The relationship between oxidative stress and apoptosis of histopathological changes in the ovary made by mad honey containing grayanotoxin.

The purpose of this study is to determine the effects of grayanotoxin in mad honey on ovarian tissue folliculogenesis in terms of cell death and nitric oxide expression. Three groups of 18 female Sprague-Dawley rats were formed. The first group received mad honey (80 mg/kg), the second group received normal honey (80 mg/kg), and the third group was the control. The first and second groups received normal and mad honey by oral gavage for 30 days before being sacrificed under anesthesia. Caspase 3 immunostaining showed a moderate to strong response, particularly in the mad honey group. In the mad honey group, immunostaining for caspase 8 and caspase 9 revealed a moderate immunoreaction in the granulosa cells of the Graaf follicles. The majority of Graaf follicles exhibited TUNEL positive in the mad honey group. The iNOS immunoreaction revealed a high level of expression in the mad honey group. In all three groups, eNOS immunostaining showed weak reactivity. According to the findings of apoptotic and nitric oxide marker expression, it was determined that mad honey may result in an increase in follicular atresia in ovarian follicles when compared to normal honey and control groups.

Anaphylactic shock following the mad honey consumption: a case report.

Introduction: Mad honey consumption is a common practice in Nepal for medicinal and consumption purposes, but it can lead to severe adverse effects. Grayanotoxin I and Grayanotoxin III isoforms found in rhododendron interfere with voltage-gated sodium channels resulting in gastrointestinal symptoms, and cardiovascular effects such as low blood pressure, abnormal heart rhythms, cardiac arrest, and abnormal electrical conduction in the heart, as well as rare central nervous system disorders. Here the authors report a case of Mad honey consumption leading to anaphylactic shock along with its investigations and management. Case presentation: The authors present a case of a 51-year-old female who developed anaphylactic shock after consuming mad honey. The patient experienced symptoms including nausea, vomiting, abdominal pain, sweating, dizziness, facial and lip swelling, but no chest pain, loss of consciousness, abnormal body movement, or dyspnoea. The patient had no prior medical conditions, regular medications, or history of allergic reactions to honey or pollen. Discussion: Mad honey intoxication is caused by grayanotoxins, with distinct cardiac effects for different types of grayanotoxins. Symptoms include bradycardia, hypotension, abdominal pain, dizziness, and nausea, which subsided within 24 h following the initial management. The presence of grayanotoxin can be detected using specialized instrumentation, but it may not be available in all medical facilities. Co-intoxication with alcohol or propolis may also occur. Conclusion: This case highlights the importance of recognizing and managing complications associated with mad honey consumption, particularly in regions where it is prevalent. Prompt medical attention is advised if unusual symptoms occur after honey consumption.

Mad honey poisoning presenting with syncopal attack: a case report.

Mad honey contains grayanotoxin, which is commonly derived from the nectar of a few Rhododendron species. It is commonly used by natives of the Himalayas in the belief of its medicinal use. Case presentation: The authors report a case of 62 years old male with mad honey poisoning who was presented to the emergency department with loss of consciousness and had bradycardia and hypotension on arrival. The patient received intravenous fluids, atropine, and vasopressor support and was closely monitored in the coronary care unit for 48 h. Discussion: Grayanotoxin I and II are believed to be primarily responsible for mad honey intoxication and act by persistent activation of voltage-gated sodium channels. Hypotension, dizziness, nausea, vomiting, and impaired consciousness are the common presentation of mad honey intoxication. Toxic effects are usually mild and close monitoring for 24-48 h is sufficient but life-threatening complications like cardiac asystole, convulsions, and myocardial infarction have also been reported. Conclusion: Most cases of mad honey intoxication only need symptomatic treatment and close observation but the potential for deterioration and life-threatening complications must also be considered.

Management of mad honey intoxication with suspected anaphylaxis in Nepal: a case report.

