Chronic kidney disease in homeless persons in Mexico.

Little is known about the prevalence of chronic kidney disease (CKD) among the homeless in Mexico. The role of substance abuse, alcoholism, and homelessness in CKD has not been properly evaluated. We screened 260 homeless individuals in the state of Jalisco, Mexico, for the presence of CKD and its risk factors, and compared their characteristics with those from a separate cohort of poor Jalisco residents and with a survey of the general Mexican population. CKD was more prevalent among the homeless than among the poor Jalisco population (22% vs. 15.8%, P=0.0001); 16.5% had stage 3, 4.3% stage 4, and 1.2% stage 5. All were unaware of having CKD. Only 5.8% knew they had diabetes, but 19% had fasting blood sugar >126 mg/dl; 3.5% knew they were hypertensive but 31% had systolic blood pressure ⩾140 mm Hg or diastolic blood pressure ⩾90 mm Hg. Alcoholism was less common than in the poor Jalisco population (23.5% vs. 32.3%, P=0.002), but tobacco smoking (34.6% vs. 21.5%, P=0.0001) and substance abuse (18% vs. 1.1%, P=0.0001) were more prevalent among the homeless. Likewise, chronic viral infections such as HIV (4.5% vs. 0.3%, P=0.0001) and HCV (7.7% vs. 1.4%, P=0.0001) were also significantly higher among the homeless than in the general population. In conclusion, CKD and its risk factors are highly prevalent among the homeless individuals in Jalisco, Mexico. Lack of awareness of having diabetes and hypertension is highly common, as is substance abuse. Programs aiming to prevent CKD and its risk factors in Mexico should specifically target this high-risk population.

HELLP syndrome and cholecystitis: case report and review of the literature.

A case of the HELLP syndrome is reported that was initially diagnosed as cholecystitis. Much overlap exists between the two diagnoses, and the emergency physician must be aware of the important differences between them. Because the HELLP syndrome and preeclampsia may occur in both the second and third trimesters, they represent serious diagnoses that must be considered when evaluating a pregnant patient with right upper quadrant abdominal pain.

Angiogenesis factor in endometrial carcinoma: a new prognostic indicator?

OBJECTIVE: Tumor angiogenesis is believed to be a prognostic indicator associated with tumor growth and metastasis. Studies of angiogenesis in breast, prostate, and lung cancer, as well as melanoma, have shown that neovascularization correlates with the likelihood of metastasis and recurrences. The purpose of this study was to evaluate microvessel density as a prognostic factor in endometrial cancer. METHODS: Between 1980 and 1991 the tumor registry identified 25 patients with a diagnosis of recurrent endometrial cancer. These patients were matched with 25 patients with nonrecurrent disease for age, stage, grade, and treatment. The histologic slides of the 50 patients were reviewed. The paraffin blocks were obtained, and the area of the deepest myometrial invasion was selected for staining. The microvessels within the invasive cancer were highlighted by means of immunocytochemical staining to detect factor VIII-related antigen. Microvessels were counted by two investigators who were blinded to the patients' clinical status. Survival data were analyzed with Kaplan-Meier survival curves. RESULTS: Microvessel count was related to likelihood of recurrence, although this trend did not reach statistical significance. Patients with tumors of low capillary density had a mean survival time of 123 months. Patients with tumors of high capillary density had a mean survival time of 75 months (p = 0.02). Among patients with recurrent disease, those with a low capillary count survived a mean of 64 months. Patients with recurrent disease with tumors of high capillary density survived a mean of 45 months (p = 0.002). CONCLUSION: Angiogenesis factor correlates with survival in endometrial carcinoma.

Reflex circulatory collapse following intrapulmonary entrapment of activated platelets: mediation via 5-HT3 receptor stimulation.

