1/10. Two patients with severe alcoholic hepatitis accompanied by hypercytokinemia and granulocytic hyperelastasemia, successfully treated by intravenous infusion of urinastarine (Miraclid).Severe alcoholic hepatitis (SAH) is not simply a disease of the liver, but it also causes infection and multiple organ failure, and therefore carries an extremely poor prognosis. We report the successful treatment of two patients with SAH. Case 1: The patient was a 55-year-old man. He was a heavy drinker whose alcohol intake had increased for some 3 years to 1.8 L sake a day. Slight clouding of consciousness, fever, and jaundice were evident on his admission to our hospital. Laboratory data showed leukocytosis with a predominance of polymorphonuclear leukocytes, and a decline in coagulability. He tested negative for various hepatitis virus markers. With the diagnosis of SAH made, steroid pulse therapy and bilirubin adsorption therapy were administered. The jaundice improved and the interleukin-8 (IL-8) level decreased. Continuous intravenous infusion of urinastarine (Miraclid) normalized the granulocyte elastase level. Improvement was also seen in coagulability, ascites, icterus and consciousness. Case 2: The patient was a 49-year-old man. He was a heavy drinker whose alcohol intake had increased for 1 month. fever, jaundice, ascites, and mild disturbance of consciousness were evident at the time of admission. Examination on admission diagnosed SAH. bilirubin adsorption and continuous intravenous infusion of urinastarine were initiated. As a result, circulating IL-8 level was decreased and coagulability was improved. Therapy for granulocytic hyperelastasemia and hypercytokinemia supervening on SAH is a new effective approach on improvement in the disease.- - - - - - - - - - ranking = 1keywords = leukocytes (Clic here for more details about this article) |
2/10. Cases from the Osler Medical Service at Johns Hopkins University.A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen.On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. urinalysis revealed an elevated specific gravity and numerous muddy granular casts. hepatitis a, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm.What is the diagnosis?- - - - - - - - - - ranking = 6.1544286177314keywords = white blood, white (Clic here for more details about this article) |
3/10. Severe alcoholic hepatitis successfully treated by leukocytapheresis: a case report.BACKGROUND: The prognosis of severe alcoholic hepatitis is poor, and there is no established method for a cure. methods: A 34-year-old man was admitted to Kurume University Hospital because of severe liver dysfunction due to excess alcohol intake. He was treated with prednisolone and two sessions of granulocyte and monocyte adsorption apheresis (GCAP) using an Adacolumn, which removes leukocytes--especially granulocytes and monocytes--from the peripheral blood. We evaluated the changes in the serum levels of interleukin-6, interleukin-8, tumor necrosis factor-alpha, and soluble intercellular adhesion molecule-1, as well as the conventional liver tests and peripheral white blood cell count. RESULTS: Prednisolone was effective in the short term but resulted in an increase in c-reactive protein (CRP), peripheral leukocytes, and serum total bilirubin. GCAP performed on the 34th and 41st hospital days produced decreases in the white blood cell count, total bilirubin, and intercellular adhesion molecule-1. The patient survived, despite the expected poor prognosis on admission. CONCLUSIONS: GCAP is recommended as a potential therapeutic option for severe alcoholic hepatitis.- - - - - - - - - - ranking = 39.25267710646keywords = white blood cell, white blood, blood cell, leukocytes, white (Clic here for more details about this article) |
4/10. Acute esophageal necrosis associated with alcoholic hepatitis: is it black or is it white?Acute esophageal necrosis is an uncommon condition diagnosed during endoscopy from the black appearance of the esophagus. We report three cases of acute esophageal necrosis, associated with severe alcoholic hepatitis. The pathogenesis was multifactorial in our patients, with gastroesophageal reflux combined with hypoperfusion probably being the key factor for the esophageal lesions. The patients presented a continuum of endoscopic appearances, ranging from the characteristic black esophageal mucosa with ulcerations to a thick white exudate that peeled away (pseudomembranes). However, esophageal biopsy specimens from all three patients had the same histological pattern of severe inflammation and necrosis. Thus, the possibility of acute esophageal necrosis should also be considered in patients with extensive necrosis covered by a white exudate, but without the characteristic pattern of a "black esophagus"; and the diagnosis should subsequently be confirmed by mucosal biopsies. Our report showed that ethanol-induced acute esophageal necrosis can appear in patients with a high alcohol intake, especially in immunosupressed patients with alcoholic hepatitis.- - - - - - - - - - ranking = 1.0320260918822keywords = white (Clic here for more details about this article) |
