Spot urine porphyrins/creatinine ratio profile of healthy Brazilian individuals adjusted for personal habits

Changes in urinary porphyrin excretion may be the result of hereditary causes and/or from environmental or occupational exposure. The objective of this study was to measure the amount of some porphyrins in spot urine samples obtained from volunteers randomly selected from a healthy adult population of São Paulo with a sensitive HPLC method and to estimate normal ranges for a non-exposed population. Spot urine samples were collected from 126 subjects (both genders, 18 to 65 years old) not occupationally exposed to porphyrinogenic agents. Porphyrin fractions were separated on RP-18 HPLC column eluted with a methanol/ammonium acetate buffer gradient, pH 4.0, and measured fluorometrically (excitation 405 nm/emission 620 nm). The amount of porphyrins was corrected for urinary creatinine excretion. Only 8-carboxyl (uro) and 4-carboxyl (copro) porphyrins were quantified as µg/g creatinine. Data regarding age, gender, occupational activities, smoking and drinking habits were analyzed by Mann-Whitney and Kruskal-Wallis tests. Uroporphyrin results did not differ significantly between the subgroups studied. Copro and uro + copro porphyrins were significantly different for smokers (P = 0.008) and occupational activities (P = 0.004). With respect to alcohol consumption, only men drinking >20 g/week showed significant differences in the levels of copro (P = 0.022) and uro + copro porphyrins (P = 0.012). The 2.5-97.5th percentile limit values, excluding those for subjects with an alcohol drinking habit >20 g/week, were 0-20.8, 11.7-93.1, and 15.9-102.9 µg/g creatinine for uro, copro and uro + copro porphyrins, respectively. These percentile limit values can be proposed as a first attempt to provide urinary porphyrin reference values for our population, serving for an early diagnosis of porphyrinopathies or as biomarkers of exposure to porphyrinogenic agents.

Spot urine porphyrins/creatinine ratio profile of healthy Brazilian individuals adjusted for personal habits.

Changes in urinary porphyrin excretion may be the result of hereditary causes and/or from environmental or occupational exposure. The objective of this study was to measure the amount of some porphyrins in spot urine samples obtained from volunteers randomly selected from a healthy adult population of São Paulo with a sensitive HPLC method and to estimate normal ranges for a non-exposed population. Spot urine samples were collected from 126 subjects (both genders, 18 to 65 years old) not occupationally exposed to porphyrinogenic agents. Porphyrin fractions were separated on RP-18 HPLC column eluted with a methanol/ammonium acetate buffer gradient, pH 4.0, and measured fluorometrically (excitation 405 nm/emission 620 nm). The amount of porphyrins was corrected for urinary creatinine excretion. Only 8-carboxyl (uro) and 4-carboxyl (copro) porphyrins were quantified as microg/g creatinine. Data regarding age, gender, occupational activities, smoking and drinking habits were analyzed by Mann-Whitney and Kruskal-Wallis tests. Uroporphyrin results did not differ significantly between the subgroups studied. Copro and uro + copro porphyrins were significantly different for smokers (P = 0.008) and occupational activities (P = 0.004). With respect to alcohol consumption, only men drinking >20 g/week showed significant differences in the levels of copro (P = 0.022) and uro + copro porphyrins (P = 0.012). The 2.5-97.5th percentile limit values, excluding those for subjects with an alcohol drinking habit >20 g/week, were 0-20.8, 11.7-93.1, and 15.9-102.9 microg/g creatinine for uro, copro and uro + copro porphyrins, respectively. These percentile limit values can be proposed as a first attempt to provide urinary porphyrin reference values for our population, serving for an early diagnosis of porphyrinopathies or as biomarkers of exposure to porphyrinogenic agents.

[Antitumor effects of liposome-entrapped carboplatin (Lipo-CBDCA) after intraperitoneal administration in rats bearing carcinomatous peritonitis].

We examined the distribution of Lipo-CBDCA after intraperitoneal administration and antitumor effects in rats. The serum levels of platinum in Lipo-CBDCA were lower than in free-CBDCA intraperitoneal or intravenous administration at 15 and 30 min. after administration. After 3 hours, Lipo-CBDCA showed higher levels of serum platinum than free-CBDCA. These data showed the slow release of Lipo-CBDCA. The antitumor effects of Lipo-CBDCA were studied in rats with peritoneal dissemination due to AH 130 tumors. Intraperitoneal treatment with Lipo-CBDCA prolonged the life span significantly compared with Lipo-CBDCA. No side effects of chemotherapy were found in the liver, kidney, spleen or small intestine. A gastric cancer patient suffering from carcinomatous peritonitis with remarkable ascites was treated with Lipo-CBDCA intraperitoneally. After several injections of Lipo-CBDCA, the ascites disappeared completely and the CEA level of ascites decreased dramatically. These results indicate that intraperitoneal chemotherapy with Lipo-CBDCA may be more effective than free-CBDCA to manage carcinomatous peritonitis, and may be therapeutically useful without toxic side effects.

Pulmonary intralobar sequestration accompanied by aneurysm of an anomalous arterial supply.

A 47-year-old woman presented with hemoptysis and her chest X-ray films showed an opacity suggesting a mass in the left lower lung field. Based on radiographic investigations, the mass was diagnosed as an aneurysm develop in an anomalous vessel and was considered to be a Pryce type I pulmonary intralobar sequestration. Resection of the left lower lobes was performed and the aneurysm was found to be filled with thrombus. It is rare for an aneurysm to form in an aberrant vessel. This complication may have been the result of regional sclerosis affecting the anomalous artery as well as systemic atherosclerosis.

[Early diagnosis of acute mesenteric artery occlusion--clinical and experimental study].

This study was undertaken for the purpose of making early diagnosis of acute superior mesenteric artery occlusion (SMAO). (Clinical Study) This study included 16 patients with SMAO. The early diagnoses by clinical, laboratory, echographic and radiologic findings which were commonly obtained in the cases of abdominal emergency, were difficult. Angiography was useful method for its diagnosis. But in its early stage, we could hardly determine which patient was subject to angiography, therefore non-invasive and simple screening modelity is needed for its early diagnosis. (Experimental Study) Portal blood flow (PVF) is considered to decrease when superior mesenteric artery (SMA) is occluded, because SMA is a main feeder of portal vein. If SMAO has specific portal hemodynamics, its early diagnosis will be possible by non-invasive PVF measurement using an ultrasonic duplex system (PD). We investigated the portal hemodynamic changes in experimental SMAO, peritonitis and ileus using 24 mongrel dogs. Our results showed that PVF to cardiac output ratios (PCR) of SMAO models were under 10% and in contrast, those of others were over 10%. So SMAO models were distinguishable from others. These suggested that PCR measured by PD and echocardiography was an useful indicator of early diagnosis of SMAO.

[A case of retroperitoneal chylous cyst developed after cholecystectomy and choledochotomy].

A 43-year-old woman complaining of upper abdominal pain was referred to our clinic. Well movable mass was detected in the right hypochondria region by palpation. Three years before, she underwent cholecystectomy and choledochotomy for cholelithiasis. After that she had been aware of painless mass in the right hypochondria region, but because of no symptom she regarded it as operative scar and had no treatment. Abdominal CT, ultrasonography, upper GI series and barium enema revealed a retroperitoneal cyst compressing the 3rd portion of the duodenum upward and the vena cava backward. Laparotomy showed an unilocular chylous cyst, 5 cm in diameter in the retroperitoneal cavity. Histologically, the cyst was cystic lymphangioma. Etiologically, the previous operation of cholecystocholedocholithiasis was supposed to be a trigger of the development of the chylous cyst.