Ascaten P

Indications

• Roundworm infections
• Hookworm infections
• Whipworm infections
• Pinworm infections
• Other helminth infections

Dosage

Children: Child 1 month–9 years: Initially 1 mg/kg daily in divided doses on the first day, then increased to 3 mg/kg daily in divided doses, dose to be increased gradually over 3 days. Child 10–17 years: Initially 1 mg/kg daily in divided doses on the first day, then increased to

Adults: 100 mg for 1 dose, if reinfection occurs, a second dose may be needed after 2 weeks.

Mechanism of action

Mebendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization into microtubules. This leads to impaired glucose uptake and depletion of glycogen stores in the parasites, resulting in decreased ATP production, immobilization, and eventual death of the helminths.

Pharmacodynamics

Mebendazole is a synthetic broad-spectrum anthelmintic. Its principal mode of action is through the inhibition of tubulin polymerization, which results in the loss of cytoplasmic microtubules. This action disrupts organelle movement and interferes with the normal physiological processes of helminths, effectively leading to their death.

Pharmacokinetics

Mebendazole is poorly absorbed from the gastrointestinal tract, which contributes to its effectiveness as an anthelmintic. After oral administration, the drug is primarily metabolized in the liver. Its low solubility limits absorption, but it can still exert its effects on the intestinal parasites present in the gastrointestinal tract. The drug's elimination half-life is variable, and it is not significantly distributed in body tissues.

Contra-indications

• Blood disorders

Adverse effects

• Abnormal sensation in eye
• Anaemia
• Appetite decreased
• Asthenia
• Asthma exacerbated
• Chest discomfort
• Coma
• Confusion
• Conjunctival haemorrhage
• Constipation
• Diarrhoea
• Difficulty standing
• Difficulty swallowing
• Dizziness
• Fever
• Gastrointestinal discomfort
• Headache
• Hepatitis
• Hypotension
• Joint disorders
• Leucopenia
• Lymphatic abnormalities
• Myalgia
• Nausea
• Oedema
• Pain
• Psychiatric disorder
• Seizure
• Severe cutaneous adverse reactions (SCARs)
• Stupor
• Tachycardia
• Tremor
• Urinary incontinence
• Vertigo
• Vomiting

Interactions

• Cimetidine (increases concentration of mebendazole)

Precautions

• Use with caution in patients with epilepsy
• Use with caution in patients with Sjögren’s syndrome

Pregnancy

Embryotoxic in animal studies, avoid if possible.

Breast-feeding

No information available.

Storage

Store in a cool, dry place away from light.

Formulations

• Chewable tablet 100 mg

Indications

• Schistosomiasis caused by Schistosoma mansoni
• Schistosomiasis caused by Schistosoma japonicum
• Tapeworm infections, including Taenia solium and Hymenolepis nana

Mechanism of action

Praziquantel is hypothesized to target the β subunits of voltage-gated Ca2+ channels in parasites such as Schistosoma mansoni and Schistosoma japonicum. This action leads to increased calcium influx, causing rapid contraction and paralysis of the worms. The drug also induces tegumental disintegration and vacuolization in schistosomes, significantly affecting adult worms more than juveniles. Secondary effects include inhibition of glucose uptake and depletion of glycogen levels.

Pharmacodynamics

Praziquantel exhibits a rapid onset of action against trematodes and cestodes, causing significant changes in the permeability of the cell membrane of the parasites. This results in muscle contraction, tegumental damage, and eventual death of the worms. It selectively targets schistosomes and is ineffective against nematodes. The drug's efficacy is notably reduced against juvenile schistosomes and may diminish after a few weeks of treatment.

Pharmacokinetics

Praziquantel is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring within 1-3 hours post-administration. It undergoes extensive hepatic metabolism, primarily by CYP450 enzymes, and has a half-life of approximately 1-3 hours. The drug is excreted mainly in urine as metabolites, with a small fraction excreted unchanged. The pharmacokinetics can be affected by co-administration with certain other drugs that alter its metabolism.

