Locomotion and morphological adaptations in the glass lizard Ophiodes cf. fragilis (Raddi, 1820) (Squamata: Anguidae).

There are few studies related to the biological and ecological aspects of the glass snake, a limbless lizard and with a wide geographic distribution. The aim of this study was to analyze the locomotion mode of specimens of Ophiodes cf. fragilis in different substrates and to investigate the morphological adaptations associated with this type of behavior. We observed that the analyzed specimens presented slide-push locomotion modes and lateral undulation in different substrates, using their hind limbs to aid locomotion in three of the four substrates analyzed. The bones of the hind limbs (proximal - femur - and distal - tibia and fibula) were present and highly reduced and the femur is connected to a thin pelvic girdle. Our data support that hind limbs observed in species of this genus are reduced rather than vestigial. The costocutaneous musculature was macroscopically absent. This is the first study of locomotor behavior and morphology associated with locomotion in Ophiodes, providing important information for studies on morphological evolution in the genus.

Congenital hepatic fibrosis associated with von Recklinghausen's disease.

Congenital hepatic fibrosis is characterized by a ductal plate malformation with duct-like structures and fibrosis. It manifests clinically with portal hypertension and may be associated with multiple congenital defects. We present the case of a 16-year-old male with splenomegaly, leukopenia and thrombocytopenia, esophageal varices, and a histopathological diagnosis of congenital hepatic fibrosis. He exhibits "café au lait" spots and "Lisch" nodules, with a diagnosis of von Recklinghausen s disease. Congenital hepatic fibrosis belongs to the so-called fibropolycystic diseases, in which there is a disordered interaction between cells and the extracellular matrix. Von Recklinghausen s disease affects tissues derived from the neural crest and its diagnosis is based on clinical criteria. It is associated with multiple diseases. We describe its association with congenital hepatic fibrosis for the first time.

Fibrosis hepática congénita asociada a enfermedad de von Recklinghausen / Congenital hepatic fibrosis associated with von Recklinghausen’s disease

La fibrosis hepática congénita se origina como consecuencia deuna malformación de la placa ductal con estructuras tipo ductalesacompañadas de fibrosis. Se manifiesta con hipertensión portal ypuede asociarse a múltiples defectos congénitos. Presentamos unvarón de 16 años con esplenomegalia, leuco- y plaquetopenia, varicesesofágicas y diagnóstico histopatológico de fibrosis hepáticacongénita. La exploración física mostraba la existencia de manchasde “café con leche” y nódulos de “Lisch” con diagnóstico de enfermedadde von Recklinghausen. La fibrosis hepática congénita formaparte de las enfermedades fibropoliquísticas donde existiría unaalteración en la interacción entre las células y la matriz extracelular.La enfermedad de von Recklinghausen afecta a los tejidos derivadosde la cresta neural y su diagnóstico se basa en criterios clínicos. Seasocia a múltiples patologías. Presentamos por primera vez su asociacióncon fibrosis hepática congénita

Congenital hepatic fibrosis is characterized by a ductal platemalformation with duct-like structures and fibrosis. It manifestsclinically with portal hypertension and may be associated withmultiple congenital defects. We present the case of a 16-year-oldmale with splenomegaly, leukopenia and thrombocytopenia,esophageal varices, and a histopathological diagnosis of congenitalhepatic fibrosis. He exhibits “café au lait” spots and “Lisch”nodules, with a diagnosis of von Recklinghausen’s disease. Congenitalhepatic fibrosis belongs to the so-called fibropolycystic diseases,in which there is a disordered interaction between cells andthe extracellular matrix. Von Recklinghausen’s disease affects tissuesderived from the neural crest and its diagnosis is based onclinical criteria. It is associated with multiple diseases. We describeits association with congenital hepatic fibrosis for the first time

Hepatotoxicity associated with the ingestion of Centella asiatica.