5/10. Alcoholic hepatitis with leukemoid reaction after surgery.Alcoholic hepatitis (AH) is a clinicopathologic syndrome resulting from an excessive intake of alcohol. Leukemoid reactions (LRs) are characterized by a strikingly elevated granulocyte count over 40,000-50,000 cells/mm(3). Although a leukocytosis of 15,000-18,000 cells/mm(3) is frequently seen in AH, LRs are rare in this context. AH-associated LRs are a sign of poor prognosis and have a high mortality. A 64-year-old male with a history of heavy alcohol intake underwent a right hemicolectomy for cecal carcinoma. Preoperative laboratory data were normal with the exception of an albumin of 2.1 g/dL. liver biopsies that were taken because of a nodular appearance revealed micronodular cirrhosis, steatohepatitis, and mallory bodies. Postoperatively, the patient developed a leukocytosis that progressively increased to 72.6 cells/mm(3). He also developed signs of impaired hepatic and renal function. Extensive workup failed to reveal a source of infection. A trial of intravenous antibiotics had no impact on the leukocytosis. methylprednisolone at a dose of 40 mg IV daily was started on postoperative day 9. The patient experienced a progressive decline in white blood count (WBC), which reached 25.2/mm(3) on postoperative day 14. However, he died on postoperative day 16. We conclude that the patient had AH-associated LR in the postoperative period, but died despite successful treatment of the LR with steroids.- - - - - - - - - - ranking = 6.1544286177314keywords = white blood, white (Clic here for more details about this article) |
6/10. Alcoholic hepatitis with hyperleukocytosis.We report a fatal case of alcoholic hepatitis with hyperleukocytosis mainly consisting of mature granulocytes in a 43-year-old woman. White blood cell count was increased in parallel with clinical deterioration to 54,800/mm3 with no immature neutrophils on a differential count. The bone marrow aspirate revealed normal maturation and no evidence of hematological malignancy. It has been postulated that severe leukocytosis accompanied by alcoholic hepatitis may be provoked by release of high levels of colony stimulating factor from damaged hepatic cells. However, the present patient showed a normal level of serum granulocyte colony stimulating factor, and could not prove the above assumption.- - - - - - - - - - ranking = 1.1660018190492keywords = blood cell (Clic here for more details about this article) |
7/10. Symptomatic zinc deficiency in experimental zinc deprivation.An evaluation of indices of poor zinc status was undertaken in five male subjects in whom dietary zinc intake was reduced from 85 mumol d-1 in an initial phase of the study to 14 mumol d-1. One of the subjects developed features consistent with zinc deficiency after receiving the low zinc diet for 12 days. These features included retroauricular acneform macullo-papular lesions on the face, neck, and shoulders and reductions in plasma zinc, red blood cell zinc, neutrophil zinc and plasma alkaline phosphatase activity. Alcohol induced hepatitis, which was suspected in this subject, may have caused a predisposition to altered zinc metabolism and possible zinc deficiency which was exacerbated by subsequent zinc deprivation. The report supports the value of neutrophil zinc concentration as an indicator of poor zinc status.- - - - - - - - - - ranking = 1.1660018190492keywords = blood cell (Clic here for more details about this article) |
8/10. High mortality among patients with the leukemoid reaction and alcoholic hepatitis.We describe a patient with severe alcoholic hepatitis, markedly elevated white blood cell count, and high fever. After review of the English literature, we discovered reports of other cases similar to our case. The striking feature in all of these cases was a high short-term mortality rate, despite predictions of a favorable outcome. We therefore believe these patients represent a subgroup of patients with alcoholic hepatitis and that the leukemoid reaction is a poor prognostic sign in this disease.- - - - - - - - - - ranking = 18.62633855323keywords = white blood cell, white blood, blood cell, white (Clic here for more details about this article) |
9/10. Acute pancreatitis in a patient treated for alcoholic hepatitis. The hypothesis of supranormal ecbolic stimulation of the pancreon.A 33-yr-old white woman treated for alcoholic hepatitis developed acute pancreatitis during her hospital stay. At autopsy, two major pathological processes were found: alcoholic cirrhosis and chronic pancreatitis. In both, there was evidence of an acute episode, i.e., acute alcoholic hepatitis and acute hemorrhagic pancreatitis superimposed on the chronic alcoholic lesions. The sequence of events would indicate that the acute pancreatic pathology was precipitated by supranormal ecbolic stimulation of the acinar segment of the "pancreon" units, triggered as a result of a high protein and fat diet.- - - - - - - - - - ranking = 0.17200434864703keywords = white (Clic here for more details about this article) |
10/10. role of serum interleukin-8 and intercellular adhesion molecule-1 in the severity of alcoholic hepatitis.Among patients with alcoholic hepatitis, three groups were distinguished by histological findings and clinico-pathological features. The aim of this study was to clarify the role of soluble intercellular adhesion molecule-1 (sICAM-1) and interleukin-8 (IL-8) in the development of severe alcoholic hepatitis. The levels of sICAM-1 and IL-8 were well correlated with the severity of liver injuries. The concentrations of serum IL-8 were significantly correlated with the number of polymorphonuclear leukocytes infiltrating the liver. Serial determination of these two markers revealed that IL-8 may be complementary in assessing the severity and prognosis of alcoholic hepatitis.- - - - - - - - - - ranking = 1keywords = leukocytes (Clic here for more details about this article) |
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