Adverse effects

• dizziness
• hepatitis
• neutropenia
• seizure
• severe cutaneous adverse reactions

Interactions

• mitotane+praziquantel: Severe (decreases exposure)
• rifampicin+praziquantel: Severe (decreases exposure)
• chloroquine+praziquantel: Moderate (decreases exposure)
• cobicistat+praziquantel: Unknown (increases exposure)
• dexamethasone+praziquantel: Unknown (decreases exposure)
• grapefruit juice+praziquantel: Unknown (increases exposure)
• cimetidine+praziquantel: Unknown (increases exposure)
• idelalisib+praziquantel: Unknown (increases exposure)

Pregnancy

Manufacturer advises avoiding use due to toxicity observed in animal studies.

Breast-feeding

Amount present in milk is too small to be harmful; however, the manufacturer advises avoiding use.

Storage

Store in a cool, dry place away from light.

Formulations

• tablets
• oral suspension

Indications

• Ethylene glycol poisoning
• Metabolic acidosis due to glycolate accumulation

Dosage

Adults: Refer to the BNF for specific dosing guidance in cases of eth

Mechanism of action

Glycollate is produced during the metabolic breakdown of ethylene glycol. The toxicity associated with ethylene glycol arises from its conversion to glycolic acid, leading to an accumulation of glycolate and other metabolites. This metabolic pathway results in metabolic acidosis and potential renal damage due to the accumulation of toxic metabolites. The exact elimination kinetics of glycolate and the associated metabolites are not fully understood, but their presence in the body contributes to the toxicological profile observed during ethylene glycol poisoning.

Pharmacodynamics

The pharmacodynamics of glycollate involves its contribution to the toxic effects seen in ethylene glycol metabolism. Glycollate, along with glycolic acid, can lead to metabolic acidosis, affecting the body's acid-base balance. The compound induces diuresis, but this effect is transient, and the accumulation of glycolate can have deleterious effects on renal function and overall metabolic status. The clinical implications of glycollate toxicity necessitate prompt identification and treatment to mitigate its effects.

Pharmacokinetics

The pharmacokinetics of glycollate are characterized by its formation through the metabolism of ethylene glycol. After administration, ethylene glycol reaches peak plasma levels within 2 hours, while glycolate peaks between 4-6 hours. The elimination half-life of ethylene glycol is approximately 1.7 hours in rats and 3.4 hours in dogs. Renal excretion plays a significant role in the elimination of both ethylene glycol and glycolate, with approximately 20-30% and 5% of the dose excreted renally, respectively. The metabolic pathways for glycollate suggest a slower rate of elimination compared to ethylene glycol.

Indications

• Lactose intolerance
• As a filler or excipient in pharmaceutical formulations

Dosage

Children: Refer to the BNF for Children for specific dosing information based on age and clinical context.

Adults: Refer to the BNF for specific dosing information based on clinical context.

Mechanism of action

Lactose is metabolized in the intestine by the enzyme lactase into its constituent monosaccharides, glucose and galactose. In individuals with lactase deficiency, unabsorbed lactose passes into the colon, where it is fermented by bacteria, leading to gas production and osmotic effects that contribute to diarrhea.

Pharmacodynamics

The pharmacodynamics of lactose are primarily related to its effects on gastrointestinal function. In healthy individuals, lactose is effectively broken down into glucose and galactose, which are absorbed and utilized for energy. In individuals with lactose intolerance, the unabsorbed lactose can cause osmotic diarrhea and colonic fermentation, leading to discomfort and symptoms associated with lactose intolerance.

Pharmacokinetics

Lactose is not absorbed in the gastrointestinal tract until it is hydrolyzed into glucose and galactose by lactase. The absorption of glucose and galactose occurs in the small intestine. The half-life is not applicable as lactose is not typically administered as a medication but is rather ingested as a natural component of food. Its metabolism primarily occurs in the intestine.

Adverse effects

• Bloating
• Diarrhea
• Abdominal pain
• Flatulence

Precautions

• Use with caution in patients with lactose intolerance.
• Consider potential for gastrointestinal upset in sensitive individuals.

Pregnancy

Lactose is generally considered safe for use during pregnancy. However, consult a healthcare professional for individual advice.