Consumption of mad honey can lead to intoxication. The exact incidence of mad honey-induced intoxication is unknown. Typically, the patients present with dizziness, nausea, syncope, and sinus bradycardia. Case presentation: The authors reported the case of a middle-aged male patient who presented with blurring of vision, passage of loose stools, vomiting, and profuse sweating after ingestion of honey. He also had a history of loss of consciousness. On presentation, he was hypotensive and tachypneic with cold, clammy extremities. His ECG showed sinus bradycardia. The authors made a diagnosis of mad honey intoxication with suspected anaphylaxis. The authors treated him with intravenous normal saline, epinephrine, and atropine. He again developed hypotension and bradycardia in a few hours, for which hydrocortisone was administered, following which his heart rate was normalized in 2 h. Overall, the recovery time in our patient was 8 h. The patient was counseled to avoid consuming mad honey and did well on his monthly follow-up. Discussion: Our patient had signs and symptoms suggesting intoxication following ingestion of mad honey with suspicion of anaphylaxis. Similar to other reported cases, the patient had sinus bradycardia and hypotension. Epinephrine and atropine were administered to treat hypotension and bradycardia, respectively. Also, refractory hypotension was managed by intravenous hydrocortisone. Usually, atropine and saline infusion are sufficient to manage these cases, and simultaneous use of epinephrine and atropine should be avoided unless indicated. Conclusion: Our case highlighted the approach to diagnosing and treating mad honey intoxication with suspected anaphylaxis.

Mad Honey and the Poisoner King: A Case of Mass Grayanotoxin Poisoning in the Roman Military.

We describe an episode of mass poisoning during the ancient Third Mithridatic War. In a brutal and well-planned ambush, forces from the Kingdom of Pontus destroyed a Roman column through the clever use of "mad honey." Incapacitated by the acute poisoning, the Romans were unable to hold off the Pontic forces. We conclude that the debilitating symptoms that the Roman soldiers experienced were due to the presence of grayanotoxins in the honey. Although they were likely self-limiting, developing these symptoms in an enemy ambush made a lethal combination. The "mad honey" environmental threat continues to persist in the Black Sea region to this day and is an etiology that modern physicians should be aware of.

Worldwide distribution and clinical characteristics of mad honey poisoning cases.

OBJECTIVES: Mad honey poisoning is a common public health problem that can be seen in many parts of the world. In this study, the symptoms and clinical findings of mad honey poisoning cases and their distribution worldwide were investigated based on current data. METHODS: PubMed, Scopus, Web of Science and Google Scholar databases were searched. The demographic characteristics of the cases, clinical findings, amount of consumed honey, duration of hospitalization, and data of the region where mad honey was produced were recorded. RESULTS: 900 cases were identified. The majority of poisoning cases (91.44%) were reported from mad honey produced in Turkey, Nepal (4.67%) came second and Korea (1.56) third. The majority of cases in Turkey were due to honey produced in the Black Sea Region. It was also determined that the mad honey was produced in the west Black Sea Region in most of the cases (35.22%), followed by the east Black Sea Region with a rate of 33.22%. In poisonous cases, it was determined that the mad honey was mostly produced in Rize, followed by Trabzon and Kastamonu, respectively. The most common signs of mad honey poisoning were bradycardia (88.48%) and hypotension (76.04%). CONCLUSION: The majority of cases have been reported from Turkey. When examining where the mad honey was produced in Turkey, it was seen that the western Black Sea Region came first, and the eastern Black Sea Region came second. Rize came first among the provinces, followed by Trabzon and Kastamonu. There is a parallelism between the distribution of mad honey poisoning cases and the distribution areas of Rhododendron species. However, although Rhododendron species show a widespread distribution throughout the world, why the majority of the cases were reported from Turkey draws attention as an issue that needs to be investigated.

Confirmed Grayanotoxin Poisoning with Bradycardia from a Gift of Imported Honey.

BACKGROUND: Human grayanotoxin poisoning is distinctly uncommon in North America, as the predominant source of human exposure is honey made by bees pollinating rhododendron species in the Mediterranean. We present a case of confirmed grayanotoxin poisoning from honey imported from Turkey. CASE REPORT: A 61-year-old man developed nausea, lightheadedness, and lost consciousness. Onset was 30 min after the ingestion of honey that was brought to the United States from Turkey. Emergency medical services found him bradycardic, hypotensive, and unresponsive. He was treated with atropine, saline, and oxygen, at which point his heart rate and blood pressure improved, and he regained consciousness. A similar episode several days earlier was followed by a brief unrevealing hospitalization. He was again hospitalized, and had a normal echocardiogram, telemetric monitoring, and complete laboratory studies. Grayanotoxins I and III were subsequently identified in the patient's blood, urine, and honey. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Grayanotoxins are diterpenoids found in rhododendron species, whose clinical effects span multiple organ systems including gastrointestinal, cardiac, and neurologic. Treatment is largely supportive, and a good response to atropine and intravenous fluids has been described. Laboratory confirmation of grayanotoxins is not available in a short enough turnaround time to be clinically useful during immediate management, but confirmatory testing may obviate further unnecessary evaluation. Grayanotoxins are likely to remain a rare source of poisoning in North America, but recurrent bradycardia without alternative etiology should prompt a thorough exposure history, which may reveal, as in this case, a treatable toxicologic etiology.