1. The role of 5-HT2 and 5-HT3 receptors in the mediation of direct and reflex vascular responses to intrapulmonary platelet activation was investigated. 2. Anaesthetized rabbits were challenged intravenously with an emulsion of autologous bone marrow that produced a sharp increase in pulmonary blood pressure, a fall in systemic blood pressure, platelet consumption and death. 3. Platelet depletion before the challenge nearly abolished all the cardiovascular effects and prevented death. Bilateral vagotomy prevented the fall in systemic blood pressure and death but did no prevent the increase in pulmonary pressure. The intravenous administration of the 5-HT2 antagonist, ketanserin, only reduced the increase in pulmonary pressure without affecting the systemic response or mortality. 4. The effects of intravenous 5-HT and of electrical stimulation of the cephalic ends of the cut vagi nerves were also explored. 5-HT injection increased the pulmonary vascular pressure but its effects on systemic blood pressure were variable. These response were modified by the 5-HT antagonists in a manner that resembles their effects on bone marrow embolism. Afferent vagal stimulation produced a fall in systemic blood pressure that was not prevented by MDL-7222. 5. This study indicates that a centrally mediated reduction of peripheral vascular tone is the cause of the potentially lethal circulatory collapse that follows the intrapulmonary entrapment of activated platelets. This reflex is initiated by the action of 5-HT on 5-HT3 receptors in the lung.

Low levels of hepatic cytochrome P-450 in Mexicans with uncomplicated cholelithiasis.

The multienzymatic complex known as cytochrome P-450 represents one of the most important hemoprotein families of the liver. It participates in the metabolism of steroids, fatty acids, prostaglandins and liposoluble vitamins, and also plays a role in the bioactivation of xenobiotic compounds (generates reactive metabolites which produce acute and chronic lesions in liver tissue). This is a report on the low concentrations of total microsomal P-450 (0.093 +/- SD = 0.069 nMoles/mg protein) found in liver biopsies of 19 mexican patients diagnosed as having biliary lithiasis, as compared to an anglosaxon population with the same liver pathology (0.415 +/- 0.105 nMoles/mg protein). These low values are in agreement with the observation of a high incidence in normal mexicans (91.7%) of poor nifedipine metabolizers. Our findings justify an analyses of hepatic RNAm and cDNA of mexican individuals according to ethnic background, diet and environmental contaminants.

[Platelet aggregation model in vivo (rabbits)]. / Modelo de agregación plaquetaria in vivo (conejos).

The purpose of this study was to establish a blood platelet aggregation model that would permit "in vivo" (New Zealand rabbits) evaluation of hemodynamic and microscopic parameters. The platelet aggregation was induced by the administration of collagen I.V. 75 micrograms/kg/min, which produced a decrease of systolic arterial pressure from mean = 69 to mean = 55 mm Hg and diastolic pressure from mean = 43 to mean = 27 mm Hg, with ventricular increase from mean = 25 to mean = 41 mm Hg. Aspirin, dypiridamol or sulfinpyrazone was administered 10 mg/kg, half hour before the administration of collagen and prostacycline 100 mg/kg/min starting 3 minutes before until 10 minutes after the collagen injection. With the joint administration of collagen and aspirin, collagen and dypiridamol both systolic and diastolic arterial pressure were lowered with no modification in the ventricular values. No hemodynamic changes were observed with the joint administration of sulfinpyrazone-collagen or prostacycline-collagen. Histology demonstrated multiple vascular lung thrombosis with the administration of collagen and in less intensity when jointly administered with an antiaggregant drug. This model permits to measure hemodynamically and histologically pro and antiaggregant substances.

Genome amplification of human papillomavirus types 16 and 18 in cervical carcinomas is related to the retention of E1/E2 genes.

The level of amplification (copy number/cell) of HPV16 and HPV18 viral genomes and its correlation with the presence of E1/E2 genes were analyzed in a sample of 42 HPV16- and 21 HPV18-positive cervical carcinomas of different clinical stages and histological types. The viral copy number/cell was assessed by dot-blot hybridization and the presence of E1/E2 genes by PCR and Southern blot. The copy number/cell was significantly lower in HPV18-positive than in HPV16-positive tumours (23 +/- 8 and 457 +/- 191 respectively). Nearly half of the HPV16s (43%) were distributed similarly to the HPV18s in the ranges of 50 or less copies, having its peak at the group of 1 to 10 copies, whereas the remaining HPV16s (57%) spread over the groups of 51 or more copies, with another peak at the group of 101 to 500. The E1/E2 region was absent in all tumours positive for HPV18 and present in 64% of those positive for HPV16. The HPV16 tumours negative for E1/E2 had a much lower viral copy number (17 +/- 12) than the positive ones (582 +/- 212), thus resembling HPV18-positive tumours. Viral copy number was negatively correlated with the clinical stage of the tumours and directly associated with the degree of histological differentiation. However, these correlations are primarily attributable to the presence or absence of an intact E1/E2 region.

