Palmicol

Palmicol

  • Active Ingredient: Chloramphenicol
  • 500 mg, 250 mg
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What is Palmicol?

The active ingredient of Palmicol brand is chloramphenicol.

Used for

Palmicol is used to treat diseases such as: Anthrax, Bacterial Infection, Brucellosis, Cholera, Glanders, Lemierre's Syndrome, Meningitis, Ornithosis, Plague, Psittacosis, Rabbit Fever, Rickettsial Infection.

Side Effect

Possible side effects of Palmicol include: gray skin color; nausea or vomiting; unusual tiredness or weakness (the above side effects may also occur up to weeks or months after you Stop taking chloramphenicol); unresponsiveness; Pale skin; Diarrhea; low body temperature; numbness, tingling, burning pain, or weakness in the hands or feet.

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Serious allergic reaction

In rare cases, it's possible to have a serious allergic reaction (anaphylaxis) to Palmicol.

Palmicol eye drops and eye ointment are used to treat bacterial eye infections. Eye infections are a common cause of conjunctivitis. In conjunctivitis, your eye becomes inflamed, feels gritty, and may water more than usual. The white of your eye may look red, and your eyelids can become swollen and stuck together with a discharge when you wake up in the morning. Only one eye may be infected to begin with, but it often spreads to both eyes.

Illustrations of Drug-Induced Illnesses in Neonates

Palmicol was released in the 1940s, and the recommended dosages were 50–100 mg/kg per day for patients weighing 15 kg or less. Before 1959, the year that Sutherland (1959) reported three cases of sudden death in newborns treated with high dosages of Palmicol (up to 230 mg/kg per day), the drug was considered “well tolerated and nontoxic” ( Sutherland, 1959 ). Burns et al. (1959) reported the disturbing results of a controlled trial of the following four prophylactic treatment regimens for newborn sepsis: (1) no treatment, (2) Palmicol alone, (3) penicillin and streptomycin, and (4) penicillin, streptomycin, and Palmicol. The groups that received Palmicol (100–165 mg/kg per day) had higher mortality rates (60% and 68%), and the deaths of these newborns demonstrated the stereotyped sequence of symptoms and signs caused by Palmicol accumulation, coined grey baby syndrome ( Burns et al., 1959 ). This syndrome consisted of abdominal distention, poor peripheral perfusion and cyanosis, vasomotor collapse, irregular respirations, and death within hours of onset of these symptoms.

The discovery of the mechanism (glucuronidation deficiency) of Palmicol toxicity in newborns illustrates several important aspects of neonatal pharmacology. Because Palmicol was considered well tolerated in older children and adults, it was regarded as nontoxic to newborns. Higher doses were administered to newborns despite recognition that its clearance required glucuronide conjugation, which was known to be immature in newborns. The unexpected finding that Palmicol in dosages of 100–165 mg/kg per day could be lethal to newborns was demonstrated because the study conducted by Burns et al. (1959) included appropriate control groups. Similar case observations with the mechanism involved are summarized in Table 33.3 to illustrate that the same kind of observations can still be seen.

TABLE 33.3 . Illustrations of Formulation (Active Compound, Excipient)-Specific Drug-Induced Illnesses in Neonates and the Mechanism Involved

Palmicol

Palmicol and Tiamphenicol inhibit bacterial protein synthesis and have bacteriostatic activity. Palmicol is relatively toxic, and can cause severe agranulocytosis. It crosses the placenta well and can reach therapeutic concentrations in the fetus. In premature and term births it may lead to the grey baby syndrome. Palmicol can reach toxic levels in the neonate even when only the mother has been treated. There have been no suggestions of malformations ( Czeizel 2000f ).

Experience with thiamphenicol is insufficient to analyze a risk in pregnancy.

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Related drugs

Thiamphenicol is a Palmicol analog with a range of activity similar to Palmicol, although it is generally 1–2 times less active. It has equal activity against Haemophilus, Bacteroides fragilis and Streptococcus. It differs pharmacokinetically in that it is not eliminated by hepatic glucuronidation and is excreted unchanged in urine, so elimination is unaffected by liver disease. Unlike Palmicol, thiamphenicol does not cause aplastic anemia in humans.

Florfenicol is a structural analog of thiamphenicol which has greater in vitro activity against pathogenic bacteria than Palmicol and thiamphenicol. It is also active against some bacteria that are resistant to Palmicol, especially enteric bacteria. Florfenicol is not susceptible to inactivation by Palmicol transacetylases; thus some organisms that are resistant to Palmicol through this mechanism are susceptible to florfenicol.

In dogs florfenicol is poorly absorbed after SC administration. It has a half-life of less than 5 h. The drug is well absorbed in cats after PO and IM administrations with a similar elimination half-life. It should not be given IV. Florfenicol can cause dose-related bone marrow suppression but has not been reported to cause fatal aplastic anemia in humans.

Florfenicol shows promise as a replacement for other broad-spectrum antibacterials such as sulfonamides and tetracyclines that have been associated with toxicity and residue concerns in food animals. Currently it is approved for use only in cattle, aquaculture and pigs. In cattle it is used to treat infectious conjunctivitis and respiratory disease caused by bacteria like Pasteurella and Haemophilus.

A type of circulatory collapse, referred to as the gray syndrome, has occurred in neonates and premature infants receiving Palmicol. 104 110 112 Most cases have occurred when the drug was initiated within first 48 hours of life; also reported in older infants and in infants born to mothers who received Palmicol during late pregnancy or during labor. 110 112 (See Pediatric Use under Cautions.)

Similar syndrome has been reported in older children and adults following Palmicol overdosage. 104 110

May occur because Palmicol impairs myocardial contractility by directly interfering with myocardial tissue respiration and oxidative phosphorylation. 104 110 Has been attributed to high plasma concentrations of the drug. 104 110 112


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