Bioactive Properties and Phytochemical Screening of Mad Honey Bee Pollen.

INTRODUCTION: Mad honey is widely used in folk medicine in the Black Sea region of Turkey for its medicinal properties, but its pollen is not collected by mad honey producers and its benefits are unknown. METHODS: In this study, water and ethanol extracts of mad honey bee pollen from four different plateaus in the Black Sea region of Turkey were researched for their antioxidant and antimicrobial properties. Phytochemical analyses were carried out and the data were supported with UV-Vis spectrophotometry. Antimicrobial activity was researched against four Gram-positive and four Gram-negative bacteria, one fungus, and one yeast. The results were compared with standard antioxidants and antibiotics. RESULTS: The ethanol extracts of the samples from Sinop (P5), Giresun (P7), and Trabzon (P8) were the most active samples as antioxidants, and almost all the extracts of R. ponticum bee pollen were effective on the tested microorganisms. However, P5-8 showed better values for B. cereus, E. feacalis, E. coli, and P. aeruginosa. CONCLUSION: It has been proven that mad honey bee pollen is a natural product with previously unknown medicinal properties and rich phytochemical content. Future research and clinical trials are important to scientifically support its benefits in complementary medicine.

Investigation of genotoxic effects of rhododendron honey using three mammalian bioassays in vivo.

Rhododendron honey (RH) is obtained from the rhododendron plants are grown in many regions around the world, causes poisoning in humans due to the grayanotoxin (GTX) compound in its structure. It is used by the public as a therapeutic for some diseases. It was aimed to study the genotoxic and cytotoxic effects of RH in mouse bone-marrow and sperm cells by using three mammalian bioassays. 25, 50 and 75 mg kg-1 concentrations of RH given to male mice via gavage for 24 and 48 h treatment periods and its active ingredient Grayanatoxin (GTX-III) 0.01 mg kg-1 by i.p. injection. Chromosome aberrations (CA), polychromatic erythrocytes (PCE)/normochromatic erythrocytes (NCE), micronucleated polychromatic erythrocytes (MNPCE) and sperm abnormalities were investigated. The results demonstrated that all the tested concentrations of RH significantly induced total abnormal cell frequency including chromosomal breaks for two time periods. In the MN assay, 75 mg kg-1 RH and 0.01 mg kg-1 GTX-III significantly increased % MNPCE and significantly reduced PCE/NCE ratios after 24 and 48 h treatments on mice demonstrating potential genotoxic and cytotoxic effect. Although there was a concentration-related increase in the percentage of total sperm abnormalities, this increase was not statistically significant compared to control. As a result, microscopic genotoxicity and cytotoxicity marker tests showed that RH and its active ingredient GTX-III have potential genotoxic and cytotoxic effect on mice bone marrow cells. It is understood that RH that is used to treat some diseases by public, should be handled carefully and used in a controlled manner.HighlightsChromosome aberration, micronucleus and sperm morphology assays are recommended as reliable biological indicators.RH and its active ingredient GTX-III have potential genotoxic and cytotoxic effect on mice bone marrow cells.Significant changes were observed upon the treatment of 75 mg kg-1 MH for MN assay.

Mad Honey Poisoning Case Series Presenting With ECG Findings Including Atrioventricular Complete Block and Symptomatic Hypotension.

Plants belonging to the Ericaceae family, which grow endemically in some parts of the world, contain grayanotoxin, which causes fatal bradyarrhythmia and circulatory collapse. Mad honey, which comes from plants with grayanotoxin, has various uses, namely, as an aphrodisiac, as an alternative therapy for GI disorders such as peptic ulcer, dyspepsia, and gastritis, and as a treatment for hypertension. However, GI, neurological and cardiac side effects may arise from its ingestion due to the grayanotoxin contained by this type of honey. Cardiac rhythm disturbances, sinus bradycardia, and other life-threatening side effects can occur, especially atrioventricular (AV) block and nodal rhythms. In this article, we present five honey poisoning cases involving adults who were admitted to our ED. Notably, one of the patients was unresponsive to atropine, so a temporary pacemaker was inserted, after which the patient was moved to the coronary ICU. Meanwhile, the cardiac rhythm of the other cases returned to normal in the follow-up after atropine administration.

