep-2013 |
Date of Acceptance | 14-Oct-2013 |
Date of Web Publication | 14-Mar-2014 |
Correspondence Address: N Gupta Department of Medicine, University College of Medical Sciences and Guru Tegh Bahadur Hospital, Delhi India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0022-3859.128819
Bristly luffa (Luffa echinata), a member of the cucurbitaceae family is an Ayurvedic medicinal plant, which has been used in the traditional system of medicine for variety of symptoms. The active constituents like cucurbitacin, saponin, echinatin, β-Sitosterol, oleanolic acid and flavonoids have important pathophysiological effects on human body. However, there is no earlier published report of any toxicity on humans. We report a case of a 50-year-old gentleman, who presented with gastrointestinal bleeding, deranged liver function and shock following consumption of dried fruits of Luffa echinata soaked overnight in water. He had antral gastritis and duodenal erosions on upper gastrointestinal endoscopy and was managed conservatively and recovered completely.
Keywords: Bristly luffa, cucurbitacin, luffa echinata, saponin
How to cite this article: Giri S, Lokesh C R, Sahu S, Gupta N. Luffa echinata: Healer plant or potential killer?. J Postgrad Med 2014;60:72-4 |
:: Introduction | |  |
Luffa echinata belongs to the cucurbitaceae family. In India, it is mainly found in Uttar Pradesh, Bihar, West Bengal and Gujarat. It is known by various names across India like Akhuvishaka, Chaturangaka, Devadali in Sanskrit, Bindaal or Ghagarabela in Hindi, Deyatada in Bengal and as Panibira in southern India. The plant is also found in many parts of Pakistan, Bangladesh, Myanmar and some parts of tropical Africa. The plant is a climber with slender stem, leaves are kidney shaped and lobbed [Figure 1]. [1] The fruits are ovoid, 2-3 cm long and are densely covered with 3-5 mm bristles, which gives its name Bristly luffa.
The fruit is intensely bitter and fibrous [Figure 2]. The dried fruits of the plant are used by the traditional Ayurvedic system of medicine, for various illnesses like chronic bronchitis, dropsy, nephritis, intestinal and biliary colic, fever and jaundice, etc. It has many proposed systemic effects, such as hepatoprotective, digestive stimulant, diuretic, purgative, anti-inflammatory, antipyretic, cough expectorant, etc. [2]
:: Case Report | |  |
A 50-year-old gentleman, presented in a drowsy state with acute onset of pain abdomen, vomiting, and bleeding per rectum. Patient attributed his symptoms to consumption of 100-150 g of dried fruits of Luffa echinata soaked in water, which he had consumed nearly 20 hours before; to improve his digestion and bloating symptoms. There was no previous history of fever, rash, gastrointestinal bleeding, bleeding diathesis or history of taking drugs like NSAIDs, aspirin, anticoagulant or corticosteroids. He was non-alcoholic. Clinical evaluation revealed feeble peripheral pulses with cold extremities and icterus. Blood pressure at presentation was 80/60 mmHg with central venous pressure of 6 cm of H 2 O. Abdominal examination revealed mild tenderness in epigastric region with no hepatosplenomegaly or free fluid. Other system examination revealed no abnormality. Routine investigations on admission showed hemoglobin of 14.8 g/dl, total leucocytes count of 12,800/μl, platelet count of 2.04 lakh/μl. Peripheral smear revealed a normocytic normochromic picture. Serum total bilirubin was 8.6 mg/dl ( normal 0.3-1.9 mg/dl), direct bilirubin was 4 mg/dl (normal 0-0.3 mg/dl), alanine transaminase (ALT) of 862 IU/L (normal <40 IU/L) , aspartate transaminase (AST) of 695 IU/L ( normal <40 IU/L), alkaline phosphatase of 424 IU/L ( normal 20-140 IU/L), lactate dehydrogenase (LDH) of 464 IU/L (normal 30-120 IU/L), creatine kinase (CPK) of 453 IU/L ( normal 60-400 IU/L) and CK MB of 10 IU/L. Prothrombin time (PT) was initially prolonged by 6 seconds and activated partial thromboplastin time (aPTT) was normal. His serial electrocardiograms and a 2D Echocardiography done on the second day of his admission were normal. Arterial Blood Gases (ABG) on three different occasions, early during presentation was also normal. Serum potassium was 4.2 meq/L. Upper gastrointestinal endoscopy on day 3 revealed diffuse antral gastritis and erosions in first part of duodenum; however colonoscopy was normal.
