Edwin H. Eigenbrodt

A randomized, double-blind, placebo-controlled trial of ursodeoxycholic acid in primary biliary cirrhosis

One hundred fifty-one patients with primary biliary cirrhosis (PBC) grouped into four strata based on entry serum bilirubin ( or +2 (strata 3 and 4). Histology was favorably affected by ursodiol in patients in strata 1 and 2 but not in strata 3 and 4. Ursodiol enrichment in fasting bile obtained at the conclusion of the trail was approximately 40% and comparable in all strata. Thus, differences in ursodiol enrichment of the bile acid pool do not explain better responses of laboratory tests and histology found in patients with less advanced PBC. Patients treated will ursodiol tended to develop a treatment failure less frequently that those who received placebo, particularly in strata 1 and 2 (ursodiol 42%, placebo 60%, P = .078). Development of severe symptoms (fatigue/pruritus) and doubling of serum bilirubin were reduced significantly in ursodiol-treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Etiology of Liver Disease in Renal-Transplant Patients

The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agents role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.

Prognostic Significance of Subacute Hepatic Necrosis in Acute Hepatitis

A retrospective analysis has been made of 57 patients with subacute hepatic necrosis demonstrated on a liver biopsy obtained during the course of an episode of acute hepatitis. Fourteen patients have been lost to follow-up. One patient died acutely with massive hepatic necrosis, while 8 have developed chronic active liver disease. Two of nine biopsies subsequently performed on patients who had shown complete clinical and biochemical resolution revealed an inactive postnecrotic cirrhosis. The incidence of these complications developing in patients with subacute hepatic necrosis was approximately 30%. These findings add qualitative support to the position that liver biopsy findings bear important prognostic value in patients with acute hepatitis.

Spectrum of Liver Disease in Renal Transplant Recipients

An evaluation of the hepatic dysfunction which occurred in the post-transplant period in 31 of 82 renal transplant recipients managed at Parkland Memorial Hospital has revealed three different patterns of liver disease. Two patients died in acute liver failure during an acute fulminant illness. Eight other patients suffered an acute, anicteric, and completely reversible hepatic disorder. Twenty-one patients have been afflicted with a chronic form of liver disease which, in a least 5, has progressed to an active cirrhosis. Infection with cytomegalovirus and other viruses is probably responsible for most of the liver disease we have observed in these patients, while hepatotoxicity related to therapy with azathioprine and other drugs has played only a minor role.

A Prospective Trial of Steroid Therapy in Severe Viral Hepatitis The Prognostic Significance of Bridging Necrosis

A prospective, double-blinded, randomized trial of corticosteroid therapy in patients with severe acute viral hepatitis has been conducted. At the same time, we have examined the prognostic significance of the presence of bridging necrosis in liver biopsies obtained from such patients as well as the predictive value of certain serologic markers. Forty-two of the 77 patients admitted to the trial were shown to have bridging necrosis on their initial biopsies. Two patients progressed to death with massive hepatic necrosis, while 5 patients developed chronic liver disease. A complicated course could not be predicted by the initial biopsy findings nor by any of the serologic markers assessed. We could not identify any clinical or epidemiologic features with prognostic impact. No advantage was demonstrated to be associated with the use of corticosteroids early in the course of severe viral hepatitis.

Intestinal graft-versus-host disease is initiated by donor T cells distinct from classic cytotoxic T lymphocytes.

In these studies, the role of T helper and T cytotoxic cells in generating intestinal graft-vs.-host disease (GVHD) was examined. Treatment of C57BL/6J (B6) splenocytes with L-leucyl-L-leucine methyl ester (Leu-Leu-OMe) selectively removes natural killer cells, cytotoxic T lymphocyte (CTL) precursors, and the capacity to cause lethal GVHD in irradiated B6xDBA/2 F1 (B6D2F1) mice while preserving T helper cell function. Neither control nor Leu-Leu-OMe-treated DBA/2 donor spleen and bone marrow cells were found to induce lethal GVHD in B6D2F1 recipients. However, extensive colonic GVHD developed in B6D2F1 recipients of DBA/2 bone marrow and spleen cells. Enteropathic GVHD in DBA/2----B6D2F1 mice was reduced in severity after anti-L3T4 + C treatment of donor cells, and was eliminated by anti-Thy1.2 + C or the combination of anti-L3T4 and anti-Lyt2 + C treatment of the donor cell inoculum. However, neither anti-Lyt2 + C, Leu-Leu-OMe, nor anti-Lyt2 + C and Leu-Leu-OMe treatment of donor cells significantly decreased severity of gut GVHD. Leu-Leu-OMe treatment of DBA/2 or B6 SpC was comparably effective in preventing in vitro or in vivo generation of B6D2F1-specific CTL. These findings, therefore, demonstrate that histologically severe enteropathic GVHD does not require participation of CTL and is not always associated with high mortality rates.