Breast-feeding

Lactose is safe to use while breastfeeding, as it is a natural sugar present in breast milk.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Powder
• Granules
• Tablets
• Syrup

Indications

• Nutritional support
• Source of carbohydrates
• Dietary fiber source
• Animal feed

Dosage

Children: As with adults, there are no specific dosing recommendations for maize for children. It can be introduced into the diet in age-appropriate forms and quantities, keeping in mind the overall dietary balance.

Adults: There are no specific dosing recommendations for maize as it is typically consumed as part of a balanced diet. It can be included in daily meals in various forms such as whole kernels, flour, or as part of dishes.

Mechanism of action

Maize primarily acts as a source of energy due to its high carbohydrate content. The complex carbohydrates in maize are broken down into glucose, which is then utilized by the body for energy production. It also contributes to dietary fiber intake, which can aid in digestive health and regulation of blood sugar levels.

Pharmacodynamics

The consumption of maize influences blood glucose and insulin levels due to its carbohydrate content. It has a relatively low glycemic index when consumed in whole form, which can help in managing blood sugar levels. The dietary fiber present in maize can also promote satiety and aid in weight management.

Pharmacokinetics

The digestion of maize begins in the mouth with salivary amylase breaking down starches into simpler sugars. In the stomach and small intestine, enzymes further break down these carbohydrates. The resultant glucose is absorbed into the bloodstream, where it is transported to cells for energy production. The absorption rate can vary based on the form of maize consumed (e.g., whole kernels versus processed forms).

Pregnancy

Maize is generally considered safe for consumption during pregnancy as it is a staple food and provides essential nutrients.

Breast-feeding

Maize is safe to consume while breastfeeding and can provide important nutrients to both the mother and the infant.

Storage

Store in a cool, dry place, away from moisture and pests. Properly sealed containers can help prolong shelf life.

Formulations

• Whole maize grains
• Maize flour (cornmeal)
• Maize starch
• Maize oil

Indications

• Ascariasis
• Partial intestinal obstruction due to Ascaris lumbricoides

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Refer to BNF for specific dosing information.

Mechanism of action

Piperazine functions as a GABA receptor agonist, selectively binding to muscle membrane GABA receptors in nematodes. This binding induces hyperpolarization of nerve endings, leading to flaccid paralysis of the worms. By blocking the response of worm muscle to acetylcholine, piperazine alters cell membrane permeability to ions, resulting in hyperpolarization and suppression of spontaneous spike potentials, thereby facilitating the expulsion of the worm through normal intestinal peristalsis.

Pharmacodynamics

Piperazine is effective as an anthelminthic, particularly for treating infections from Ascaris lumbricoides. It induces reversible muscle paralysis in nematode parasites by hyperpolarizing their cell membranes. The primary clinical use is in addressing complications such as partial intestinal obstruction caused by these worms, a condition more frequently encountered in children.

Pharmacokinetics

The pharmacokinetics of piperazine, including absorption, distribution, metabolism, and excretion, have not been well-characterized in the available literature. However, it is generally understood that piperazine is absorbed from the gastrointestinal tract and is metabolized in the liver. Further detailed studies may be required to elucidate its complete pharmacokinetic profile.

Adverse effects

• Nausea
• Vomiting
• Abdominal pain
• Diarrhea
• Headache
• Dizziness

Precautions

• Use with caution in patients with renal impairment
• Consider potential interactions with other central nervous system depressants

Pregnancy

Limited data are available on the safety of piperazine during pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Piperazine is excreted in breast milk; use with caution and consider the need for monitoring the infant.

Storage

Store in a cool, dry place away from light. Keep out of reach of children.

Formulations

• Piperazine citrate
• Piperazine hydrate

Indications

• Preoperative skin antisepsis
• Wound irrigation and cleansing
• Management of minor cuts and abrasions
• Treatment of minor skin infections
• Disinfection of mucous membranes

Dosage

Children: Refer to specific product guidelines for concentration and application method, as doses may vary by formulation.

Adults: Refer to specific product guidelines for concentration and application method, as doses may vary by formulation.