He was managed conservatively with intravenous fluids, one unit of whole blood, fresh frozen plasma (FFP), vitamin K, vasopressors and proton pump inhibitors. His haemoglobin repeated on the same day was 11.2 g/dl. Bleeding per rectum was stopped on 2nd day, PT became normal on day 3, liver enzymes and bilirubin levels were gradually improved over a period of 7-10 days and patient was successfully discharged after 12 days.
:: Discussion | |  |
Luffa echinata (Bristly luffa) belongs to the cucurbitaceae family. Mainly the fruits of the plant have been used in traditional Ayurvedic medicine. The active constituents of the plant include Saponins, Hentriacontane, Gypsogenin, Sapogenin Cucurbitacin-B and E, β-Sitosterol, Echinatol-A and B, Oleanolic acid, Elaterin glycoside, Chrysoeriol-7-glucoside, Sitosterol glycosides, etc. [2],[3] These active constituents are known to have a wide variety of pathophysiological effects on human body [Table 1]. Although there is no earlier published report of human toxicity due to Luffa echinata, few reports of human toxicity due to other cucurbits have been reported. Khan, et al[4] reported five cases of bloody diarrhoea due to colocynth toxicity. Nadkarni, et al[5] reported hematemesis due to bitter gourd juice ingestion. Puri, et al[6] have reported a large series of 15 cases with gastrointestinal bleed and hypotension following ingestion of the juice of bitter bottle gourd. The US-FDA database on poisonous plants also includes this plant. | Table 1: The role of different active principles of the fruit responsible for the various presenting symptoms and their postulated mechanisms are incorporated in a tabular form
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All cucurbits produce variable quantities of a complex substance known as Cucurbitacin. This is responsible for the bitter quality of the plant, which produces a characteristic aroma and protects it from insects and animals. Cucurbitacin B and C are cytotoxic they causes G2 cell cycle arrest and apoptosis of malignant cells via reactive oxygen species dependent mechanism. They also inhibit STAT3 and JAK/STAT pathways. They have been tried in many cancers such as pancreatic cancer, melanoma, breast cancer, colon cancer. [7] Cucurbitacin also have hepatoprotective, anti-inflammatory and cardiovascular effects. The anti-inflammatory activities of some of the cucurbitacin are linked to inhibition of cyclooxygenase enzyme (COX). Saponins of various plants have been used as anti-oxidants and anti-carcinogens. It reduces serum cholesterol and improve immunity but excess saponins can cause hemolysis and cytotoxicity. [8] β-Sitosterol is a phytosterol, mainly used to treat hypercholesterolemia, benign prostatic hyperplasia, and as an immunomodulator and anticancer agent. Excess Sitosterol can cause hemolysis in patients of sitesterolemia, but not in normal individuals. [9]
Chrysoeriol, a flavonoid has anti-oxidant, anti-inflammatory, anti-thrombogenic, anti-atherogenic and anti-cancer properties. Flavonoids and their synthetic analogues have been intensively investigated in the treatment of different cancers. They inhibit the promotion stage of carcinogenesis by inhibiting oxygen radical-forming enzymes or enzymes that contribute to DNA synthesis or act as ATP mimics and inhibit protein kinase that contribute to proliferative signal transduction. They may prevent tumor development by inducing tumor cell apoptosis by inhibiting DNA topoisomerase II and p53 down regulation or by causing mitochondrial toxicity. Toxicity of flavonoids is an active area of investigation, excess flavonoids can cause hemolysis, liver failure, contact dermatitis, etc. [10] Methanol extracts of Luffa echinata caused apoptosis of human colon cancer cells by activating mitochondrial apoptosis pathway in vitro. [11] The various glycosides can cause cardiac suppression and hypotension. [2] Aerial parts of Luffa echinata dose dependently decreases gastric content, total acidity, ulcer index and increase pH of gastric fluid in pylorus ligation ulcer models in rat. [12] In a recent study. Sharma et al[13] found free radical scavenging, anti inflammatory and analgesic effects of Luffa echinata seed extract in a dose-dependent manner. Echinatin, another important constituent have been shown to disturb the mitochondrial energy transfer reactions and membrane permeability in animal studies. [14] The role of some other active ingredients is not known.
