Caso clínico: Rabdomiolisis secundaria al consumo de cocaína / Case report: Rabdomuolisis after cocaine consumption

Introducción: Las múltiples causas de Rabdomiolisis se pueden separar en 5 categorías según el mecanismo de daño del miocito: Hipóxicas, físicas, químicas, biológicas e idiopáticas. Como primera causa se describe el consumo de drogas ilícitas/alcohol, seguido por medicamentos, trauma, inmovilidad y ejercicio extenuante. Las causas químicas representan hasta el 80% de los casos de rabdomiolisis. En esta categoría se encuentran los medicamentos, alcohol y drogas donde destaca la cocaína. Se presenta el caso de un paciente masculino que cursa con insuficiencia renal aguda secundario a una rabdomiolisis por consumo de cocaína.

Introduction: The multiple causes of rhabdomyolysis can be separated into 5 categories according to the myocyte damage mechanism: hypoxic, physical, chemical and biological. However, a cause will not always be identified. The consumption of illicit drugs / alcohol has been identified as the first cause, followed by medication, trauma, immobility and extenuating exercise. The chemical causes represent up to 80% of cases of rhabdomyolysis. This category includes medications, alcohol and drugs, where cocaine stands out. Cocaine is a strong stimulant used mainly as a recreational drug that has considerably increased its consumption in the country so it should be considered. Next, we present the case of a male patient with acute renal failure secondary to rhabdomyolysis due to cocaine use. The physiopathology, diagnostic process and current management will be discussed according to the latest guidelines.

Endohelminth parasites from salmonids in intensive culture from southern Chile.

A total of 228 salmonids (90 Oncorhynchus mykiss, 48 Oncorhynchus kisutch, and 90 Salmo salar) from 8 intensive aquaculture centers in the south of Chile were examined for endohelminths parasites between December 2008 and May 2009. The body cavities of 2 O. mykiss were infected by Diphyllobothrium sp. plerocercoids (prevalence: 6.7%, mean intensity: 1.0, mean abundance: 0.07) from the Lake Tarahuin hatchery on the south of Chiloé Island. Also, tetraphyllidean plerocercoids (prevalence: 3.3%, mean intensity: 1, mean abundance: 0.03) and fourth-stage larvae of Hysterothylacium aduncum (prevalence: 6.7%, mean intensity: 1, mean abundance 0.07) were observed in O. kisutch from a marine hatchery in Chiloé. The occurrences of Diphyllobothrium sp. in a lake and a tetraphyllidean plerocercoid from marine cultured salmonid in Chiloé are reported for first time. No muscular infection by helminths was recorded in the fish examined.

Chiral inversion of (R)-(-)-fenoprofen in guinea-pigs pretreated with clofibrate.

The influence of clofibrate on the stereoconversion of fenoprofen (FPF) was studied in guinea pigs. This hypolipidaemic agent has been related to some biochemical changes in the liver leading to an increase in the chiral inversion process. Two groups of animals (n = 6 per group) were pretreated with oral doses of clofibrate (280 mg/kg per day) for three days and were then given (R)- or (S)-FPF (5 mg/kg, IV). The FPF enantiomers were extracted from the guinea-pigs' plasma using a solid phase procedure and analysed by HPLC with previous derivatization with L-leucinamide. Pretreatment with clofibrate increased the chiral inversion of (R)-FPF in favour of the pharmacologically active (S)-FPF enantiomer. Before this metabolic interaction can be applied to therapy with fenoprofen, the toxic effects of (S)-(+)-FPF on the gastrointestinal and renal tracts and the interference by (R)-(-)-FPF with the metabolism of lipids should be thoroughly evaluated.

Late protective effects of the anticalmodulin drug fluphenazine on carbon tetrachloride-induced liver necrosis.

Fluphenazine (FP) treatment (50 mg/kg bw, ip in saline) 30 min before or 6 or 10 h after CCl4 administration (1 ml/kg ip in olive oil) significantly prevented the liver necrosis produced by the hepatotoxin at 24 h. FP had enhancing effects on the covalent binding of CCl4 reactive metabolites to cellular constituents and on CCl4 induced lipid peroxidation. FP lowered body temperature of the CCl4-poisoned animals during the 24 h observation period. The obtained results are compatible but do not prove the hypothesis that calmodulin (CaM) had participation in late occurring events preceding necrosis. FP lowering action on body temperature, however, might also play a role in the effects of this drug on the onset of CCl4 induced liver necrosis. FP levels in liver tissue as determined by gas chromatography-mass spectrometry evidenced the presence of the drug in amounts sufficient to inhibit CaM and that suggests that not all preventive effects of FP are due to its indirect actions on the central nervous system via decreased body temperature.

Trifluopromazine late preventive effects on carbon tetrachloride-induced liver necrosis.

Trifluopromazine (TFPro) administration to rats (50 mg/kg, ip) 30 min before or 6 or 10 hr after CCl4 treatment (1 ml/kg ip in olive oil) partially prevented necrogenic effects of this compound at 24 hr. TFPro has only minor effects on the covalent binding (CB) of CCl4-reactive metabolites to cellular constituents and even an enhancing action on CCl4-promoted lipid peroxidation (LP). Determination of TFPro levels in liver 1 and 3 hr after administration by gas chromatography/mass spectrometry showed its presence in that tissue at concentrations well above those needed for calmodulin (CaM) inhibitory effects of this drug. TFPro lowered body temperature in CCl4-treated animals during the 24-hr observation period. Protective effects of TFPro at 6 or 10 hr, when most of the CB and all of the LP has already occurred, suggest but do not prove a role for CaM in late stages of CCl4-induced necrogenic effects. Decreases in the body temperature of CCl4-poisoned animals provoked by TFPro might also play a role in the preventive actions of this drug.

Nicotinamide late protective effects against carbon tetrachloride-induced liver necrosis.

Nicotinamide (NIC) is known to increase the synthesis of pyridine nucleotides and also to inhibit the hydrolysis of them to ADP-ribose, which in turn is involved in Ca2+ release from mitochondria via the ADP ribosylation of crucial mitochondrial proteins. In this work, we test the potential ability of NIC to be a late protective agent against CCl4-induced liver necrosis. We observed that 1 g/kg po NIC, 30 min before or 6 or 10 hr after CCl4 (1 ml/kg), given ip as a 20% (v/v) solution in olive oil, was able to significantly prevent the necrogenic effect of the hepatotoxin at 24 hr as evidenced by determination of isocitric dehydrogenase activity in plasma or by histological observation. NIC administration 6 hr after CCl4 prevented fatty liver induced by hepatotoxin at 24 hr. NIC did not modify CCl4-induced lipid peroxidation process at 1 hr after CCl4 and decreased the covalent binding of 14CCl4 to lipids. NIC decreased the levels of 14CCl4 reaching the liver when given 30 min before hepatotoxin but not when given 6 hr after it. NIC lowered body temperature of rats at 1, 3, and 6 hr and augmented it at 24 hr after CCl4. NIC concentrations in liver as determined by GC/MS/SIM analysis were 21 micrograms/g liver 1 hr after administration and 53 micrograms/g at 3 hr. Late preventive effects of NIC against CCl4 induced liver necrosis when given at 6 or 10 hr after CCl4 are compatible with the hypothesis that NIC restores mitochondrial ability for Ca2+ uptake. This hypothesis remains to be proved and is being further challenged in our laboratory.