BACKGROUND: Hepatotoxicity due to herbal remedies is being increasingly recognized. Centella asiatica (Centella asiatica Linn Urban) is commercialized for multiple conditions. Its active principles are pentacyclic triterpenic saponosides (asiaticoside, madecassoside). CLINICAL CASE STUDIES: We present three women (61, 52 and 49 years old) who developed jaundice after taking Centella asiatica for 30, 20 and 60 days. Respective laboratory tests: ALT: 1193, 1694 and 324 U/L; ALP: 503, 472 and 484 U/L; bilirubin: 4.23, 19.89 and 3.9 mg/dl. The first patient also had ASMA 1/160 and AMA 1/320. Respective pathological diagnoses: granulomatous hepatitis with marked necrosis and apoptosis; chronic hepatitis with cirrhotic transformation and intense necroinflammatory activity, and granulomatous hepatitis. All patients improved with Centella asiatica discontinuation, and ursodeoxycholic acid 10 mg/kg/day. The first patient took Centella asiatica again, with recurrence of the damage. The second one had taken this herb a year before. CONCLUSIONS: Many plants synthesize hepatotoxic compounds. Germander, Skullcap and Glycyrrhizin contain di- or triterpenic active principles, which can produce hepatic injury by promoting apoptosis and altering cell membranes. We hypothesize that these mechanisms may have resulted in injuries associated with Centella asiatica. The presence of autoantibodies and granulomas also favors an immune-mediated mechanism. Ursodeoxycholic acid has anti-apoptotic properties, but we cannot rule out that Centella asiatica discontinuation alone may have resulted in patient improvement.

Hepatotoxicidad asociada al consumo de Centella asiática / Hepatotoxicity associated with the ingestion of Centella asiatica

Introducción: la hepatotoxicidad por hierbas medicinales esreconocida cada vez más frecuentemente. Centella asiática (Centellaasiatica Linn Urban) es comercializada para múltiples afecciones.Sus principios activos son saponósidos pentacíclicos triterpénicos(asiaticósido, madecasósido).Casos clínicos: presentamos 3 mujeres (61, 52 y 49 años)que presentaron ictericia después de consumir Centella asiáticapor 30, 20 y 60 días. Analíticas respectivas: ALT: 1193, 1694 y324 U/l; FAL: 503, 472 y 484 U/l; bilirrubina: 4,23, 19,89 y3,9 mg/dl. La primera presentó ASMA 1/160 y AMA 1/320.Diagnósticos anatomopatológicos: respectivamente hepatitisgranulomatosa con marcada necrosis y apoptosis; hepatitis crónicacon transformación cirrótica e intensa actividad necroinflamatoriay hepatitis granulomatosa.Todas mejoraron al suspender Centella asiática y con ácidoursodeoxicólico 10 mg/kg/día.La primera volvió a ingerir Centella asiática, repitiendo las lesiones.La segunda había ingerido esta sustancia un año antes.Conclusiones: muchos vegetales sintetizan compuestos hepatotóxicos.Camedrio, escutelaria y glicirricina poseen principiosactivos di- o triterpénicos que pueden lesionar el hígado promoviendoapoptosis y alterando membranas celulares. Hipotetizamosque estos mecanismos pueden haber producido las lesiones asociadasa Centella asiática. La presencia de autoanticuerpos y granulomastambién favorecen un mecanismo inmunológico. El ácidoursodeoxicólico posee propiedades antiapoptóticas, aunque nopodemos descartar que la sola discontinuación de Centella asiáticahaya determinado la mejoría de las pacientes

Background: hepatotoxicity due to herbal remedies is beingincreasingly recognized. Centella asiatica (Centella asiatica LinnUrban) is commercialized for multiple conditions. Its active principlesare pentacyclic triterpenic saponosides (asiaticoside, madecassoside).Clinical case studies: we present three women (61, 52 and49 years old) who developed jaundice after taking Centella asiaticafor 30, 20 and 60 days. Respective laboratory tests: ALT:1193, 1694 and 324 U/L; ALP: 503, 472 and 484 U/L; bilirubin:4.23, 19.89 and 3.9 mg/dl. The first patient also had ASMA1/160 and AMA 1/320.Respective pathological diagnoses: granulomatous hepatitiswith marked necrosis and apoptosis; chronic hepatitis with cirrhotictransformation and intense necroinflammatory activity, andgranulomatous hepatitis.All patients improved with Centella asiatica discontinuation,and ursodeoxycholic acid 10 mg/kg/day.The first patient took Centella asiatica again, with recurrenceof the damage. The second one had taken this herb a year before.Conclusions: many plants synthesize hepatotoxic compounds.Germander, Skullcap and Glycyrrhizin contain di- ortriterpenic active principles, which can produce hepatic injury bypromoting apoptosis and altering cell membranes. We hypothesizethat these mechanisms may have resulted in injuries associatedwith Centella asiatica. The presence of autoantibodies andgranulomas also favors an immune-mediated mechanism. Ursodeoxycholicacid has anti-apoptotic properties, but we cannotrule out that Centella asiatica discontinuation alone may have resultedin patient improvement

Steroid receptors and heat-shock proteins in patients with primary biliary cirrhosis.

