Diagnostic Role of Platelet Lymphocyte Ratio(PLR) in Pancreatic Head Masses

Masses in and around pancreas constitute an important clinical entity in gastrointestinal surgical practice. Most common being adenocarcinoma of head of pancreas followed by inflammatory masses due to chronic pancreatitis. Accurate diagnosis is of central importance as therapeutic strategies range from observation to complete surgical removal including total pancreatectomy.Several tumor markers are available which could help in prognostication and diagnosis of carcinoma pancreas. Carbohydrate antigen 19-9(CA 19-9) is traditionally accepted best marker available. The role of new tumor marker platelet lymphocyte ratio (PLR) has been defined recently in prognostication of carcinoma pancreas. Role of PLR in diagnosing and its efficacy after combining it with CA 19-9 is not known. The aim of study was to assess the demographics of histologically proven neoplastic and inflammatory pancreatic head masses in our department. To assess the role of CA19-9 and platelet lymphocyte ratio(PLR) in determining nature of pancreatic head mass. Data consisted of histologically proven 45 patients .23 having head mass due to chronic pancreatitis and 22 because of neoplastic lesions. Demographics in terms of age, sex, previous pain episodes, presence of jaundice, history of alcohol intake were compared in both groups. Also tumor markers CA 19-9 and PLR individually and in combination were compared in both groups. Cancer pancreas significantly (p < 0.001) occurred in older age group, was significantly associated with jaundice (p = 0.005) and weight loss (p < 0.001). Accuracy in diagnosis of cancer pancreas was similar with CA 19-9 and PLR (68.89 %), where as combining CA 19-9 with PLR showed increased sensitivity(81.82 %) and accuracy(71.11 %) in diagnosing cancer pancreas. Other combinations showed no advantage. PLR is at least as good as CA 19-9 as diagnostic marker to differentiate between malignant and inflammatory head mass of pancreas.     

Hematological response of pancytopenia to glucocorticoids in patients with Sheehan’s syndrome

Sheehan??s syndrome presents with panhypopituitarism after childbirth, usually preceded by post partum hemorrhage. Hematological abnormalities like pancytopenia with hypocellular marrow in these patients are reported rarely. Though multiple hormone deficiencies may contribute to Pancytopenia in Sheehan??s syndrome, complete recovery is observed after achieving eucortisolemic and euthyroid state. The predominant role of thyroxine or glucocorticoids in reversing pancytopenia in these patients has not been studied. We present the clinical, hormonal, hematological course and response to glucocorticoids in a patient of Sheehan??s syndrome presenting with pancytopenia. Complete recovery of pancytopenia was observed after achieving eucortisolemic state thus concluding that gulcocorticoid replacement is sufficient to reverse pancytopenia in these patients.     

Myocardial protection during ischemia by prior feeding with the creatine analog: cyclocreatine

The ability of 1-carboxymethyl-2-iminoimidazolidine (cyclocreatine), a synthetic creatine analog, to protect myocardium during global ischemia was assessed in isovolumic rat hearts using phosphorus-31 nuclear magnetic resonance spectroscopy. Wistar rats were fed a 1% cyclocreatine diet. After 2 weeks, cyclocreatine-fed (n = 8) and control (n = 7) rats were anesthetized, the heart was excised and retrograde perfusion was begun at 10 ml/min per g with 37 degrees C, phosphate-free buffer containing glucose and oxygen. Hemodynamic and spectroscopic data were obtained during baseline, ischemia and recovery periods (each 24 min). During ischemia, the heart of control rats developed a rigor-like increase in tonic pressure (ischemic contracture) not seen in the heart of cyclocreatine-fed rats (22 versus 1 mm Hg, p less than 0.01). This change was associated with significantly more adenosine triphosphate (ATP) at end-ischemia in the cyclocreatine group (1.6 versus 0.6 mumol/g, p less than 0.01) and delayed development of acidosis (p less than 0.001). With reperfusion, the heart of cyclocreatine-fed rats spontaneously defibrillated sooner than did the heart in control rats (178 versus 346 s, p less than 0.03). Diastolic pressure remained significantly elevated throughout recovery in control hearts compared with treated hearts (p less than 0.001). Prior feeding with cyclocreatine preserves myocardial adenosine triphosphate during ischemia, delays the development of acidosis and ischemic contracture and improves recovery of mechanical function on reperfusion.     

Sl/Sld mouse bone marrow stroma in vitro contains an active radiation- sensitive inhibitor of normal hemopoiesis

Sl/Sld mice have a defective hemopoietic microenvironment. It has been assumed, based upon previous studies, that the primary abnormality in these mice is simply lack of a necessary supportive or inductive material within the hemopoietic stroma. We used in vitro long-term bone marrow cultures to characterize further the nature of the hemopoietic microenvironmental defect in Sl/Sld mice. Sl/Sld mouse bone marrow cells consistently produced less than 10% of the total hemopoietic cells and multipotent and unipotent hemopoietic progenitor cells produced in cultures of marrow from normal, congenic +/+ mice. If fresh Sl/Sld and +/+ marrow cells were mixed prior to establishing long-term marrow cultures, there was a direct correlation between number of Sl/Sld cells added and degree of inhibition of +/+ hemopoiesis. A pre- established, confluent Sl/Sld adherent stromal layer inhibited hemopoiesis by fresh +/+ marrow cells by nearly 70%, as compared with dishes with irradiated +/+ or no stroma. This inhibitory effect was abrogated by irradiation of the Sl/Sld stroma prior to addition of the fresh +/+ marrow cells. Similarly, unirradiated, but not 9 to 200 Gy irradiated Sl/Sld stroma inhibited proliferation of the factor- dependent FDC-P1 hemopoietic progenitor cell line. Thus, the Sl/Sld hemopoietic microenvironment actively inhibits hemopoiesis in vitro, and this inhibition can be at least partially eliminated by irradiation of the Sl/Sld stroma.