Evaluation of Electrocardiographic Parameters and the Presence of Interatrial Block in Patients with Mad Honey Intoxication.

Mad honey intoxication (MHI) is a food-induced clinical condition that usually presents with cardiovascular symptoms and can lead to life-threatening arrhythmias if not diagnosed and treated early. No data exist in the literature on the presence of interatrial block (IAB) after food intoxication. In our study, we sought to investigate atrioventricular electrocardiography (ECG) parameters and determine the frequency of IAB in patients with MHI. In total, 76 patients diagnosed with MHI were included in our retrospective study. Twelve-lead ECGs were performed and participants were divided into two groups according to the presence of IAB in the reference ECG. The P maximum (Pmax), P minimum (Pmin), P dispersion (Pdisp), T peak to T end (Tp-Te) interval and QT dispersion (QTdisp) values were compared between the two groups. IAB was detected in 28 (35.5%) of 76 MHI patients included in the final analysis. Pmax duration (122 ± 8; p < 0.001) and PD (69 ± 11; p < 0.001) were significantly higher in the IAB ( +) group. During regression analysis, Pmax [odds ratio (OR) 1.158, 95% confidence interval (CI) 1.036-1.294; p = 0.010] and Pd (OR 1.086, 95% CI 1.001-1.017; p = 0.046) were independently associated with IAB. Pmax and Pd area under the receiver operating characteristic curve values for IAB prediction were 0.926 (95% CI 0.841-1,000; p < 0.001) and 0.872 (95% CI 0.765-0.974; p < 0.001), respectively. ECG changes are common in patients presenting with MHI. These patients need to be followed up clinically in terms of progression to arrhythmic events that may occur in the future.

Determination of the dose-dependent toxic effects of mad honey on mouse liver using ATR-FTIR spectroscopy.

Mad honey (MH) is obtained from Rhododendron plants, which are extensively grown in some regions of the world such as Europe, North America, Tropical Asia and Turkey. Although it has been known that MH induces adverse effects in the body due to grayanotoxin (GTX) in it, it is widely used for some medical purposes by the public. In this study, the effects of MH (25, 50 and 75 mg/kg) and GTX-III (0.01 mg/kg), which is the pure form of the most toxic type of the GTXs in MH, were investigated on the mouse liver at molecular level via Attenuated Total Reflection-Fourier Transform Infrared (ATR-FTIR) spectroscopy. The results showed that 25 and 50 mg/kg of MH didn't cause any significant alterations in the liver tissue except a decrease in the glycogen amount. However, significant differences were observed between 75 mg/kg MH and GTX-III treated groups and control group. For example, the amounts of saturated lipids, nucleic acids and proteins increased in the 75 mg/kg MH and GTX-III treated groups. A decrease in the ratios of unsaturated/saturated lipid, CH2/lipid and carbonyl/lipid and an increase in the ratio of CH3/lipid were observed after the administration of 75 mg/kg MH and GTX-III, all of which may be a consequence of lipid peroxidation. Moreover, 75 mg/kg MH and GTX-III caused a decrease in the membrane order, an increase in the membrane fluidity and some important changes on the secondary structure of proteins indicating protein denaturation. In addition, Hierarchical Cluster Analysis (HCA) and Principal Component Analysis (PCA) confirmed these findings. These results revealed that MH induces significant dose-dependent toxic effects in the structure and function of the liver tissue. This study also showed that ATR-FTIR spectroscopy provides a rapid and sensitive monitoring of the changes induced by a toxic compound on biological tissues at molecular level.

Rapid identification of "mad honey" from Tripterygium wilfordii Hook. f. and Macleaya cordata (Willd) R. Br using UHPLC/Q-TOF-MS.

Cases of honey poisoning have been reported widely, meaning there is a need for methods that detect "mad honey" or honey contaminated with plant-derived toxins to protect human health. In this study, we compared whole flower extracts and honey from Tripterygium wilfordii Hook. f. (TwHf) and Macleaya cordata (Willd) R. Br (McRB) using QuEChERS (quick, easy, cheap, effective, rugged, and safe) and ultra-high-performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UHPLC/Q-TOF-MS). The results revealed several compounds common to whole flowers and honey samples. Triptolide and protopine were selected as potential markers for identifying "mad honeys" from these plants. The developed method can easily detect different honey varieties that were spiked with 5% TwHf and McRB honey samples. Additionally, 90 commercial honey samples were analyzed and determined as free from contamination. The method described in this report could be useful for studies on honey from other poisonous nectar and pollen plants.