Mechanism of action

Povidone-iodine exerts its antiseptic effects primarily through the release of free iodine, which penetrates microbial cell walls and disrupts protein and nucleic acid synthesis. This leads to cell lysis and death of a wide variety of pathogens. The mechanism involves the oxidation of essential cellular components, thus rendering microorganisms inactive.

Pharmacodynamics

Povidone-iodine demonstrates rapid bactericidal activity, effectively reducing the microbial load on the skin and in wounds. The antimicrobial efficacy is influenced by factors such as concentration, exposure time, and the presence of organic matter. Its broad-spectrum action makes it effective against gram-positive and gram-negative bacteria, fungi, and viruses, making it a versatile antiseptic.

Pharmacokinetics

Povidone-iodine is not significantly absorbed through intact skin; however, some absorption may occur with large or prolonged applications, especially on compromised skin. The elimination half-life of iodide is approximately 24 hours, with the majority excreted unchanged in the urine. Iodine levels can be temporarily elevated in the serum after application, particularly in patients with pre-existing thyroid conditions.

Contra-indications

• Hypersensitivity to povidone-iodine or any of the excipients
• Thyroid dysfunction
• Use in infants less than 2 months of age

Adverse effects

• Skin irritation
• Burning sensation
• Allergic reactions
• Staining of skin and clothing
• Thyroid dysfunction
• Electrolyte imbalance (with prolonged use)

Interactions

• May interfere with thyroid function tests
• Incompatibility with other antiseptics or disinfectants

Precautions

• Avoid contact with eyes
• Use with caution in patients with thyroid disease
• Not for deep puncture wounds or serious burns

Pregnancy

Generally considered safe for topical use, but should be used with caution. Consult a healthcare professional for guidance.

Breast-feeding

Suitable for topical use, but excessive use should be avoided. Consult a healthcare professional for guidance.

Storage

Store at room temperature, away from direct sunlight. Keep container tightly closed.

Formulations

• Topical solution
• Ointment
• Surgical scrub
• Swab sticks

Indications

• Nutritional supplementation
• Energy source in enteral nutrition
• Excipient in pharmaceutical formulations

Dosage

Children: Refer to specific guidelines or product inserts for dosing information, as it can vary based on the context of use.

Adults: Refer to specific guidelines or product inserts for dosing information, as it can vary based on the context of use.

Mechanism of action

Starch is broken down into glucose units by enzymes such as amylase during digestion. The glucose is then absorbed in the intestines and utilized for energy production in the body's cells. This pathway involves hydrolysis of the glycosidic bonds, converting starch into simpler sugars.

Pharmacodynamics

Starch primarily serves as an energy source. Its digestion and absorption lead to an increase in blood glucose levels, which provides energy for metabolic processes. In this context, it plays a crucial role in maintaining energy homeostasis in the body.

Pharmacokinetics

Starch is not absorbed in its polymeric form; it must first be enzymatically hydrolyzed into simpler sugars such as maltose and glucose. The digestion and absorption of starch occur predominantly in the small intestine, with glucose being readily absorbed into the bloodstream. The rate of absorption can vary depending on the type of starch and its physical form.

Adverse effects

• Allergic reactions
• Gastrointestinal discomfort
• Diarrhea
• Constipation

Precautions

• Use with caution in individuals with known allergies to starch or starch derivatives
• Monitor for gastrointestinal symptoms in patients with a history of digestive disorders

Pregnancy

Starch is generally considered safe for use during pregnancy. However, it should be consumed in moderation as part of a balanced diet.

Breast-feeding

Starch is deemed safe for nursing mothers when used in moderation as part of a balanced diet.

Storage

Store in a cool, dry place away from moisture and direct sunlight.

