Female predominance is a common characteristic for autoimmune diseases attributed to the combined effect of hormonal influence and genetic factors. Since X chromosome has immunologically important genes, the age related X chromosome loss could contribute to the development of autoimmunity. X chromosome monosomy (XCM) has been associated with primary biliary cirrhosis (PBC) and systemic sclerosis. Herein, using fluorescence in situ hybridization (FISH) with specific centromeric probes, we report the rate of XCM in interphase nuclei in women with Reynolds syndrome (RS), an overlapping condition of PBC and systemic sclerosis (SSc). Frequency of nuclei with XCM was 12.1% (CI 95%, 8.5–17.1) in RS, 10% (7.1–13.9) in PBC, 9.2% (6.0–13.9) in SSc and 6.4% (5.1–8) in age-matched healthy controls. We found a significantly higher XCM frequency in RS PBC and SSc groups of patients when compared with controls, p < 0.01, p < 0.05 and p < 0.05 respectively. XCM was highest in the RS group but not statistically different from PBC and SSc patients. Fetal–maternal microchimerism prevalence evaluated by Q-PCR for SRY sequences varies among groups, although no statistical differences were observed. Besides the above, we found an apparently important additive effect (89.1%) of PBC and SSc on the prevalence of XCM cells in RS patients. Another interesting finding was that the prevalence of XCM cells seems not to be dependent on the time of evolution of the AID studied. Moreover, the shorter time of evolution and the higher prevalence of XCM interphase nuclei observed in RS patients sustain our hypothesis of the additive effect abovementioned.

Reported maximum weight loss after Roux-en-Y Gastric Bypass (RYGB) is close to 70% and generally occurs during the first postoperative year. Both, amount and pattern of weight loss may be different among populations. The aim of the study was to identify the pattern of weight loss during the first year after RYGB in a Mexican population.

Since mechanical retractors in endoscopic plastic surgery cause certain drawbacks, we developed a model in dogs, which, by insufflating CO2 into a subcutaneous cavity, we were able to maintain. We evaluated the magnitude of subcutaneous emphysema and absorption of CO2 by insufflating different pressures and the efficacy of external pressure on the skin with the purpose of limiting the subcutaneous emphysema. Sixteen dogs were divided in 3 groups, A, B, and C. We controlled the pulmonary function by using a volume-cycle ventilator. In all groups, we maintained a subcutaneous cavity by insufflating CO2. Groups A and C were insufflated at 15 mm Hg; group B, at 8 mm Hg. We placed circumferential Esmarch bandages on the thorax of groups B and C to delimit superiorly and inferiorly the surgical area. Arterial blood gas analyses (ABGA) were taken from the femoral artery 60 minutes after intubation, 60 minutes after Esmarch bandage was placed and at the end of the CO2 insufflation. Statistically, results were analyzed by Wilcoxon test. P < 0.05 was considered statistically significant. Group A showed extensive subcutaneous emphysema. Two dogs died. The systemic increase of the CO2 showed a median of 9.6 mm Hg (P < 0.05). In Group B, Esmarch bandages caused increase in CO2, with a median of 1.65 mm Hg (P < 0.028). None of these dogs showed subcutaneous emphysema during the insufflation after CO2 insufflation pressure augmented with a median of 3.7 mm Hg (P < 0.028). In Group C, chest restriction increased CO2 median of 6.1 mm Hg (P < 0.043), and subcutaneous emphysema shown was less extensive than group A. The CO2 increased after insufflation a median of 16 mm Hg (P < 0.043). Conclusions:Subcutaneous cavities can be maintained open with CO2 insufflation at 8 mm Hg, limiting perfectly the surgical area; as done with Esmarch bandages, it reduces CO2 absorption and makes this procedure safe.

The clinical suspicion of hereditary spherocytosis (HS) must be confirmed at the clinical laboratory. The osmotic fragility test (OFT) and the autohemolysis test (AHT) are the worldwide accepted assays to establish a definite diagnosis of HS; however, they have some disadvantages. We describe herein our experience with the cryohemolysis test (CHT) as a tool to confirm the HS diagnosis. We included four groups of subjects, namely, patients with clinical HS, patients with mechanical heart valve prosthesis, malignant hematological diseases and healthy blood donors. CHT was carried out in all the groups, while OFT and AHT only in the HS patients and healthy individuals. OFT and AHT were performed according to previously described techniques. CHT was performed using red blood cells incubated in a hypertonic solution, preheated for 10 min and then transferred to an ice bath for an additional 10 min. The resulting cryohemolysis was determined measuring the free hemoglobin in the sample. There were no differences among the groups in terms of general characteristics. All HS suspicious patients had a positive OFT and AHT. CHT was positive in all patients from the HS group but in none of the subjects from the control groups (p < 0.001). We found that CHT is a faster and easier-to-perform assay compared with OFT and AHT. Moreover, using CHT, the zone between normal and abnormal results is wider than OFT or AHT. We propose 0.7 to 11% hemolysis as reference values for CHT.

