Acetic Acid Ingestion Research Articles

THERAPEUTIC AND ANTAGONIST VILLI INSURGENCY OF GARCINIA KOLA ON ACETIC ACID INDUCED EROSIVE SMALL INTESTINAL ULCER OF WISTAR ALBINO RATS MODEL

The small bowel, also known as the small intestine, is a key component of the digestive system responsible for the majority of nutrient absorption from food. Positioned between the stomach and the large intestine, it receives digestive enzymes from bile and pancreatic juice via the pancreatic duct. The small intestine measures approximately 18 feet (6.5 meters) in length and is intricately folded to fit within the abdominal cavity. The Garcinia Kola plant was recognized by the Department of Pharmacology at Niger Delta University, located on Wilberforce Island, Amasomma, Bayelsa State. The seeds of this plant were collected from Amasomma and subjected to a drying process under natural sunlight for 14 days. Subsequently, they were ground into a fine powder and distributed into various beakers. After allowing the mixture to settle for three days, it was filtered using Watchman's No. 1 filter paper. For this research, thirty albino rats with weights ranging from 150g ± 3.5 to 205g ± 2.6 were utilized. These rats were sourced from the animal facility of the Pharmacology Department at Niger Delta University. They were kept in a controlled environment with temperatures maintained between 20°C and 27°C and a 12-hour cycle of light and darkness. The rats were grouped and provided with standard feed pellets from Guinea Feed Nigeria Plc and unlimited access to clean water for the duration of the study, which included a two-week acclimatization period. The handling of the animals adhered to the institution's guidelines for animal experimentation. The study spanned two months, with an initial four-week acclimatization phase. Post-acclimatization, the 30 rats were randomly assigned to seven groups (A to G). Group A (control) received a diet of pelleted growers feed (mash) and water. Group B (chronic exposure group) was given 1ml of 4% acetic acid orally, along with the standard diet, for 30 days. Group C (subchronic exposure group) received the same acetic acid treatment for 14 days. Groups D and E (sub-chronic exposure groups) were treated with acetic acid and varying doses of Garcinia Kola extract for 14 days. Groups F and G (chronic exposure groups) underwent a similar regimen with Garcinia Kola extract for 30 days. At the end of the treatment period, the rats were euthanized using chloroform anesthesia, and vital organs were harvested and preserved in 10% formalin. The tissues underwent standard histological processing and were stained with Haematoxylin and Eosin at the Histopathology laboratory of the Niger Delta Teaching Hospital (NDUTH) in Okolobiri. Histological examination revealed that the control group's villi and submucosal walls remained intact. However, plates 4.2 to 4.4 displayed erosion of the submucosal layer, interruption of the villi, and aggregation of white blood cells. Plate 4.5 indicated mild erosion of the mucosal layer and the presence of inflammatory cells. The findings suggest that oral ingestion of acetic acid for 30 days can cause inflammation and necrosis in the stomach tissues of lab animals. Additionally, it was noted that administering Garcinia Kola seed extract alone had minimal impact on the animals' histology.

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Acetic acid ingestion can cause chemical burns of the upper airways and upper digestive tract (mouth-throat-esophagus-stomach-duodenum) with the risk of development of respiratory distress, perforation, oesophageal strictures and systemic complications, such as coagulopathy, hemolysis and kidney damage. The initial symptoms include mouth pain, dysphagia and stridor. The first priority is an urgent assessment of the respiratory tract, and if the respiratory tract is affected, it is necessary to carry out final debridement, including anti-edema inhalations, steroids. An effective means of preventing renal damage as a result of the development of hemolysis as well as correcting methabolic acidosis is alkaline diuresis with sodium bicarbonate injections, with the control of urine pH. In those patients with a stable airway and no clinical or radiological signs of perforation, an urgent oesophagogastroduodenoscopy (OGDS) should be done within the first 24 h to assess the degree of injury and to make long-term prognosis. Effective methods of treatment are the use of proton pump inhibitors, H2 antagonists, antacids and antibacterial therapy. Grade II b circular lesions of the oesophagus tend to cause strictures. Мonitoring via OGDS is needed for 14-18 days after the ingestion as well as treatment of the developed strictures in a specialized surgical department. The main reason of acetic acid poisoning in children is its storage in containers for beverages. In this regard, we consider it necessary for pediatricians to regularly inform parents about the safety rules.