Investigation of mad honey use as an alternative treatment in patients admitted to the pulmonary clinic: Ordu, Turkey example

Abstract This study assessed mad honey use in alternative treatments. The universe of this descriptive study was patients admitted to the pulmonary disease clinic located in the Ordu province of the Black Sea region between 15 December 2014 and 15 February 2015. We did not use a sampling method and patients who agreed to participate were included in the study (n=353). In order to collect the data, we used a questionnaire prepared by the researchers. In this study, 77% of the participants stated that mad honey was beneficial to health, 44.5% used mad honey, and 53.5% consumed it daily. Furthermore, 28.7% used mad honey for asthma, 6.4% for cough, 12.1% for gastrointestinal diseases, and 3.2% for hypertension. There was a significant relationship between the gender, family structure, age, and chronic disease status of participants and the status of consuming mad honey (p<0.05). In this study, participants used mad honey for asthma, gastrointestinal diseases, hypertension, and cough. Health professionals should provide training and counseling on the health effects and risks of mad honey to improve public health.

Cardiovascular, psychiatric, and neurological phenomena seen in mad honey disease: A clinical case report.

Mad Honey Disease is characterized by intoxication symptoms secondary to over-ingestion of grayanotoxin found in honey produced from rhododendron nectar. Cardiovascular symptoms are common, but psychiatric and neurological phenomena are rarely seen in this condition. Our case details a patient who presented with florid symptomology in all three aforementioned areas.

The effect of different types of honey on healing infected wounds.

OBJECTIVE:: To investigate the effects of treatments of 'mad honey', blossom honey and nitrofurazone on infected wound healing. METHOD:: Male albino Wistar rats were randomly divided into four groups: 'mad honey' (MH), blossom honey (BH), nitrofurazone (N) and control (C). All rats were anaesthetised intraperitoneally. A circular skin incision was made to the back regions. Grafts containing slime-producing Staphylococcus epidermidis were placed on the incision area and then sutured to the skin. Infection in the wound area was confirmed after 48 hours. Wounds were dressed twice daily with the various treatment materials. Rats were randomly euthanised on days 7 or 14, and tissue samples taken. Tissue samples were assessed for hydroxyproline (HP), tensile strength (TS) and macroscopic measurement (area and intensity). RESULTS:: HP levels were higher in the treatment groups (MH, BH, N) at days 7 and 14 compared with the control group. 'Group x day' interaction was found in the HP levels (p=0.015). Increases in HP levels in the MH and N groups between days 7 and 14 were significantly higher than those in the other groups (p<0.05). Intensity was significantly lower in the control group and significantly higher in group MH compared with the other groups. Significant 'group x day' interaction was observed in intensity (p=0.006). TS was significantly lower on day 7 than on day 14 (p=0.022). No marked difference was observed between the groups, nor any 'group x day' interaction, in terms of TS. CONCLUSION:: Honey administration successfully healed infected wounds. However, there was no significant difference between the effect of MH and that of N in terms of wound healing.

Grayanotoxin levels in blood, urine and honey and their association with clinical status in patients with mad honey intoxication.

OBJECTIVES: The purpose of this study was to investigate whether there is an association between grayanotoxin levels in urine and blood of patients with mad honey intoxication and in the honey consumed, and the resulting clinical picture. The pilot data acquired from this study was analysed in National Forensic Service, Daejeon Institute, South Korea and first results were published as a preliminary study. PATIENTS AND METHODS: This descriptive study was conducted at a university hospital emergency department in Turkey. 25 cases diagnosed with mad honey intoxication were obtained the study. Samples of mad honey consumed by patients were obtained. Blood and urine specimens were collected at presentation to the emergency department. GTX 1 and GTX 3 levels from patients' blood, urine and honey consumed were investigated simultaneously using the LC-MS/MS system. RESULTS: Mean GTX 1 concentration in blood was 4.82 ng/mL and mean GTX 3 level 6.56 ng/mL. Mean GTX concentration in urine was 0.036 µg/mL and mean GTX 3 level 0.391 µg/mL. Mean GTX I concentration in honeys consumed was 8.73 µg/gr and mean GTX 3 level 27.60 µg/gr. CONCLUSION: This descriptive study is show grayanotoxin levels in body fluids of patients with mad honey intoxication. No association was determined between grayanotoxin levels in blood and clinical data.

A Comparison of the Effects of Grayanotoxin-Containing Honey (Mad Honey), Normal Honey, and Propolis on Fracture Healing.