Primary biliary cirrhosis has a definite female preponderance. Increased estrogen levels have been found in patients with this disease; however no studies indicate the status of sex hormone steroid receptors in primary biliary cirrhosis patients. In this study the occurrence and distribution of estrogen receptors, progesterone receptors and androgen receptors in liver biopsy specimens from patients with primary biliary cirrhosis were examined and compared with these receptors in the normal liver. In addition, three heat-shock proteins associated with steroid receptors (90 kD, 70 kD and 27 kD) were examined. All of the receptor proteins were detected on immunocytochemical study using specific receptor antibodies; monoclonal and polyclonal antibodies were also used to detect the heat-shock proteins. Normal bile duct epithelial cells displayed low-to-moderate amount of estrogen receptors and abundant 90- kD, 70- kD and 27-kD heat-shock protein expression, whereas normal hepatocytes showed moderate estrogen receptor and 90-kD heat-shock protein and high 70-kD heat-shock protein expression. Expression of 70-kD heat-shock protein was due mainly to the constitutive form of this protein (hsc72). In patients with primary biliary cirrhosis, significant increases in estrogen receptor and 90-kD heat-shock protein content were seen in bile duct cells and in hepatocytes. Levels of 27-kD heat-shock protein were also increased in some of the primary biliary cirrhosis biopsy specimens. The expression of progesterone receptor and androgen receptor was very low in normal and primary biliary cirrhosis bile duct cells and hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Tratamiento esclerosante de las varices esofagicas / Sclerosing treatment of esophageal varices

Se presentan los resultados del tratamiento de las várices esofágicas en dos tipos de pacientes cirróticos. A) trescientos cincuenta y un que habían experimentado una hemorragia y que fueron tratados con esclerosis ya sea en el episodio agudo o en los intervalos libres. B) Noventa enfermos cirróticos en quienes se fectuó el tratamiento profiláctico. De los 67 enfermos tratados durante el episodio agudo 6(9%) fallecieron por hemorragia, 6(9%) por isuficicencia hepática y 1 (1,5%) por sepsis. Noventa enfermos cirróticos recibieron tratamiento profiláctico. Se los dividió en tres grupos. El primero de 30 enfermos, 15 fueron esclerosados y 15 no recibieron tratamiento. El segundo de 32 enfermos, 16 recibieron propranolol y se compararon los 16 de control. El tercero de 28 pacientes, 14 recibieron propranolol y esclerosis y 14 ningún tratamiento. En los tres grupos tratados la hemorragia disminuyó de manera estadísticamente significativa. L sobrevida fue la misma en los grupos tratados y en los controles. La mayoría falleció a raíz de una insuficiencia hepática

Tratamiento esclerosante de las varices esofagicas / Sclerosing treatment of esophageal varices

Se presentan los resultados del tratamiento de las várices esofágicas en dos tipos de pacientes cirróticos. A) trescientos cincuenta y un que habían experimentado una hemorragia y que fueron tratados con esclerosis ya sea en el episodio agudo o en los intervalos libres. B) Noventa enfermos cirróticos en quienes se fectuó el tratamiento profiláctico. De los 67 enfermos tratados durante el episodio agudo 6(9%) fallecieron por hemorragia, 6(9%) por isuficicencia hepática y 1 (1,5%) por sepsis. Noventa enfermos cirróticos recibieron tratamiento profiláctico. Se los dividió en tres grupos. El primero de 30 enfermos, 15 fueron esclerosados y 15 no recibieron tratamiento. El segundo de 32 enfermos, 16 recibieron propranolol y se compararon los 16 de control. El tercero de 28 pacientes, 14 recibieron propranolol y esclerosis y 14 ningún tratamiento. En los tres grupos tratados la hemorragia disminuyó de manera estadísticamente significativa. L sobrevida fue la misma en los grupos tratados y en los controles. La mayoría falleció a raíz de una insuficiencia hepática (AU)

Estrogen receptors, progesterone receptors and heat-shock 27-kD protein in liver biopsy specimens from patients with hepatitis B virus infection.