Estimation of the risk of local and systemic effects in infants after ingestion of low-concentrated weak acids from descaling products

Introduction The accidental ingestion of diluted household descaling products by infants is a phenomenon that poison control centers regularly encounter. Feeding infants with baby milk prepared with water from electric kettles still containing descaler is a common way of exposure. This study aimed to determine the risks related to ingestion of (diluted) descalers by infants. Methods pH measurements were performed using acetic acid and three different commercially available electric kettle descalers. The pH of different dilutions was measured in the absence or presence of baby milk powder. In addition, an overview was made of pH values of different electric kettle descalers as given by the product information of the manufacturer. Finally, a simple pharmacokinetic (PK) model was used to predict changes in blood pH in infants after ingestion of acetic acid, which is the most commonly used descaler. Results Several commercially available electric kettle descalers have a pH <2. Even after diluting such descalers up to 10 times the pH can remain low. The addition of milk powder increases the pH of descalers containing weaker acids, with a pH >1.5, while descalers with stronger acids and pH <1 show little pH increase after the addition of milk powder. Finally, a simple PBPK model for the ingestion of acetic acid predicted that the ingestion of larger amounts of acetic acid (>1000 mg) by an infant could result in relevant changes in blood pH. Conclusions Commercially available electric kettle descaling products may pose a health risk to infants in case of accidental ingestion since the pH of some of these products can be very low, even when diluted 10-times or in the presence of baby milk powder. Oral exposure of infants to the common descaler acetic acid, after accidental preparation of baby milk with cleaning vinegar, will probably not result in serious local effects, but changes in blood pH cannot be excluded when larger amounts of acetic acid are ingested.

Corrosive poisoning: Case report

Introduction: Acids are corrosive compounds which extract water from the tissues, coagulate the proteins to form the acid of albumin and convert hemoglobin to the acid hematin. On the world map of toxicology, Serbia is considered to be the country with high percentage of caustic intoxication. In developed countries corrosive poisoning is extremely rare due to unavailability of the products and forbidden free sale. Aim: To highlight the importance, size and frequency of corrosive poisoning, to show fatal acetic acid ingestion and the model of pre-hospital and hospital care for acutely poisoned with corrosives, as well as suggest measures to reduce these intoxications. Material and methods: Case history was used of the Clinic for Endocrinology, Diabetes and Metabolism Disorders, Toxicology Department, Clinical Centre Niš and a forensic autopsy report of the Institute for Forensic Medicine Niš. Case report: The circumstances of poisoning: A female patient drank deliberately about 200ml of acetic acid at about 9 p.m. on 21st February 2014 with suicidal intentions due to disagreements in the family. She was brought conscious in Admission and Triage Department of the hospital in Vranje at 9:49 p.m., where she gave the information on the intentional self-intoxication. She vomited, a urinary catheter was placed and haematuria in the urine was obtained. It was the first suicide attempt, not treated psychiatrically so far. She was transported to the Clinical Centre Niš at 0:35 a.m. on 22nd February 2014. She was examined by an ENT specialist and submitted to urgent EGDS (esophagogastroduodenoscopy). Objective status: severe patient with PSS (poisoning severity score) 4. Hyperaemic skin around the lips, with burns, oral cavity hyperaemic, edematous. Abdomen: painfully sensitive to palpation diffusely, urine bag with 1500ml of the haematurian urine. Lab: Gly 39.9; Urea 10.9-12.6; Crea 133.0-167.3; Amy 606.7; Acid-base status pH 7.19; BE -18.9, HCO3 10.3. Urgent EGDS: In the esophagus, stomach, duodenal bulb and postbulbar duodenum, mucous membranes are livid whitish with hyperaemic parts. Conclusion: The female patient was hospitalized after intentional intoxication with corrosive substances (acetic acid) in the severely bad general condition. During hospitalization tracheotomy was performed due to respiratory failure and developed anuria leading to acute renal failure. Despite all resuscitation measures there was a lethal outcome at 1:40 a.m. on 22nd February 2014. Macroscopic autopsy findings: the tongue is flubby, covered with dirty-brownish deposits that are easily removed. Moderate amount of dirty-dark-brownish-liquid content is present in the esophagus, its mucous membranes darkly painted over the entire surface, thin, lacking its upper layer. About 100 cc of brown-greenishmushy content present in the stomach. Its mucosal folds deleted, swollen, peeling of the mucous membranes, almost completely darkly painted over, finely granular in places. Conclusion: Emphasis should be placed on preventive measures. The management of the intoxicated patient distinguishes pre-hospital and hospital measures. Possible complications include an esophageal stricture, stenosis of the pylorus and the esophagus, or gastric cancer. Highly concentrated acetic acid is still frequently ingested with a high mortality rate. Patients with higher grades of gastrointestinal injury, pneumonia, renal injury and higher amount of acid ingested should be more carefully monitored as they are more susceptible to develop fatal consequences.

Severe Renal Function Impairment in Adult Patients Acutely Poisoned with Concentrated Acetic Acid

Acetic acid is a widely used organic acid with corrosive properties that depend on its concentration. If acetic acid is ingested in concentrations above 30 % it may severely damage the upper gastrointestinal tract and cause intravascular haemolysis, which can result in severe kidney and liver disorders and disseminated intravascular coagulation. In this retrospective study, we analysed acetic acid ingestion data collected at the University Clinic for Toxicology of Skopje, Macedonia from 1 January 2002 to 31 December 2011. The analysis included systemic complications, kidney damage, and the outcomes in particular. Over the ten years, 84 patients were reported at the Clinic to have ingested highly concentrated acetic acid. Twenty-eight developed kidney disorders, while the remaining 56 had no complications. Fatal outcome was reported for 11 patients, seven of whom had systemic complications and four severe gastrointestinal complications.