OBJECTIVES: Delayed healing and non-union of fractures have a significant effect upon patient morbidity. Studies have therefore largely concentrated on accelerating fracture healing. This study was intended to compare the effect of "mad honey" and propolis on fracture healing using radiological and histopathological analysis. SUBJECTS AND METHODS: Femur fracture was surgically performed on 48 rats, followed by fixation. Animals were then divided into 8 groups: 2 control groups (15- and 30-day) and 6 treatment groups (15- and 30-day normal honey, 15- and 30-day "mad honey," and 15- and 30-day propolis). Rats were sacrificed at the end of these periods, and radiological and histological examinations were performed. RESULTS: Radiological healing in the propolis group after 15-day therapy was statistically better than in the control (p = 0.004) and normal honey (p = 0.006) groups. After 30-day therapy, healing in the propolis group (p = 0.005) and grayanotoxin-containing "mad honey" group (p = 0.007) were significantly better than in the control group. Histologically, there was a statistically significant difference between the 15-day propolis group and the other groups (control, honey, mad honey: p = 0.003, p = 0.003, and p = 0.002, respectively). We also found a statistically significant difference when the 30-day propolis group (p = 0.005) and "mad honey" group (p = 0.007) were compared to the control group. CONCLUSIONS: This study shows that grayanotoxin-containing "mad honey" and propolis can accelerate fracture healing.

Effect on oxidative stress, hepatic chemical metabolizing parameters, and genotoxic damage of mad honey intake in rats.

A total of 66 male Wistar rats were used and six groups (control: 10 animals and experimental: 12 animals) were formed. While a separate control group was established for each study period, mad honey application to the animals in the experimental group was carried out with a single dose (12.5 g kg-1 body weight (b.w.); acute stage), at a dose of 7.5 g kg-1 b.w. for 21 days (subacute stage), and at a dose of 5 g kg-1 b.w. for 60 days (chronic stage). Tissue and blood oxidative stress markers (malondialdehyde (MDA), nitric oxide (NO), 4-hydroxynonenal (HNE), superoxide dismutase, catalase, glutathione (GSH) peroxidase, and glucose-6-phosphate dehydrogenase), hepatic chemical metabolizing parameters in the liver (cytochrome P450 2E1, nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase, nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome c reductase (CYTC), GSH S-transferase (GST), and GSH), and micronucleus and comet test in some samples were examined. Findings from the study showed that single and repeated doses given over the period increased MDA, NO, and HNE levels while decreasing/increasing tissue and blood antioxidant enzyme activities. From hepatic chemical metabolizing parameters, GST activity increased in the subacute and chronic stages and CYTC activity increased in the acute period, whereas GSH level decreased in the subacute stage. Changes in tail and head intensities were found in most of the comet results. Mad honey caused oxidative stresses for each exposure period and made some significant changes on the comet test in certain periods for some samples obtained. In other words, according to the available research results obtained, careless consumption of mad honey for different medical purposes is not appropriate.

Mad Honey Disease.

A 46-year-old woman presented to the emergency room with acute onset of nausea, vomiting and prostration. She appeared ill and was poorly responsive to verbal stimuli. Physical examination showed a systolic blood pressure of 60 mmHg and a pulse of 40 bpm. ECG was notable for slight ST-elevations in the inferior leads. Right ventricular myocardial infarction with cardiogenic shock and bradycardia was suspected. Supportive therapy with catecholamines was initiated and an emergency coronary angiography was arranged. However, laboratory results showed normal troponin levels and a subsequent echocardiogram showed the absence of abnormal wall motion. Thorough history taking with the spouse revealed that the patient had consumed Turkish honey approximately 1 h before the symptoms began. The patient made a full recovery within 24 h with only supportive therapy. In retrospect, the clinical presentation was highly indicative of poisoning with grayanotoxins from the rhododendron plant, which contaminate some types of honey in the Black Sea area. A pollen analysis confirmed the presence of rhododendron in a honey sample. Historically this poisoning is referred to as mad honey disease. The ST-elevations in the ECG were a sign of early repolarization, a non-pathological finding. LEARNING POINTS: ST-elevation in the inferior leads of an ECG in the context of hypotension and bradycardia does not always indicate right myocardial infarction.In the proper context, intoxication with grayanotoxins should be included in the differential diagnosis of hypotension and bradycardia.Study of diseases occurring in the past in a particular region offers the physician the chance to make a diagnosis otherwise missed.