cocaine/necrosis

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Cocaine hepatotoxicity: influence of hepatic enzyme inducing and inhibiting agents on the site of necrosis.

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Cocaine-induced hepatotoxicity has been reported in human beings and is well documented in mice. One interesting feature of this toxicity that appears to be common to both species is an apparent shift in the intraacinar site of necrosis under circumstances known to alter cocaine metabolism. However,

Shifting necrosis: butylated hydroxytoluene (BHT) and phenobarbital move cocaine-induced hepatic necrosis across the lobule.

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Cocaine (60 mg/kg i.p.) caused centrilobular necrosis in the livers of 55% of DBA/2Ha mice. Pretreatment with phenobarbital (PB, 3 x 80 mg/kg i.p.) increased the incidence of necrosis to 70% and shifted this damage to the midzonal region. Pretreatment with butylated hydroxytoluene (BHT, 0.1% in

Palpable purpura complicated by streptococcal toxic shock syndrome resulting in limb necrosis and amputation: a case of levamisole and cocaine coingestion.

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Palpable purpura resulting from cocaine and levamisole coingestion has been reported with increasing frequency over the last several years as distribution of this drug combination becomes more universal. Toxicity from ingestion of this dangerous combination is difficult to diagnose due to the

Cocaine-Induced raynaud's phenomenon and ischaemic finger necrosis.

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A 37-year-old man with ischaemic finger necrosis and recent-onset Raynaud's phenomenon associated with cocaine abuse is reported. Initial therapy with systemic vasodilators, low-molecular-weight heparin and aspirin failed. Resolution of the ischaemia and ulcer healing was rapidly achieved with

Acute multifocal skin necrosis: synergism between invasive streptococcal infection and cocaine-induced tissue ischaemia?

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A 30-year-old pregnant woman with full thickness skin necrosis following parenteral abuse of cocaine and heroine is described. Three lesions occurred simultaneously on the trunk and right knee subsequent to an abscess on the left thigh from which S. pyogenes group A and S. aureus were isolated.

Modulation of tumor necrosis factor and gamma interferon production by cocaine and morphine in aging mice infected with LP-BM5, a murine retrovirus.

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The actions of retroviral infections, aging, and cocaine and morphine injection on cytokine production were investigated in C57BL/6 female mice. Retroviral infection with LP-BM5 murine leukemia virus was further developed as a model of murine acquired immunodeficiency syndrome (AIDS). The effects of

[Palatal necrosis due to cocaine abuse].

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The easier access to cocaine allows chronic and intensive consumption. Nasally inhaled cocaine causes important midfacial lesions called: Cocaine Induced Midline Destructive Lesions. These lesions are due to several factors, the anesthetic, vasoconstrictive, locally prothrombotic properties of

Simultaneous Bilateral Avascular Necrosis of the Femoral Heads Associated With Cocaine Use

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We present a case of a 38-year-old female patient, presenting with debilitating simultaneous bilateral avascular necrosis of the femoral head (AVNFH) 10 years after cocaine detoxification, making her wheelchair-bound for six months. This case is reported for the rarity of association of cocaine with

[Middle facial necrosis secondary to cocaine abuse].

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The middle facial necrosis is a rare pathology that can be found related to multiple processes that can provoque it: traumatic, chemical, infections, inflammatory and tumorals. So for its diagnosis we require a wide differential diagnosis. We present a clinic case of a nose aspirated cocaine female

Role of protein binding in cocaine-induced hepatic necrosis.

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The hepatotoxicity of cocaine in the mouse is associated with a significant amount (greater than 2 nmol/mg) of irreversible binding of a cocaine metabolite to hepatic protein. The drug-induced hepatic necrosis correlated with the degree of radiolabeled cocaine binding to hepatic protein and both

Myocardial necrosis and cocaine. A quantitative morphologic study in 26 cocaine-associated deaths.

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A quantification of different forms of acute myocardial necrosis, myocardial leukocytic infiltrates and myocardial fibrosis was accomplished in 26 chronic cocaine abusers who died of cocaine intoxication and compared to 45 normal subjects who died from head trauma and 38 who died of acquired

[Midfacial necrosis secondary to cocaine-abuse].

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Midfacial necrosis due to the abuse of inhaled cocaine is a new entity that is included in the differential diagnosis of the midline destructive diseases such as Wegener's granulomatosis, polymorphic reticulosis, nasal lymphoma, infections and the idiopathic midline destructive disease. We report

Cocaine modulation in vitro of tumor necrosis factor production by macrophages from retrovirally infected mice.

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The effect of cocaine and LP-BM5 murine leukemia retrovirus infection on tumor necrosis factor (TNF) production were investigated. Three types of macrophages were used 1) peritoneal macrophage (PM), 2) thioglycollate induced peritoneal macrophage (TPM), and 3) alveolar macrophage (AM). Cells were

[Centrofacial necrosis secondary to cocaine use].

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We report the medical case of a 40-year-old man with a history of years of cocaine abuse. He was admitted to our hospital for a septic process and purulent rhinorrhea. The clinical examination and craniofacial computed tomography revealed severe necrosis of the nasal septum, maxillary sinus,

[Nasal osteocartilaginous necrosis caused by cocaine. Our experience with two patients].

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Sinonasal osteocartilaginous necrosis induced by the abuse of inhaled cocaine must be considered in the differential diagnosis of those pathologies that produce facial midline destructions. We report two cases corresponding to women admitted in our Hospital because of such entity. There were

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