Highly Concentrated Acetic Acid Poisoning: 400 Cases Reviewed

Background: Caustic substance ingestion is known for causing a wide array of gastrointestinal and systemic complications. In Russia, ingestion of acetic acid is a major problem which annually affects 11.2 per 100,000 individuals. The objective of this study was to report and analyze main complications and outcomes of patients with 70% concentrated acetic acid poisoning. Methods: This was a retrospective study of patients with acetic acid ingestion who were treated at Sverdlovsk Regional Poisoning Treatment Center during 2006 to 2012. GI mucosal injury of each patient was assessed with endoscopy according to Zargar’s scale. Data analysis was performed to analyze the predictors of stricture formation and mortality. Results: A total of 400 patients with median age of 47 yr were included. GI injury grade I was found in 66 cases (16.5%), IIa in 117 (29.3%), IIb in 120 (30%), IIIa in 27 (16.7%) and IIIb in 70 (17.5%). 11% of patients developed strictures and overall mortality rate was 21%. Main complications were hemolysis (55%), renal injury (35%), pneumonia (27%) and bleeding during the first 3 days (27%). Predictors of mortality were age 60 to 79 years, grade IIIa and IIIb of GI injury, pneumonia, stages “I”, “F” and “L” of kidney damage according to the RIFLE scale and administration of prednisolone. Predictors of stricture formation were ingestion of over 100 mL of acetic acid and grade IIb and IIIa of GI injury. Conclusion: Highly concentrated acetic acid is still frequently ingested in Russia with a high mortality rate. Patients with higher grades of GI injury, pneumonia, renal injury and higher amount of acid ingested should be more carefully monitored as they are more susceptible to develop fatal consequences.

Preliminary evidence that regular vinegar ingestion favorably influences hemoglobin A1c values in individuals with type 2 diabetes mellitus

This report examined whether daily acetic acid ingestion as vinegar, dill pickle, or commercial vinegar pill influenced hemoglobin A1c in diabetic patients. Hemoglobin A1c values fell 0.16% with vinegar use but rose 0.06% and 0.22% for pill and pickle use respectively ( p = 0.018). Hence, regular vinegar use modestly improved glycemic control.

Systemic manifestations following ingestion of small amounts of acetic acid by a child

Acetic acid ingestion can cause hemolysis, DIC, respiratory and renal insufficiency, and hepatic necrosis. Only a few cases of acetic acid ingestion have been described in the past, most of which caused hemolysis, and one description of hepatic necrosis. All of these were reported in adults, usually as a suicide attempt with ingestion of large amounts. Severe symptoms have not been reported so far in children following accidental ingestion of small amounts of acetic acid. We report of a 3-year-old child who ingested a minimal amount of 60% acetic acid and developed hemolysis and hepatic dysfunction.

Role of endogenous glucocorticoids in the healing of gastric erosions and chronic gastric ulcers in rats

To investigate the role of endogenous glucocorticoids in the healing of gastric lesions, we compared the healing of indomethacin- or cold-restraint-induced gastric erosions as well as aceticacid-induced ulcers in sham-operated rats, adrenalectomized rats and adrenalectomized rats with corticosterone replacement. Adrenalectomy was performed immediately after the formation of gastric erosions (4 h after indomethacin administration or 6 h after the onset of cold-restraint stress) or chronic ulcers (in 3 days after ingestion of acetic acid into the luminal side of the stomach). All ulcerogenic stimuli caused an increase in corticosterone production. Adrenalectomy created corticosterone deficiency and delayed the healing of gastric erosions and chronic ulcers. Replacing corticosterone reversed the deleterious effect of adrenalectomy on healing of gastric damage in adrenalectomized rats. These results suggest that glucocorticoids participate in natural healing processes of injured gastric mucosa. The data obtained also indicate that participation of glucocorticoid in the healing of gastric lesions is more evident under prostaglandin deficient conditions.

Concentrated (80%) acetic acid ingestion

Concentrated (80%) acetic acid ingestion

Acute Pancreatitis After Ingestion of Acetic Acid

Acute Pancreatitis After Ingestion of Acetic Acid

Disseminated Intravascular Coagulopathy Caused by Acetic Acid Ingestion

A case of disseminated intravascular coagulopathy following ingestion of 100% acetic acid is presented. The patient was successfully treated with fresh frozen plasma and cryoprecipitate. Complete resolution of the bleeding diathesis and the disturbed coagulation tests was achieved.

Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice.

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased transmucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.

Aggravating Effect of Serotonin on Gastric Ulceration Induced by Thermocautery Under the Healing Process in Mice

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased trans-mucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.

Production and utilization of free acetate in man.

THE concentration of acetate in the blood determined enzymatically1 in a number of experimental subjects was found to be about 2 µgm./ml., independent of the nutritional regime (see Table 1). Attempts to raise the level of acetate in the blood by oral ingestion of acetic acid or acetates were unsuccessful, because the experimental subjects were not able to consume a sufficient quantity of those substances.