Low flow veno-venous ECMO: an experimental study.

Clinical use of extracorporeal membrane oxygenation (ECMO) and carbon dioxide removal (ECCO 2R) have become well established techniques for the treatment of severe respiratory failure; however they require full cardiopulmonary bypass, representing major procedures with high morbidity. We theorized the possibility of an efficient low flow veno-venous extracorporeal membrane gas exchange method. Four mongrel 12 kg dogs were submitted to veno-venous extracorporeal membrane gas exchange via a jugular dialysis catheter using a low flow (10 ml/min) roller pump and a membrane oxygenator for a period of four hours. Respiratory rate was set at 4 breaths/min with a FiO 2 of 21% and ventilatory dead space was increased. Adequate gas exchange was obtained (pO 2139, pCO 224, Sat 99.4%), without major hemodynamic changes or hematuria. Our results demonstrate the feasibility of a low flow, less aggressive system. Further research should be considered.

[Trans-Kehr postoperative cholangiography in upright and horizontal positions: the morphofunctional aspects of the biliary tract]. / La colangiografía postoperatoria trans Kehr en posiciones orto y horizontal: aspectos morfológico-funcionales de las vías biliares.

To change from the lying position to the upright position, in patients without their gallbladder, causes: a) a rapid and partial emptying of the biliary ducts towards the duodenum by the amplification of the opening phasic waves activity of the sphincter of Oddi (S. O.); b) an important reduction caliber of the main biliary duct (M. B. D) and c) stability of the intraductal pressure with slight raising in upright position. These physiological concepts allow a better cholangiographic exploration by means of a drip of 60 to 70 drops per minute of diluted tri-iodic in: 1) Upright position, which gives a good image regarding the terminal choledochus; of the biliary duodenal flow, and of the reduction of the caliber of the MBD. 2) In lying down position which allows: the filling up of the complete biliary-tree with possible scarcity of information about the distal choledochus-duct; the appreciation of the degree of the expansion of the MBD, and the measuring of the delay of the emptying out of the X-ray-opaque substance in relation to what was found in the upright position. The elasticity of the walls of the biliary ducts acts efficiently in the compliance of the container and contained. In normal choledochal ducts, the top level images in the upright position do not go beyond the hepatic duct. When there are problems with the flow through the S. O., there is a filling up of the intrahepatic biliary ducts with the contrast substance introduced in the upright position.

Anionic currents of chick sensory neurons are affected by a phospholipase A2 purified from the venom of the taipan snake.

A neurotoxic phospholipase A2 was purified from the venom of the taipan snake Oxyuranus scutellatus scutellatus by three consecutive chromatographic steps on ion exchange resins, followed by an affinity column prepared with a phosphatidylcholine derivative attached to Sepharose. The phospholipase was shown to be of type A2 (specific activity of 85 units/mg protein), and an apparent molecular weight of 16,000. Amino acid analysis shows the presence of approx. 150 residues with the N-terminal amino acid sequence: NLAQFGFMIRCANGGSRSALDYADYGC, different from all the phospholipases described until now. This enzyme is lethal to experimental mice (LD50 = 10 micrograms/20 g mouse weight) and affects ionic currents in chick (Gallus domesticus) dorsal root ganglion cells, measured by the whole-cell clamp technique. In symmetrical external/internal ionic solutions, after suppression of Na+, K+ and Ca2+ currents, external application of phospholipase at a low concentration (30 nM) was shown to increase the baseline current in a reversible manner. The augmented response was voltage-dependent and the effect was much greater for negative currents. In the presence of a salt gradient across the membrane (out 40 mM NaCl/in 140 mM CsCl), the current reversal potential revealed a shift in the positive direction typically due to Cl- ion flux through the membrane. External application of a 50 microM concentration of picrotoxin caused a reversible reduction of the phospholipase-induced chloride current. Moreover, no appreciable current block was detected after addition of 50 microM DIDS.

