[Hypertriglyceridemic pancreatitis during pregnancy. A report of a case]. / Pancreatitis hipertrigliceridémica durante el embarazo. Comunicación de un caso.

Acute pancreatitis during pregnancy is an uncommon complication. The usual cause is biliary tract disease. Cholesterol and triglyceride plasma levels physiologically increase during pregnancy. Pregravidic hypertriglyceridemia (as much primary as secondary) may be exacerbated and occasionally act as the trigger. Early diagnosis and treatment are the keys because related morbidity and mortality are high. We report a case of diabetic ketoacidosis and hypertriglyceridemia-induced gestational pancreatitis (tryglicerid level of 12,100 mg/dL) treated successfully with conservative management. The clinical, biochemical and therapeutic aspects comment in addition of this pathology, as well as its prevention

[Leptin and its influence on the main gynecoobstetric diseases]. / Leptina y su influencia en los principales padecimientos ginecoobstétricos.

Leptin is a protein hormone synthesized and secreted by adipose tissue and also probably in other organs and systems in human body. It has multiple functions such as to regulate feed intake and energy balance, gonadal regulation, action in the hypothalamo-pituitary-gonadal axis, regulates the metabolism of the fetal-placental unit in the pregnancy, fertility and reproductive systems, actions in the endometrium, mammary gland with corresponding influences on important physiologic processes such as menstruation, pregnancy and lactation. In the gynecologic surgery the serum leptin concentration is also modified. The knowledge of serum leptin concentration in the oncological diseases is going-up. Leptin is modified in the choriocarcinoma, Meigs' syndrome and other tumors. A better understanding of regulatory mechanisms will have direct clinical significance, as leptin has been proposed to impact on those causes of human perinatal morbidity and mortality that are associated with abnormalities of fetal maturity and development, general concept growth, trophoblast endocrinology, and placental sufficiency. Further investigations in this area will be necessary to improve new knowledge and a better understanding of the actions about this hormone.

[Response of gastrin after an oral calcium load in healthy women and in postmenopausal patients without hormone replacement therapy]. / Respuesta de la gastrina ante una carga bucal de calcio en mujeres normales y pacientes climatéricas sin terapia hormonal de reemplazo.

BACKGROUND: Gastrin has a wide variety of functions on the digestive system including the regulation of gastric acid secretion, being a growth factor for the non antral gastric mucosa and the stimulation of mucosal proliferation in the large and small intestines. Animals studies showed that various diseases of the digestive system have better clinical evolution in the presence of estrogens as is the case of peptic ulcers, now little is known in humans about this phenomenon. OBJECTIVE: To evaluate the response of gastrin after an oral calcium load in normal and postmenopausal women without hormone replacement therapy. PATIENTS AND METHODS: We studied 10 healthy women with mean age 25.3 +/- 1.79 yr (range: 23-28 yr) and 7 postmenopausal women without previous treatment and a mean age 56.5 +/- 6.4 yr (range: 50-70 yr). A permeable vein with physiologic solution was obtained in order to maintain a permeable vein in the antecubital fossa to obtain blood samples for the determination of gastrin. Before an oral administration of 1 g of calcium baseline samples were taken at time 0 and thereafter on 30, 60, 90, 120, 150, and 180 minutes. Gastrin levels were determined by RIA using CIS Bio-International commercial kits. RESULTS: Basal gastrin levels were x: 72.54 +/- 15.9 pg/mLK in normal women and x: 61.1 +/- 39.62 in postmenopausal women. Basal gonadotrophins were x: 62.1 +/- 26 and x: 32.9 +/- 7.3 for FSH and LH respectively and estradiol level of x: 13.9 +/- 4.2 pg/mL. Normal volunteers had a peak secretion of x: 173.4 +/- 15 pg/mL at 90 minutes and in postmenopausal women a peak of x: 66.2 +/- 50 at 60 minutes. Comparing the magnitude of the response between the healthy volunteers and the postmenopausal women at 90 and 120 minutes the statistical significance was a (p < 0.005) and (p < 0.001), respectively. CONCLUSIONS: These results demonstrate the lack of response of gastrin levels to the calcium stimulus in postmenopausal women probably due to the lack of hormone replacement therapy. Further studies are needed to best understand the role of sexual hormones on the synthesis and secretion of gastrin in the digestive system especially the role of the estrogens.

[Analysis of Bcr-abl type transcript and its relationship with platelet count in Mexican patients with chronic myeloid leukemia]. / Análisis del tipo de transcrito bcr-abl y su relación con la cuenta plaquetaria en pacientes mexicanos con leucemia mieloide crónica.

