Remote ischemic preconditioning as treatment for non-ischemic gastrointestinal disorders: beyond ischemia-reperfusion injury

Common gastrointestinal diseases such as radiation enteritis (RE), acute pancreatitis, inflammatory bowel diseases (IBD) and drug-induced hepatotoxicity share pathophysiological mechanisms at the molecular level, mostly involving the activation of many pathways of the immune response, ultimately leading to tissue injury. Increased oxidative stress, inflammatory cytokine release, inflammatory cell infiltration and activation and the up-regulation of inflammatory transcription factors participate in the pathophysiology of these complex entities. Treatment varies in each specific disease, but at least in the cases of RE and IBD immunosuppressors are effective. However, full therapeutic responses are not always achieved. The pathophysiology of ischemiareperfusion (IR) injury shares many of these mechanisms. Brief and repetitive periods of ischemia in an organ or limb have been shown to protect against subsequent major IR injury in distant organs, a phenomenon called remote ischemic preconditioning (RIP). This procedure has been shown to protect the gut, pancreas and liver by modulating many of the same inflammatory mechanisms. Since RIP is safe and tolerable, and has shown to be effective in some recent clinical trials, I suggest that RIP could be used as a physiologically relevant adjunct treatment for non-ischemic gastrointestinal inflammatory conditions

Social networks in medical practice

The number of social network users is rising meteorically, a trend that also includes health-care workers. Even though social networking can serve educational functions and is an effective means of communicating medical resources, it is associated with a variety of important challenges. Misuse of social networks by health-care workers can have dire consequences, ranging from seemingly simple issues such as affecting the doctor’s reputation to serious legal matters. Maintaining professionalism and preserving the concepts of confidentiality and privacy is essential. In this review we will analyze some of the dilemmas that have been brought about by the use of social networks in the healthcare environment, as well as existing guidelines on the matter

Mean platelet volume in the differential diagnosis of tuberculous and bacterial meningitis

Abstract Introduction: Mean platelet volume (MPV) has been shown to reflect the inflammatory burden in different inflammatory and autoimmune diseases. Our objective was to analyze the MPV in patients with tuberculous (TBM) and bacterial meningitis (BM). Methodology: The demographic and clinical data of 73 consecutive patients that presented with either BM (n = 35) or TBM (n = 38) were retrospectively analyzed, as well as that of 28 age- and sex-matched controls. Results: MPV was 8.78 ± 1.58 fL in patients with BM and 6.42 ± 1.39 fL in the TBM group (p < 0.05). In the control group, MPV was 7.4 ± 0.66 fL, significantly higher and lower when compared with TBM and BM, respectively. MPV was significantly associated with diagnosis (adjusted OR: 5.15, 95% CI: 1.090–23.7; p = 0.03). With the optimal cut-off value of 7.62 fL, MPV had 82% sensibility and 78% specificity for the differential diagnosis of TBM versus BM. Lower platelet counts, higher serum creatinine, higher white blood cell counts, and higher blood-cerebrospinal fluid glucose ratio were also predictive of BM. Conclusions: Platelet counts were lower and MPV was higher in patients with BM compared to patients with TBM. Platelet indices, available in routine bloodwork, could be useful in the early differential diagnosis of these entities. Key words: meningitis; mean platelet volume; inflammation; platelets; thrombocytopenia

1,25-dihydroxyvitamin D and PTHrP mediated malignant hypercalcemia in a seminoma

Background: Seminomas have been rarely associated with malignant hypercalcemia. The responsible mechanism of hypercalcemia in this setting has been described to be secondary to 1,25-dihydroxyvitamin D secretion. The relationship with PTHrP has not been determined or studied. The aim of this study is to describe and discuss the case and the pathophysiological mechanisms involved in a malignant hypercalcemia mediated by 1,25-dihydroxyvitamin D and PTHrP cosecretion in a patient with seminoma. Case presentation: A 35-year-old man was consulted for assessment and management of severe hypercalcemia related to an abdominal mass. Nausea, polyuria, polydipsia, lethargy and confusion led him to the emergency department. An abdominal and pelvic enhanced CT confirmed a calcified pelvic mass, along with multiple retroperitoneal lymphadenopathy. Chest x-ray revealed “cannon ball” pulmonary metastases. The histopathology result was consistent with a seminoma. Serum calcium was 14.7 mg/dl, PTH was undetectable, 25-dihydroxyvitamin D was within normal values and PTHrP and 1,25 dihydroxyvitamin were elevated (35.0 pg/ml, and 212 pg/ml, respectively). After the first cycle of chemotherapy with bleomycin, etoposide and cisplatin, normocalcemia was restored. Both PTHrP and 1,25-dihydroxyvitamin D, dropped dramatically to 9.0 pg/ml and 8.0 pg/ml, respectively. Conclusion: The association of seminoma and malignant hypercalcemia is extremely rare. We describe a case of a patient with a seminoma and malignant hypercalcemia related to paraneoplastic cosecretion of 1,25-dihydroxyvitamin D and PTHrP. After successful chemotherapy, calcium, PTHrP and 1,25-Dihydroxyvitamin D returned to normal values

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion

Hepatoprotective effect of commercial herbal extracts on carbon tetrachloride-induced liver damage in Wistar rats