Verapamil does not block the spastic response of Praziquantel on the larvae of Taenia pisiformis.

This paper describes that the previous addition of Verapamil does not block the spastic response to Praziquantel (Pz) in larvae of Taenia pisiformis kept in vitro, where opposite results were found in the literature using mammalian tissue. It is possible that Pz stimulates other Ca++ transport channels not sensitive to Verapamil action and promotes Ca++ liberation from calcareous corpuscles stimulating phospholipase C of the tegument surface generating inositol triphosphate. These hypotheses require experimental approaches to define the exact mechanism of action.

Thromboxane and prostacyclin generation by human umbilical veins after thrombin.

Prostacyclin (PGI2) and Thromboxane B2 (TxB2) production induced by thrombin in human umbilical veins (HUV) was studied. Successive stimulations of HUV segments were performed with and without restoration of arachidonic acid (AA). Thrombin consistently stimulated the production of both substances. The magnitude of the increment declined with progressive stimuli. The addition of exogenous AA could restore the production of TXB2 but not that of PGI2. These results suggest that sustained stimulation of AA release may lead to an imbalance in the TXA2/PGI2 ratio perhaps through an effect of unknown products of AA oxidation on PGI2 synthase.

Nitric oxide synthesized from L-arginine regulates vascular tone in the coronary circulation of the rabbit.

1. The role of nitric oxide (NO) in the regulation of the vascular tone of the coronary circulation of the Langendorff-perfused rabbit heart was investigated. 2. NG-monomethyl-L-arginine (L-NMMA; 10-100 microM), a specific inhibitor of NO formation from L-arginine (L-Arg), but not its D-enantiomer (D-NMMA; 100 microM) produced a dose-related, sustained increase in the coronary perfusion pressure (CPP). In addition, L-NMMA inhibited the vasodilator responses of acetylcholine (ACh), unmasking in some instances its direct vasoconstrictor effect. These effects of L-NMMA were attenuated by L-Arg. 3. L-NMMA (10 and 30 microM), but not D-NMMA (30 microM), caused a long-lasting inhibition of NO formation which was reversed by L-Arg (30 and 100 microM), but not by D-Arg (100 microM). 4. This study indicates that the formation of NO from L-Arg in the coronary circulation of the rabbit plays a role both as a regulator of vascular tone and as a mediator of the vasodilatation induced by ACh.

Experimental uterine eosinophilia in the rat. The role of some inhibitors of arachidonic acid metabolism.

The mechanism of estrogen induced eosinophilia is not well understood. It has been proposed that type II estrogen receptors, present both in eosinophils and uterine tissues, can act as anchorage mechanism for the attachment of eosinophils within the uterus. However an explanation based on the existence of chemotactic mediators is more likely. We studied the effects of the lipoxygenase inhibitor BW755 and two different doses of indomethacin in a model of acute uterine eosinophilia promoted by 17-beta-estradiol in young rats; simultaneously estrogen receptors were studied with immunocytochemical methods using monoclonal antibodies. BW755 and a high dose of indomethacin sharply reduced the estrogen induced eosinophilia, whereas a low dose of indomethacin enhanced the steroid effect. No estrogen receptors were found with immunohistochemical methods neither in eosinophils nor in endothelial cells in any of the groups. A role for the lipoxygenase products of arachidonic acid, mainly leukotrine B4 as the chemical mediators responsible of eosinophil chemotaxis in be estrogen primed uterus is suggested.

Acetylcholine induces vasodilatation in the rabbit isolated heart through the release of nitric oxide, the endogenous nitrovasodilator.