PROBLEM: It has been suggested that type of chimeric mRNA is associated with differences in the clinical and hematologic characteristics of chronic myeloid leukemia (CML). However, prognostic value of type of chimeric mRNA bcr-xabl (b3a2 or b2a2) is still controversial. METHODS: We analyzed 97 cases of Philadelphia-positive CML to determine mRNA type by reverse-polymerase chain reaction (RT-PCR) and its relationship with clinical features. RESULTS: We detected b3a2 bcr-abl transcripts in 27 (28%) cases, b2a2 in 57 (59%) cases, and 13 (13%) with both mRNA transcripts b3a2/b2a2. These frequencies were the total reverse of other reports. Age, sex, hemoglobin, and white-cell counts showed no significant difference for those with either b3a2 or b2a2 bcr-abl transcripts. However, platelet counts of b3a2 patients were significantly higher than those of b2a2 patients (743.3 vs 477.3 x 109/L; p = 0.01). In addition, in the subgroup of patients whose white-cell count at diagnosis was < 100 x 10(9)/L, those with b3a2 transcript had a significantly higher platelet count (679.1 vs. 352.2 x 10(9)/L; p = 0.001). CONCLUSIONS: We observed reversed frequency of bcr-abl transcripts in this population, but agreement with other Latin-American reports. In addition, our data suggested that there is different CML biological behavior in our population and that there is a subpopulation of CML patients in whom b3a2 is associated witH higher thrombopoietic activity.

Response of patients with advanced prostatic cancer to administration of somatostatin analog RC-160 (vapreotide) at the time of relapse.

BACKGROUND: The aim of this study was to evaluate the effects of administration of the somatostatin analog RC-160 (vapreotide) at the time of relapse in patients with androgen independent prostate cancer. METHODS: Our study included 13 patients with biopsy-proven prostate cancer, stage D3. Eight patients had been treated with a depot formulation of the agonist D-Trp-6-LH-RH, with a median remission time of 68 (range 48-102 months). Five patients were initially treated by surgical orchiectomy, but relapsed after a median time of 33 months (range 17-91 months). A new remission period with a median duration of 10 months (range 2-29 months) was induced with Ketoconazole in the orchiectomy group. At the relapse time, all the patients received 1 mg of vapreotide t.i.d., by subcutaneous route, in addition to D-Trp-6-LH-RH, or Ketoconazole in the orchiectomy group. RESULTS: Eight of 13 patients demonstrated clinical improvement after 3 months of therapy with vapreotide, six showing a decrease in serum prostate specific antigen (PSA) from 234.5 +/- 308.5 to 68.2 +/- 60.5 ng/ml (mean decline 71 +/- 8%; P < 0.05). Two additional patients presented a fall in serum prostatic acid phosphatase (PAP). Responding patients showed a decrease in the bone pain score from 2.62 +/- 0.48 to 0.37 +/- 0.69 and an increase in the Karnofsky performance status from 72.3 +/- 4.21 to 83.6 +/- 23.2 (P < 0.05). In accord with the ECOG criteria, two patients had a complete response; four had partial response, and two had a stable response. Four patients did not respond and one was not evaluable. Two patients died in remission, one at 16 months due to myocardial infarction and the other at 24 months due to pneumonia. Three patients relapsed at 5, 17, and 19 months respectively. Three patients who have been followed-up for more than 3 years continued in remission (79, 45, and 45 months) respectively. Vapreotide was well tolerated, only three patients having transitory mild diarrhea. CONCLUSIONS: Our results indicate that therapy with the somatostatin analog vapreotide at the time of relapse can induce objective clinical responses in some patients with prostate cancer who are refractory to androgen ablation induced by LH-RH analogs or orchiectomy.

Pentoxifylline in the treatment of refractory nephrotic syndrome secondary to lupus nephritis.

OBJECTIVE: To evaluate the efficacy of pentoxifylline in the treatment of refractory nephrotic syndrome secondary to lupus nephritis. METHODS: We studied 11 patients who met the following inclusion criteria: (1) systemic lupus erythematosus (SLE) according to the American College of Rheumatology criteria; (2) lupus nephritis class III, IV, or V according to the World Health Organization; (3) proteinuria in the nephrotic range (> or = 3 g/24 h) for at least 6 months despite treatment. All patients received pentoxifylline 800-1600 mg/day. Clinical and laboratory data, including creatinine, urine test, creatinine clearance, and 24-h urinary protein, were collected monthly for 6 months. No changes in treatment were allowed, except for alterations in the dose of prednisone. RESULTS: All patients had received corticosteroids and immunosuppressants for at least 6 months. All patients showed a decrease in proteinuria concentrations after use of pentoxifylline from a median of 5.5 to 2.0 (p = 0.003). No patient discontinued the drug due to side effects. One patient had nausea and one had anxiety that disappeared after decreasing the dosage. CONCLUSION: Pentoxifylline seems to be effective in the treatment of refractory nephrotic syndrome secondary to lupus nephritis.