Formulations

• Powder
• Granules
• Tablets
• Suspensions

Mechanism of action

Mebendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies. Although the exact mechanism of anthelmintic activity of mebendazole has not been fully elucidated, the drug appears to cause selective and irreversible inhibition of the uptake of glucose and other low molecular weight nutrients in susceptible helminths; inhibition of glucose uptake appears to result in endogenous depletion of glycogen stores in the helminth. Mebendazole does not inhibit glucose uptake in mammals. Mebendazole appears to cause degenerative changes in the intestine of nematodes and in the absorptive cells of cestodes. The principal anthelmintic effect of the drug appears to be degeneration of cytoplasmic microtubules within these intestinal and absorptive cells. Microtubular deterioration results in inhibition of organelle movement and interferes with the absorptive and secretory function. As a result of excessive accumulation of intracellular transport secretory granules, hydrolytic and proteolytic enzymes are released and cause cellular autolysis. This irreversible damage leads to death of the parasite. Vermicidal; may also be ovicidal for ova or most helminths; mebendazole causes degeneration of parasite's cytoplasmic microtubules and thereby selectively and irreversibly blocks glucose uptake in susceptible adult intestine-dwelling helminths and their tissue-dwelling larvae; inhibition of glucose uptake apparently results in depletion of the parasite's glycogen stores; this, in turn, results in reduced formation of adenosine triphosphate (ATP) required for survival and reproduction of the helminth; corresponding energy levels are gradually reduced until death of the parasite ensues; mebendazole does not appear to affect serum glucose concentrations in humans, however. Benzimidazoles produce many biochemical changes in susceptible nematodes, eg, inhibition of mitochondrial fumarate reductase, reduced glucose transport, and uncoupling of oxidative phosphorylation ... /but/ the primary action ... /should be/ to inhibit microtubule polymerization by binding to beta-tubulin. The selective toxicity of these agents derives from the fact that specific, high-affinity binding to parasite beta-tubulin occurs at much lower concn than does binding to the mammalian protein ... Benzimidazole-resistant Haemonchus contortus display reduced high-affinity drug binding to beta-tubulin and alterations in beta-tubulin isotype gene expression that correlate with drug resistance ... Two identified mechanisms of drug resistance in nematodes involve both a progressive loss of "susceptible" beta-tubulin gene isotypes together with emergence of a "resistant" isotype with a conserved point mutation that encodes a tyrosine instead of phenylalanine at position 200 of beta-tubulin. While this mutation may not be required for benzimidazole resistance in all parasites, eg, Giardia lamblia, benzimidazole resistance in parasitic nematodes is unlikely to be overcome by novel benzimidazole analogs, because tyrosine also is present at position 200 of human beta-tubulin. /Benzimidazoles/

Pharmacodynamics

Mebendazole is a (synthetic) broad-spectrum anthelmintic. The principal mode of action for Mebendazole is by its inhibitory effect on tubulin polymerization which results in the loss of cytoplasmic microtubules.

Mechanism of action

Although the exact mechanism of action is unknown, praziquantel was hypothesized to target the β subunits of voltage-gated Ca₂₊ channels, particularly in Schistosoma mansoni and Schistosoma japonicum, due to the lack of two conserved serine residues in these subunits. This is supported by the finding that co-administration of calcium channel blockers like nicarpidine and nifedipine renders 50% of Schistosoma mansoni resistant to praziquantel. Increased exposure of antigens on the worm surface was also observed, but little research has been done to elucidate on the mechanism of action.

Pharmacodynamics

In vitro studies on trematodes and cestodes have shown that praziquantel induces a rapid contraction of schistosomas by a specific effect on the permeability of the cell membrane. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased Ca2⁺-influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is specific to trematodes and cestodes; nematodes (including filariae) are not affected. Praziquantel is active against schistosoma (for example, Schistosoma mekongi, Schistosoma japonicum, Schistosoma mansoni and Schistosoma hematobium), and infections due to the liver flukes, Clonorchis sinensis/Opisthorchis viverrini. Published in vitro data have shown a potential lack of efficacy of praziquantel against migrating schistosomulae. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks.