The traditional system of medicine recommends a dose of 1-3 g/day of dry fruits of Luffa. [2] A study by Abraham, et al[15] defined the lethal dose of Luffa echinata in mice (LD50 ≥ 21.5 mg/kg body weight). Our patient consumed nearly 100-150 g of the dried fruits and presented with above-mentioned symptoms. The various active ingredients of this plant may explain shock, gastrointestinal bleeding and hepatotoxicity in our patient.
:: Conclusions | |  |
Excess consumption of the fruits of Luffa echinata may be toxic to humans, due to different active ingredients that it contains. This is a cause for concern in a country like India where a large population strongly believes in traditional system of medicine and people indulge in self-medication with such medicinal herbs.
:: References | |  |
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2. | Luffa. In: Khare CP, editor. Indian Herbal Remedies: Rational Western Therapy, Ayurvedic, and Other Traditional Usage, Botany. New York: Springer; 2004. p. 294.  |
3. | Ahmed B, Alam T, Khan SA. Hepatoprotective activity of Luffa echinata fruits. J Ethnopharmacol 2001;76:187-9.  |
4. | Khan SA, Shelleh HH, Bhat AR, Bhat KS. Colocynth toxicity. A possible cause of bloody diarrhea. Saudi Med J 2003;24:904-6.  |
5. | Nadkarni N, D′Cruz S, Sachdev A. Hematemesis due to bitter melon (Momordica charantia) extract-induced gastric ulcerations. Indian J Gastroenterol 2010;29:37-8.  [PUBMED] |
6. | Puri R, Sud R, Khaliq A, Kumar M, Jain S. Gastrointestinal toxicity due to bitter bottle gourd (Lagenaria siceraria) - a report of 15 cases. Indian J Gastroenterol 2011;30:233-6.  |
7. | Duangmano S, Sae-Lim P, Suksamrarn A, Patmasiriwat P, Domann FE. Cucurbitacin B causes increased radiation sensitivity of human breast cancer cells via G2/M Cell Cycle arrest. J Oncol 2012;2012:601682.  |
8. | Available from: http://www.phytochemicals.info/phytochemicals/saponins.php [Last accessed on 2012 Aug 10].  |
9. | Available from: http://www.drugs.com/npp/beta-sitosterol.html [Last accessed on 2012 Aug 10].  |
10. | Galati G, O′Brien PJ. Potential toxicity of flavonoids and other dietary phenolics: Significance for their chemo preventive and anticancer properties. Free Radic Biol Med 2004;37:287-303.  |
11. | Shang LH, Li CM, Yang ZY, Che DH, Cao JY, Yu Y. Luffa echinata Roxb. Induces human colon cancer cell (HT-29) death by triggering the mitochondrial apoptosis pathway. Molecules 2012;17:5780-94.  |
12. | Kailasiya D, Jain SK, Verma M, Yadav RD, Kanaujia V. Antiulcer activity ofaerial parts of Luffa Echinata Roxb. Ethanolic extracts in diclofenac sodium induced rats. Pharma Sci Monitor 2012;3:109-17.  |
13. | Sharma T, Arora R, Gill NS. Evaluation of free Radical scavenging, Anti inflammatory and Analgesic potentials of Luffa Echinata seed extract. J Med Sci 2012;12:99-106.  |
14. | Inoue B, Inaba K, Mori T, Izushi F, Eto K, Sakai R, et al. The effects of echinatin and its related compounds on the mitochondrial energy transfer reaction. J Toxicol Sci 1982;7:245-54.  [PUBMED] |
15. | Abraham Z, Bhakuni DS, Garg HS, Goel AK, Mehrotra BN, Patnaik GK. Screening of Indian Plants for Biological Activity: Part XII. Indian J Exp Biol 1986;24:48-68.  [PUBMED] |
[Figure 1], [Figure 2]
[Table 1]
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