Subject(s)
Interferon-alpha/therapeutic use , Mesenteric Veins/pathology , Polycythemia Vera/complications , Polycythemia Vera/drug therapy , Polyethylene Glycols/therapeutic use , Thrombocythemia, Essential/complications , Thrombocythemia, Essential/drug therapy , Venous Thrombosis/etiology , Humans , Interferon-alpha/administration & dosage , Interferon-alpha/adverse effects , Polycythemia Vera/diagnosis , Polycythemia Vera/etiology , Polyethylene Glycols/administration & dosage , Polyethylene Glycols/adverse effects , Prospective Studies , Recombinant Proteins/administration & dosage , Recombinant Proteins/adverse effects , Recombinant Proteins/therapeutic use , Thrombocythemia, Essential/diagnosis , Thrombocythemia, Essential/etiology , Venous Thrombosis/diagnosis , Venous Thrombosis/therapyABSTRACT
This study was conducted to determine the ion transport mechanisms in the normal mouse cecum and compare them to an inbred mouse model of colitis. The Ussing chamber-voltage clamp technique was used to monitor the short circuit current (I(sc)). The basal I(sc) in the normal cecum was 82.6 +/- 5.8 microA/cm2. It was not affected by bumetanide, 9-anthracene carboxylate, amiloride, and phenamil or by removal of Cl- ions; but was abolished by the removal of Na+ ions. Flux measurements revealed the presence of neutral NaCl transport. In the colitic cecum, the basal current was significantly higher than the normal cecum. Basal current in the normal cecum was due primarily to Na+ absorption through a Na+ channel, while in the colitic cecum it was due to Cl- ion secretion. cAMP addition in colitic cecum did not increase Cl- secretion, further suggesting that the tissue is already secreting at a maximal rate.
Subject(s)
Cecum/metabolism , Colitis/metabolism , 8-Bromo Cyclic Adenosine Monophosphate/pharmacology , Animals , Atropine/pharmacology , Cecum/drug effects , Cecum/pathology , Cecum/physiopathology , Colitis/pathology , Colitis/physiopathology , Electric Conductivity , Female , Ion Transport , Mice , Mice, Inbred C3H , Muscarinic Antagonists/pharmacology , Reference Values , Tetrodotoxin/pharmacologyABSTRACT
Fulminant hepatic failure is a devastating illness that carries considerable mortality and affects patients with previously healthy livers. Although the etiology of FHF remains unclear in a significant number of cases, viral hepatitis and drug-induced liver injury account for the majority of identifiable causes. The clinical presentation varies widely, but is always characterized by the presence of encephalopathy. Markedly elevated transaminases are seen, but do not correlate with extent of liver injury. Prothrombin time, bilirubin, creatinine, and arterial pH are prognostic indicators of survival in FHF. FHF and its consequences must be readily recognized so that appropriate triage and treatment can be administered. All patients should be managed in an intensive care setting pending transfer to a liver transplantation center. Supportive care remains the mainstay of treatment, with liver transplantation reserved for select patients.
Subject(s)
Hepatic Encephalopathy , Diagnosis, Differential , Hepatic Encephalopathy/complications , Hepatic Encephalopathy/diagnosis , Hepatic Encephalopathy/etiology , Hepatic Encephalopathy/therapy , Humans , Multiple Organ Failure/etiologyABSTRACT
Histamine levels are elevated in inflammatory bowel disease. We investigated the mechanism by which histamine affects electrolyte transport in the mouse cecum. Using the Ussing-chamber voltage clamp technique, histamine was found to cause a transient concentration-dependent increase in short-circuit current, a measure of total ion transport across the epithelial tissue. This increase was not affected by amiloride pretreatment, but was significantly inhibited by bumetanide and completely inhibited when chloride was substituted in the bathing buffer by gluconate. A histamine-induced increase in short-circuit current was also significantly reduced by inhibitors of the cyclooxygenase pathway indicating the involvement of prostaglandin E2 in its action. Prostaglandin E2 levels were increased in histamine treated tissue and this increase was reversed by indomethacin. These data suggest that histamine causes its effect on mouse cecum largely through increasing arachidonic acid metabolism resulting in increased levels of prostaglandins which in turn increase Cl- secretion in the epithelial cells.
Subject(s)
Cecum/metabolism , Histamine/physiology , Ion Channels/metabolism , Animals , Arachidonic Acid/metabolism , Cecum/drug effects , Cholinergic Antagonists/pharmacology , Dinoprostone/metabolism , Female , Hexamethonium/pharmacology , Histamine/pharmacology , Histamine Antagonists/pharmacology , In Vitro Techniques , Ion Channels/drug effects , Ion Channels/physiology , Mice , Mice, Inbred C3H , Patch-Clamp Techniques , Receptors, Histamine/drug effects , Tetrodotoxin/pharmacologySubject(s)
Adenocarcinoma/diagnosis , Appendiceal Neoplasms/diagnosis , Urinary Bladder Neoplasms/diagnosis , Uterine Neoplasms/diagnosis , Adenocarcinoma/pathology , Aged , Aged, 80 and over , Appendiceal Neoplasms/pathology , Diagnosis, Differential , Female , Humans , Laparotomy , Neoplasm Invasiveness , Tomography, X-Ray ComputedABSTRACT
Disease of the epiploic appendage remains a diagnostic challenge. We have seen a patient whose main preoperative findings were limited to an abnormal small bowel loop with thickened folds on a small bowel series, an association not previously reported, to our knowledge. We review the pertinent medical and radiological literature.
Subject(s)
Colon/blood supply , Infarction/diagnosis , Adult , Crohn Disease/diagnosis , Diagnosis, Differential , Humans , MaleABSTRACT
An 85-yr-old female presented with diversion colitis after surgery with a resultant colostomy and excluded rectal segment. Treatment with 5-aminosalicylic acid (Rowasa) enemas resulted in both endoscopic and histological resolution. This is the first case of diversion colitis treated with 5-aminosalicylic acid enemas.