Background: The antioxidant and anti-inflammatory effects of arbutin protect against a number of diseases. Objectives: The present study evaluated the protective effect of arbutin against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. Methods: Sixty-three Wistar rats were divided into nine groups. Groups I and II were the normal control groups. Group III, the hepatotoxic group, was given CCl4. Groups IV, VI, and VIII received different dosages of arbutin along with CCl4. Groups V, VII, and IX were administered different dosages of arbutin. The albumin content, total protein, and bilirubin were assayed to determine their serum and antioxidant levels; lipid peroxidation was assessed in the serum and liver tissue. Histological studies were carried out to confirm the biochemical results. Results: Treatment with CCl4 for 28 d decreased the levels of total protein and albumin and increased the level of bilirubin and lipid peroxidation. Arbutin treatment raised the level of albumin and lowered the lipid peroxidation to normal levels. Necrosis and fibrosis were observed in the liver tissue of CCl4-injected rats, and the administration of arbutin had a protective effect on the liver tissue. Conclusions: The results of this study showed that arbutin may protect the liver against CCl4-induced oxidative damage in rats. This hepatoprotective effect might be correlated with the antioxidant and free radical scavenger effects of arbutin

Temporal relationship of serum markers and tissue damage during acute intestinal ischemia/reperfusion

OBJECTIVE: It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chius classification to grade the histopathological damage. METHODS: We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ¡ standard deviation and compared the baseline and maximum values for each marker using Student’s t-test. RESULTS: The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group. CONCLUSION: For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion

Coma hipopotasémico: a propósito de un caso

Introduction: coma is the extreme degradation of consciousness. A syndrome characterized by a loss of vegetative functions, as an expression of acute and severe brain dysfunction.Presentation of the case: a 65-year-old male patient who two years ago commenced showing signs of loss of consciousness for two days In inter-crisis periods the studies did not confirm positive results. He was brought to the emergency room in a state of hyporeflexic coma. All parameters were normal except for a very discrete metabolic alkalosis and severe hypokalemia with 1,3 millimoles of potassium. General measures and complementary examinations were performed. Potassium values were replenished. As the potassium values standardized, a process of consciousness recovery was initiated. It was interpreted as a hypokalemic coma.Conclusions: hypopotassemia is a common imbalance, with repercussions in the different systems; this imbalance can result in alterations of the cardiovascular dynamics, progressive muscle weakness and coma. Therefore, in case of symptoms similar to hypokalemia, it is required to work on its diagnosis and treatment.Introducción: El coma es la máxima degradación del estado de conciencia. Síndrome caracterizado por una pérdida de las funciones de la vida de relación y conservación de las de la vida vegetativa, como expresión de una disfunción cerebral aguda y grave.Presentación del caso: paciente masculino de 65 años de edad que hace dos años comenzó con cuadros de pérdida de conciencia por espacio de dos días. En períodos intercrisis los estudios no arrojaron resultados positivos. Es traído a servicio de urgencia en estado de coma hiporrefléctico. Se tomaron medidas generales y se realizaron complementarios. Todo en parámetros de normalidad excepto por una muy discreta alcalosis metabólica y una hipocaliemia severa con 1,3 mili moles de potasio. Se reponen valores de potasio. En la medida que los valores de potasio se recuperaban se iniciaba un proceso de recuperación de la conciencia. Se interpreta como un coma hipopotasémico.Conclusiones: la hipopotasemia es un desbalance común, con repercusiones en los diferentes sistemas, que puede causar desde alteraciones de la dinámica cardiovascular, debilidad muscular progresiva y coma.  De ahí que ante sintomatologías similares a una hipopotasemia se deba trabajar en su diagnóstico y tratamiento.

Arachidonic Acid Derivatives and Their Role in Peripheral Nerve Degeneration and Regeneration

After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes. The enzymes responsible for their production, cyclooxygenases and lipooxygenases, also participate in nerve degeneration and regeneration. The interactions between signals for nerve regeneration and neuroinflammation go all the way down to the molecular level. In this paper, we discuss the role that AA derivatives might play during WD and nerve regeneration, and the therapeutic possibilities that arise

Clinical Features and Outcome of Mucormycosis

Mucormycosis (MCM) is a life-threatening infection that carries high mortality rates despite recent advances in its diagnosis and treatment. The objective was to report 14 cases of mucormycosis infection and review the relevant literature. We retrospectively analyzed the demographic and clinical data of 14 consecutive patients that presented with MCM in a tertiary-care teaching hospital in northern Mexico. The mean age of the patients was 39.9 (range 5–65). Nine of the patients were male. Ten patients had diabetes mellitus as the underlying disease, and 6 patients had a hematological malignancy (acute leukemia). Of the diabetic patients, 3 had chronic renal failure and 4 presented with diabetic ketoacidosis. All patients had rhinocerebral involvement. In-hospital mortality was 50%. All patients received medical therapy with polyene antifungals and 11 patients underwent surgical therapy. Survivors were significantly younger and less likely to have diabetes than nonsurvivors, and had higher levels of serum albumin on admission. The clinical outcome of patients with MCM is poor. Uncontrolled diabetes and age are negative prognostic factors