1. Acetylcholine (ACh, 0.03-3.0 microM) induced a dose-dependent vasodilatation in the isolated Langendorff-perfused heart of the rabbit. The vasodilatation was mimicked by exogenous nitric oxide (NO, 0.045-4.5 nmol). 2. There was no detectable vascular relaxing activity in the cardiac effluent when these concentrations of ACh or NO were injected through the heart, even in the presence of an infusion of superoxide dismutase (SOD). 3. Acetylcholine (0.03-3.0 microM), however, induced the release into the cardiac effluent of a material which produced a chemiluminescent signal when reacted with ozone, a response which could be mimicked with exogenous NO (0.045-4.5 nmol) injected through the heart. 4. The effects of ACh, but not those of NO, were antagonized by atropine (2 microM). Prostacyclin (1 microM) injected through the heart induced vasodilatation without the release of a biologically active or chemiluminescent material. 5. During passage through the heart, greater than 99% of the biological activity of exogenous NO disappeared, whereas there was approximately 50% reduction of its chemiluminescent response. This indicates complete transformation into a mixture containing approximately 50% NO2- and 50% of other non-chemiluminescent material(s), presumably NO3-. 6. This study suggests that ACh induces endothelium-dependent vasodilatation in the coronary circulation through the release of the endogenous nitrovasodilator, NO, which is rapidly converted to NO2- and NO3-.

Protection against thallium hepatotoxicity by silymarin.

The effect of silymarin (100 mg/kg i.p.) on the biochemical indicators of liver damage induced by thallium (10 mg/kg p.o.) was studied in rats. The production of malondialdehyde and the content of reduced glutathione in the liver were measured as indicators of lipid peroxidation. Thallium intoxication increased the serum activities of glutamic pyruvic transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase and the liver concentration of triglycerides. Thallium decreased the activity of alkaline phosphatase and increased that of gamma-glutamyl transpeptidase in the liver cell membrane. It also abolished the membrane activity of Na+/K+ ATPase. Lipid peroxidation was enhanced by thallium as malondialdehyde production was increased and the content of reduced glutathione was decreased in the liver. Silymarin completely prevented all these changes. It is suggested that thallium toxicity is due, at least in part, to the promotion of lipid peroxidation. The membrane stabilizing effect of silymarin observed in this and in other models of liver toxicity is due to some antioxidant property, possibly related to its ability to scavenge free oxygen radicals.

Protective effect of colchicine on acute liver damage induced by carbon tetrachloride.

Pretreatment of rats with colchicine (10 micrograms/day) for 7 days protected against CCl4-induced acute liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of glutamic-pyruvic transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase. Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane gamma-glutamyl transpeptidase activity were found. Colchicine increased the LD50 of CCl4 2.5-fold and prevented the release of intracellular enzymes, as well as the decrease in gamma-glutamyl transpeptidase activity in the plasma membrane. It also completely prevented the lipid peroxidation produced by CCl4 and limited the extent of the histological changes. Our results suggest that the protective effect of colchicine may be mediated through its action on an early toxic event, because treatment of the animals with colchicine produced a significant decrease in CCl4-induced lipid peroxidation.

Aspirin disposition in rats acutely intoxicated with CCl4.

The profile of urinary salicylate metabolites was determined after an oral administration of acetylsalicylic acid (ASA) to: 1, control rats; 2, rats treated with CCl4 and 3, rats intoxicated with CCl4 and also pretreated with colchicine for 7 days. The following enzymatic activities were determined: liver and plasma ASA-esterase, liver UDP-glucuronyltransferase and liver aniline hydroxylase. The time course of plasma concentration of salicylates in similar groups were followed after the intraperitoneal administration of acetylsalicylic acid (ASA), salicylic acid (SA) or gentisic acid (GA). The animals acutely intoxicated with CCl4 showed a reduction in urinary excretion of glucuronates and an increased urinary excretion of gentisic and salicylic acids. The activities of plasma and liver ASA-esterases were significantly increased in CCl4-treated rats while the aniline hydroxylase was reduced and the UDP-glucuronyltransferase remained unchanged. The plasma half lives of salicylates were reduced in CCl4-treated rats regardless of the administered parent compound. Colchicine pre-treatment completely prevented the alterations produced by acute intoxication with CCl4. The heterogeneity of liver metabolic dysfunctions present in acute liver damage was evidenced. It is emphasized that the pharmacokinetic alterations produced by acute liver injury can be the result of complex factors that may involve changes in circulation, hepatic binding protein and other routes of elimination.