Tumor ovárico de células esteroideas productor de andrógenos: informe de caso / Ovarian steroid cell tummors producing androgens

Los tumores del ovario con repercusión endócrina constituyen 5 por ciento de las neoplasias de este órgano, ocupan el primer término las productoras de estrógenos, las de andrógenos en segundo y son excepcionales las de progesterona, corticosteroides y renina. En la nomenclatura de estos tumores ha existido una serie de sinónimos empleados que indican la confusión acerca de su histogénesis y la dificultad para su manejo en la literatura. Informe del caso. Femenina de 23 años de edad que presentó opsomenorreas de varios años de evolución, amenorrea secundaria, voz grave e hirsutismo rápidamente progresivo. Peso: 98,500 kg, talla: 1.74m. Índice de masa corporal (IMC): 32.61 kg/m2 de supeficie corporal. Vello en cara (barba y bigote), distribución androide en abdomen, antebrazos, muslos y piernas (Ferriman 20), acné e involución mamaria bilateral. Todos los paraclínicos efectuados fueron normales. La cuantificación de gonadotrofina coriónica en orina de 24 horas fue negativa. Imagenología. Ultrasonido de cavidad pélvica y la tomografía axial computada de abdomen demostraron tumoración ovárica derecha. El estudio citogenético fue 46XX. Los estudios endocrinológicos prequirúrgicos fueron: basales hormonales de testosterona libre y total de 14.30 pg/mL y 3.55 ng/mL respectivamente, insulina de 43.3 µU/mL y péptido C de 5.7 ng/mL. La curva de tolerancia oral a la glucosa (CTGO) demostró intolerancia a carbohidratos. Durante el transoperatorio los niveles hormonales de la vena ovárica derecha fueron: testosterona total de 2.70 ng/mL y la libre de 12.70 pg/mL, normalizándose a las 12 horas del postoperatorio. Otras hormonas esteroideas determinadas fueron normales seis meses después del acto quirúrgico la paciente presentaba un puntaje de Ferriman de 10, eumenorreica y con peso: 98,100 kg, CTGO y niveles basles hormonales normales. La ultraestructura mostró datos característicos de tumor productor de esteroides sin cristaloides de Reinke.

Influencia de la administración transdérmica de 17-b estradiol sobre la liberación de hormona de crecimiento mediante la hormona liberadora de la hormona de crecimiento (gh-rh-1-29) en mujeres climatéricas pre y postratamiento / Influence of transdermal 17-ß estradiol administration on growth hormones secretion in menopausal women before and after treatment under the stimulus of growth hormonereasing hormone (GH-RH)

Antecedentes. En la actualidad se ha generado gran interés en el papel que juega la disminución de la hormona liberadora de la hormona de crecimiento y la hormona de crecimiento y su repercusión en varias partes del organismo como factores responsables de los cambios observados en la mujer climatérica, en especial en el sistema nervioso central, cardiovascular, genitourinario, digestivo y osteomuscular. Objetivo. Evaluar la influencia de la administración transdérmica de 17-b estradiol sobre la liberación de la hormona de crecimiento en mujeres climatéricas pre y postratamiento mediante la administración de la hormona liberadora de la hormona de crecimiento. Material y método. Se incluyeron cinco pacientes con edad promedio de 51 ñ 4.1 años, con cuadro clínico y bioquímico de climaterio. Tiempo de evolución: 5.4 ñ 4.61 (rango: 1-13 años). Se monitorizó la pulsatilidad de la hormona de crecimiento durante los primeros 120 minutos y tres horas más después de la administración de la hormona liberadora de la hormona de crecimiento (GH-RH-1-29-NH2), I.V. en bolo (50 µg). La obtención del suero para determinar la hormona de crecimiento se realizó cada 15 minutos antes y después del estímulo. Inmediatamente después se inició la sustitución hormonal con el 17-b estradiol transdérmico (parches de 50 µg) dos veces por semana. La evaluación clínica y el estudio mediante la estimulación con GH-RH-1-29 se realizaron al tiempo 0 (basal), 1, 3 y 6 meses de iniciado el tratamiento con las mismas condiciones descritas previamente. Resultados. La pulsatilidad de la hormona de crecimiento antes de iniciada la sustitución estrogénica en los cinco pacientes fue de: X:0.48 ñ 0.22; 0.38 ñ 0.17; 0.45 ñ 0.25 y 0.69 ñ 0.29 (Basal, 1, 3 y 6 meses, respectivamente) y de 2.74 ñ 1.21; 3.48 ñ 1.32 (p > 0.05); 4.91 ñ 1.57 (p < 0.05) y 6.04 ñ 1.69 (p < 0.05) (p en relación con la basal) postestímulo con GH-RH-1-29, Basal, 1, 3 y 6 meses, respectivamente, postestrogenoterapia transdérmica. Los niveles basales de gonadotrofinas descendieron de 54.68 ñ 27 a 33.20 ñ 11.23 y de 40.48 ñ 12 a 28.30 ñ 6.70 (FSH y LH, respectivamente, pre y postratamiento) y los valores basales de estradiol se incrementaron de 1.82 ñ 4.06 a 25.95 ñ 5.96 después de iniciada la estrogenoterapia