It has been proposed that in the human liver, the estrogen receptor gene may become inappropriately expressed as a consequence of HBV integration, contributing to cell transformation. This study was undertaken to examine estrogen receptor status in patients with hepatitis B virus infection and to analyze the expression of progesterone receptor and of a heat-shock 27,000-D protein (hsp27), both of which are estrogen regulated in estrogen target tissues. Receptor proteins were detected in liver biopsy specimens by immunocytochemistry using antireceptor monoclonal antibodies; a monoclonal antibody was also used to detect hsp27. Estrogen receptor and progesterone receptor were mainly seen in the nuclei of hepatocytes. The presence of hepatitis B virus infection did not always result in elevated estrogen receptor expression, but in general the expression of this receptor protein was higher in hepatitis B virus-positive patients than in patients with the same pathological findings (hepatitis, cirrhosis, hepatocarcinoma) but without hepatitis B virus. This was more clearly seen in the patients with hepatitis. Although estrogen receptor expression was moderate to high in many samples, the expression of the two biochemical markers of estrogen action at postreceptor levels (progesterone receptor and hsp27) was low or absent in most of the liver tissues examined, suggesting that in the liver the interaction of estrogen-estrogen receptor-DNA has characteristics inherent to this tissue.

[Sclerosing treatment of esophageal varices]. / Tratamiento esclerosante de las várices esofágicas.

The results of esophageal varices treatment in two groups of patients are shown. The first group consists of 351 patients who suffered an hemorrhage and were treated with sclerosing varices during the acute period or in the intervals of bleedings. The second group consists of 90 cirrhotic patients to whom a prophylactic treatment was administered. From 67 patients treated during acute hemorrhage 6 (9%) died due to hemorrhage, 6 (9%) due to hepatic failure and 1 (1.5%) due to sepsis. The 90 cirrhotic patients with prophylactic treatment were divided in 3 groups. In the first group of 30, 15 were sclerosized and 15 did not get treatment. From the second group of 32, 16 got propranolol and 16 no treatment. In the third group of 28, 14 got propranolol and were sclerosized and 14 were not treated. In all three groups with treatment hemorrhage ceased in a statistically significative manner. Surviving was the same in the treated and non-treated groups. Most patients died due to an hepatic failure.

Tratamiento esclerosante de las várices esofágicas. / [Sclerosing treatment of esophageal varices]

The results of esophageal varices treatment in two groups of patients are shown. The first group consists of 351 patients who suffered an hemorrhage and were treated with sclerosing varices during the acute period or in the intervals of bleedings. The second group consists of 90 cirrhotic patients to whom a prophylactic treatment was administered. From 67 patients treated during acute hemorrhage 6 (9

) died due to hemorrhage, 6 (9

) due to hepatic failure and 1 (1.5

) due to sepsis. The 90 cirrhotic patients with prophylactic treatment were divided in 3 groups. In the first group of 30, 15 were sclerosized and 15 did not get treatment. From the second group of 32, 16 got propranolol and 16 no treatment. In the third group of 28, 14 got propranolol and were sclerosized and 14 were not treated. In all three groups with treatment hemorrhage ceased in a statistically significative manner. Surviving was the same in the treated and non-treated groups. Most patients died due to an hepatic failure.

[Effect of somatostatin and ranitidine in acute hemorrhage of the upper digestive tract]. / Acción de la somatostatina y de la ranitidina en las hemorragias agudas del tracto digestivo superior.

The effects of Somatostatin and Ranitidine were studied in 46 patients with acute hemorrhages of the upper digestive tract, 23 were medicated with Somatostatin, 12 with acute gastric hemorrhages of medicamental etiology and 11 with ulcers. The doses was 500 micrograms bolus and than infusion of 250 micrograms/h. 23 patients were treated with 300 mg/day I.V. of Ranitidine, 12 had acute gastric hemorrhages also of medicamental etiology and 11 with ulcers. Somatostatin stopped the bleeding in 100% of the patients with hemorrhagic gastritis, meanwhile Ranitidine only in 76%. This is statistically significative (p less than 0.04648). Hemorrhages in patients with ulcers were stopped by Somatostatin in 73% and by Ranitidine in 64%. This is not statistically significative (p = 0.4995). No collateral effects were observed in both groups of patients.