Mechanism of action

Ethylene glycol toxicity results from its metabolism to glycolic acid and other toxic metabolites. The accumulation of glycolate and the elimination kinetics of ethylene glycol and its metabolites are not well understood, so studies with male Sprague-Dawley rats and mixed breed dogs have been carried out. Ethylene glycol was administered by gavage to rats and dogs which were placed in metabolic cages for urine and blood sample collection at timed intervals. The peak plasma level of ethylene glycol occurred at 2 hr after dosing and that of glycolate between 4-6 hr. The rate of ethylene glycol elimination was somewhat faster in rats with a half-life of 1.7 hr compared to 3.4 hr in dogs. The maximum plasma level of glycolate was greater in rats although the pattern of accumulation was similar to that in dogs. Glycolate disappeared from the plasma at the same time as ethylene glycol, suggesting a slower rate of elimination of the metabolite than that of ethylene glycol. Renal excretion of ethylene glycol was an important route for its elimination accounting for 20-30% of the dose. Renal excretion of glycolate represented about 5% of the dose. Ethylene glycol induced an immediate, but short lived diuresis compared to that in control rats. Minimal clinical effects (mild acidosis with no sedation) were noted at these doses of ethylene glycol (1-2 g/kg) in both rats and dogs. The results indicate that the toxicokinetics of ethylene glycol and glycolate were similar in both species. The effect of 0.35 to 0.8 mmol/kg glycolic acid and 1.0 to 4.4 mmol/kg sodium glycolate on cyclopropane-epinephrine induced cardiac arrhythmias was examined using dogs. Doses of 0.35 to 0.5 mmol/kg glycolic acid increased the duration of arrhythmias in the 13 dogs tested, whereas doses >0.5 mmol/kg decreased or totally eliminated the arrhythmias in each of 11 dogs. Depression was observed for many of the dogs at higher doses. Sodium glycolate was much less effective in decreasing the arrhythmias, with 3 mmol/kg being required and its action being transient.

Mechanism of action

Piperazine is a GABA receptor agonist. Piperzine binds directly and selectively to muscle membrane GABA receptors, presumably causing hyperpolarization of nerve endings, resulting in flaccid paralysis of the worm. While the worm is paralyzed, it is dislodged from the intestinal lumen and expelled live from the body by normal intestinal peristalsis. Piperazine blocks the response of the /target species/ worm muscle (best studied in Ascaris), causing flaccid paralysis of the worm. While the worm is paralyzed, it is dislodged from the intestinal lumen and expelled live from the body by normal intestinal peristalsis. The predominant effect of piperazine on /the target species/ Ascaris is to cause a flaccid paralysis that results in expulsion of the worm by peristalsis. ... Piperazine blocks the response of Ascaris muscle to acetylcholine, apparently by altering the permeability of the cell membrane to ions that are responsible for the maintenance of the resting potential. The drug causes hyperpolarization and suppression of spontaneous spike potentials with accompanying paralysis. Piperazine citrate causes reversible muscle paralysis in intestinal nematodes, presumably by causing hyperpolarization of nerve endings /in this target species/. /Piperazine citrate/ Piperazine and its salts, as a gamma-aminobutyric acid (GABA)-like substance, induce a reversible flaccid paralysis in the /target/ nematode parasites. This is provoked by a hyperpolarization of the cell membrane followed by suppression of spontaneous spike potentials. THe paralyzed nematodes are expelled from the gut lumen by normal peristaltic actions. In mammals, motorcortical GABAa inhibition is important for initiation of smooth flexion and/or extension movements of the extremities affecting motor and postural control. When injected into the hand motor cortical area of three infant macaque monkeys, the GABA agonist muscimol disrupted forelimb movement showing a posture of dropped wrist and fingers as if the radial nerve were paralysed. Interestingly, the three investigated animals exhibited large inter-individual differences in sensitivity to the action of the same dose of muscimol, being low in one, moderate in the second and substantial in the third. Injection into the medial segment of globus pallidus elicited choreiform movements and injections into substantia nigra pars reticulata provoked severe axial posture anomalies with rotational behaviour as well as contralateral hypotonia. Although the symptoms induced by piperazine in sensitive species exhibits some of these features, it is possible that its effects in mammals also involve other modes of action as well, in as much as a nicotinic action on rat sympathetic ganglia in vitro was reported in one series of experiments.

Pharmacodynamics

Piperazine is an anthelminthic especially useful in the treatment of partial intestinal obstruction caused by Ascaris worms, which is a condition primarily seen in children. Piperazine hydrate and piperazine citrate are the main anthelminthic piperazines.