Background.The prevalence of Helicobacter pylori in patients with alcoholic and nonalcoholic cirrhosis is uncertain. The present study was aimed at determining the prevalence of H. pylori infection among cirrhotic patients and to explore its relationship to demography, etiology of cirrhosis, and liver function.Materials and Methods.Thirty‐three cirrhotic patients were included. H. pylori infection was determined by the 14C urea breath test (n = 30) and endoscopy with antral biopsy (n = 4). Etiology of cirrhosis was classified as alcoholic or nonalcoholic. The rate of H. pylori infection was related to age, gender, etiology, Child‐Pugh grading, portal hypertension, and portal‐systemic encephalopathy (PSE). None of the patients received antibiotics for at least the last 3 months.Results.Twelve alcoholic and 21 nonalcoholic cirrhotics, with a median age of 57 years and a male:female ratio of 1 : 1.4 were studied. Overall H. pylori prevalence was 45.5%. This prevalence varied from 47.1% to 43.8% in those younger and older than the median age, and from 35.7% to 52.6% in men and women, respectively. Fifty percent of alcoholic and 42.9% of nonalcoholic cirrhotics were H. pylori–positive. According to Child‐Pugh grading, 69% of grade A, 40% of grade B, and 0% of grade C were infected ( p = .03). Among patients with PSE, 25% were H. pylori–positive compared to 52% of those without PSE ( p = .24).Conclusions.The prevalence of H. pylori infection in cirrhotics is 45.5%. Prevalence was unrelated to age, gender, and etiology of cirrhosis. An inverse relation to the Child‐Pugh grading and a tendency to a lower prevalence in PSE was found.

Post-remission high dose chemotherapy has been an important advance in the treatment of adult acute leukemia (AAL). Without the use of colony-stimulating factors (CSFs) in this program, the mortality rate varies from 5 to 17%, and infectious complications arise in more than 50%. These findings limit the widespread use of such forms of therapy. The use of high-dose ara-C (HIDAC) alone or in combination with other drugs is the most common regimen studied, however neither other drug combinations nor the addition of supporting CSFs have been extensively explored. For this reason we studied the effect of high-dose cyclophosphamide-etoposide (CECY) plus recombinant human granulocyte-macrophage (rHuGM)-CSF with the intention of decreasing morbimortality and prolonging disease-free survival (DFS). Since 1992 we have included 51 complete remission patients with AAL in the CECY plus rHuGM-CSF protocol. The maximal myelosuppression occurred in a mean of 6.4 days, and the mean days required for absolute neutrophil count recovery was 13 days and for platelets 21 days (p < 0.0001). No toxic deaths occurred and only two serious infectious complications were seen, After two years of follow-up, 50% of de novo acute myelogenous leukemia patients had relapsed at 13 months, and 50% of de novo adult acute lymphocytic leukemia patients had relapsed at 15 months. In a recent update, we have not seen a significant difference when compared to historic groups. The CECY protocol does not appear to be superior in prolonging DFS compared to HIDAC as a post-remission strategy for newly diagnosed AAL. The main difference was the absence of toxic deaths and minimal serious infectious complications in the CECY protocol. Therefore, we suggest that the use of rHuGM-CSF in post-remission programs should be included in future studies.

Rats treated with puromycin aminonucleoside (PAN) developed characteristics of the nephrotic syndrome, including albuminuria, hypoalbuminemia and hyperlipidemia. To study the regulation of apolipoprotein (apo) A-1 and apo E gene expression in nephrotic rats, we analyzed the steady-state levels (SSLs) of hepatic and intestinal apo A-1 and apo E mRNA using the Northern technique, and the plasma levels of high-density lipoprotein (HDL) by biochemical methods. Male Wistar rats were treated with PAN and compared with pair-fed and untreated control rats at different stages of disease. Nephrotic rats presented with marked hypoalbuminemia and albuminuria at between 6 and 11 days after PAN treatment. During this stage of disease, plasma levels of HDL were elevated in correlation with an increase of both hepatic and intestinal apo A-1 mRNA. In liver of nephrotic rats, high levels of apo A-1 mRNA together with low levels of apo E mRNA caused an increase in the ratio of apo A-1/apo E mRNA, reaching a maximum 6 days after treatment. Apo E mRNA was barely detected in small intestine of pair-fed controls and PAN-treated rats. However, contrary to nephrotic rats, the ratio apo A-1/apo E mRNA was inverted in liver of pair-fed rats due to an increase in apo E mRNA. In conclusion, in nephrotic rats, the SSL of apo A-1 mRNA is increased in liver and small intestine and appears to regulate the plasma levels of apo A-1. These results also suggest a coordinated regulation of the apo A-1 and apo E gene expression in liver of nephrotic and pair-fed rats.