Acción de la somatostatina y de la ranitidina en las hemorragias agudas del tracto digestivo superior. / [Effect of somatostatin and ranitidine in acute hemorrhage of the upper digestive tract]

The effects of Somatostatin and Ranitidine were studied in 46 patients with acute hemorrhages of the upper digestive tract, 23 were medicated with Somatostatin, 12 with acute gastric hemorrhages of medicamental etiology and 11 with ulcers. The doses was 500 micrograms bolus and than infusion of 250 micrograms/h. 23 patients were treated with 300 mg/day I.V. of Ranitidine, 12 had acute gastric hemorrhages also of medicamental etiology and 11 with ulcers. Somatostatin stopped the bleeding in 100

of the patients with hemorrhagic gastritis, meanwhile Ranitidine only in 76

. This is statistically significative (p less than 0.04648). Hemorrhages in patients with ulcers were stopped by Somatostatin in 73

and by Ranitidine in 64

. This is not statistically significative (p = 0.4995). No collateral effects were observed in both groups of patients.

[Importance of apolipoproteins A-1 and B in acute viral hepatitis and hepatic cirrhosis]. / Importancia de las apolipoproteínas A-1 y B en la hepatitis viral aguda y en la cirrosis hepática.

APO A-1 and B HDL cholesterol in 15 cases of acute hepatitis and 13 cases of hepatic cirrhosis were comparatively studied with different biochemical parameters. The decrease in APO A-1 and HDL revealed an alteration of the hepatic function. When the APO A-1 and HDL returned to normal a recovery of the hepatic function was observed.

Importancia de las apolipoproteínas A-1 y B en la hepatitis viral aguda y en la cirrosis hepática. / [Importance of apolipoproteins A-1 and B in acute viral hepatitis and hepatic cirrhosis]

APO A-1 and B HDL cholesterol in 15 cases of acute hepatitis and 13 cases of hepatic cirrhosis were comparatively studied with different biochemical parameters. The decrease in APO A-1 and HDL revealed an alteration of the hepatic function. When the APO A-1 and HDL returned to normal a recovery of the hepatic function was observed.

Primary sclerosing cholangitis.

Primary sclerosing cholangitis was diagnosed in 6 patients (4 men and 2 women), with ages ranging from 33 to 71 years. Four of them had ulcerative colitis, with an evolution from 8 to 21 years, the other two had Crohn's disease with 2 and 3 years of evolution. 66% of the patients had pain in the right upper quadrant; 50% complained of itching, 33% presented with fever, jaundice, weight loss and hepatomegaly and 16% had splenomegaly. 50% of these patients were diagnosed as having Sjörgren's syndrome. Alkaline phosphatase and gamma GT were elevated in 100% of the cases; SGOT and SGPT were slightly elevated in all cases; bilirubin was elevated only in 50% of the cases. Cholelithiasis was found in 2 patients with Crohn's disease and 1 patient with ulcerative colitis. All were subjected to laparoscopy. 2 of them were diagnosed as having persistent chronic hepatitis and the remaining patient had hepatic fibrosis. ERCP revealed alterations in the intrahepatic ducts and there was stenosis of the end of the common bile duct in one of them. The most frequent histological findings were periportal reactions with lymphocytes, plasma cells of macrophages, and periductal fibrosis with obliteration of the canaliculae.

[Results and prognostic factors in the treatment of chronic active hepatitis with prednisone and azathioprine]. / Resultados y factores de pronóstico en el tratamiento de las hepatitis crónicas activas con prednisona y azathioprina'

Fifty-two patients with active chronic hepatitis (A.C.H.) were treated with prednisone and azathioprine simultaneously. Seventy-three per cent of the patients were cured. Healing was obtained in 94% of the patients who did not reveal necrotic bridging prior to treatment, while only 43% of the patients who had this sign was cured. Eighty-one per cent of the cases with no A- no B active chronic hepatitis was cured, while only in 66% of patients with B A.C.H. remission was obtained. All the Non A- Non B A.C.H. patients who recovered did so in less than 3 years, while only 40% of the B + A.C.H. patients obtained complete remission in the same period of time. The remaining 60% of the B + A.C.H. group recovered in a period ranging from 3 to 12 years. In the B + A.C.H. group 75% patients of the male sex were cured, while only 33% of the females recovered. Active cirrhosis was seen in 7.6% of cases. All of them were B+. Mortality rate was 3.8 and only the B + group was affected. In conclusion it must be remarked that the presence of necrotic bridging, virus B and female sex were the factors that revealed the worst prognosis as response of A.C.H. to the combined treatment of prednisone and azathioprine.