Cirrhosis After Repeated Trichloroethylene and 1,1,1-Trichloroethane Exposure

Acute hepatotoxicity has been described in patients exposed to either trichloroethylene or 1,1,1-trichloroethane, but there have been no previous reports of chronic liver disease induced by these agents. We describe a patient who developed cirrhosis and portal hypertension after repeated bouts of acute hepatotoxicity caused by trichloroethylene and a final episode of 1,1,1-trichloroethane-induced liver injury.

Cat scratch disease

Abstract An unusual case of cat scratch disease with large hepatic defects is presented. We describe a previously healthy 16-yr-old black man presenting with a neck mass, hepatosplenomegaly, and systemic symptoms. Pathology of the neck mass revealed a lymph node with chronic inflammation and focal necrosis. An abnormal computed tomography scan showed large hepatic defects which were confirmed at peritoneoscopy; biopsy specimens are described. Routine and special stains for bacteria and fungi were all negative. Serologic studies were unremarkable but a cat scratch skin test was positive. Follow-up examinations revealed resolution of all findings. Cat scratch disease should be considered in the differential diagnosis of diseases causing lymphadenopathy, systemic symptoms, and hepatic fand splenic) defects.

Cranial nerve deficit: A clue to the diagnosis of ethylene glycol poisoning

CASEREPORTS Patient 1 A 57-year-old white man was transferred to the Dallas Veterans Administration with a four-day history of mild abdominal pain and anuria. Past medical history was significant for a femoral-femoral bypass. On examination the patient was alert, oriented, lucid, and appeared well. Vital signs were normal. Mild diffuse abdominal tenderness without rebound was noted. The following values were obtained during laboratory evaluation (mEq/L): sodium 138, potassium 4.2, chloride 100, and bicarbonate 22; the blood urea nitrogen level was 67 mg/dL, and the creatinine level was 12.5 mg/dL. Urinalysis revealed 300 mg/dL protein by dipstick, greater than 50 red blood cells per high-power field, occasional granular casts, and no crystals (X3). The hematocrit was 34.7%, and the white blood cell count was 9,800/mm3. Renal sonographic results were normal. Given persistent anuria, the history of peripheral vascular disease, and abdominal pain, a diagnosis of renal artery occlusion was entertained. Results of a renal arteriogram were completely normal. Hemodialysis was begun 10 days after the patient’s initial admission. On Day 11 of hospitalization, the patient was noted to be dysarthric and to have evidence of cranial nerve V, VII, and VIII abnormalities. Physical examination demonstrated drooping of the right side of the face and an inability to completely close the right eye. Decreased sensation to pinprick was present on the right side of the face, and the patient was deaf bilaterally. Results of computerized tomographic examination of the brain were normal. Examination of the cerebrospinal fluid showed 51 to 70 white blood cells/mm3 (90% polymorphonuclear leukocytes), protein 198 mg/dL, and glucose 52 mg/dL. VDRL, cryptococcal antigen, and all microbial culture specimens were negative. On the twelfth, day of hospitalization, the patient developed bilateral facial diplegia and sensory loss. The left cornea1 reflex was absent and a gag reflex could no longer be elicited. Nerve conduction studies confirmed the presence of bilateral peripheral VII nerve palsies. On Day 13, the patient’s sensorium decreased; by Day 14, frank coma was present, and the patient required

Liver histopathologic findings in women with sickle cell disease given prophylactic transfusion during pregnancy

Forty women with a major sickle hemoglobinopathy (hemoglobin SS, SC, or S-beta-thalassemia) were given red blood cell transfusions prophylactically during pregnancy. A mean of 13.6 units of erythrocytes per woman was given and none received more than 28 units. Direct-vision needle biopsy of the liver was performed in conjunction with cesarean section or puerperal sterilization. Although iron deposition in hepatocytes and Kupffer cells was identified commonly, neither cirrhosis nor widespread hepatocellular necrosis was found. We conclude that the risk of irreversible hepatic damage is negligible in women with sickle hemoglobinopathies who are given erythrocytes prophylactically during one pregnancy.