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Biomedical subjects

R S Koff

Publications and source records attributed to R S Koff.

At least 109 records · Page 6Linked to original sources
PubMed1980

Prognostic indicators in chemotherapy for head and neck carcinoma: alkaline phosphatase levels.

Serum alkaline phosphatase (AP), total bilirubin, total protein, serum albumin, and serum glutamic oxaloacetic transaminase (SGOT) were determined in 55 patients with biopsy proven carcinoma of the head and neck prior to their induction chemotherapy with cis-platinum and bleomycin. Of the 55 patients, 40 (73%) exhibited either a complete or partial response (tumor mass decreased by over 50%) to the chemotherapy. Responses were noted more frequently in patients with elevated AP levels. Nine of the 10 patients (90%) with AP levels greater than 100 mU/ml experienced a major response; whereas, only 8 of 16 patients (50%) with AP levels less than 60 mU/ml demonstrated a favorable response to the chemotherapeutic agents. The source of the elevated AP levels has not yet been established. Possible sources include liver, bone, kidney, intestinal mucosa, or the tumor itself. Total bilirubin, total protein, serum albumin, and SGOT levels did not differentiate the responders from the non-responders as accurately as did the AP levels.

Alkaline Phosphatase↗
PubMed1980

Polycythemia vera with myelofibrosis and myeloid metaplasia. Acute hepatic failure following splenectomy.

Myelofibrosis with myeloid metaplasia developed during the course of polycythemia vera in a middle-aged man. Severe megakaryocytopenia and thrombocytopenia were early features of this illness and were unresponsive to splenectomy. After splenectomy, hepatic enlargement and acute hepatic failure developed. Extensive extramedullary hematopoiesis dilating hepatic sinusoids and compressing liver cells was the major pathologic finding in the liver. The mechanism of hepatic failure in this disorder is uncertain.

Adult↗
PubMed1980

Wilson's disease: diagnostic difficulties in the patient with chronic hepatitis and hypoceruloplasminemia.

Wilson's disease presents as a classical hereditary syndrome of clinical and biochemical abnormalities. Life-long treatment with copper-chelating agents may dramatically alter the subsequent course and outcome. Hence, considerable attention has been drawn to early recognition and treatment. Since the presentation of Wilson's disease may simulate chronic active hepatitis of unknown etiology, it has been emphasized that the diagnosis of the genetic disorder should be suspected and excluded in this clinical setting. In this report we describe the difficulties encountered in the evaluation of a patient with non-Wilsonian chronic active hepatitis and low serum ceruloplasmin levels. This case illustrates that the distinction between the Wilson's disease homozygote and the hypoceruloplasminemic patient with idiopathic chronic active hepatitis may be difficult to establish and requires a critical evaluation of data to avoid diagnostic pitfalls.

Adult↗
PubMed1979

Neuropsychological dysfunction in acute viral hepatitis.

Neuropsychological dysfunction may precede, occur simultaneously with, or follow the icteric phase of viral hepatitis. Encephalitic and meningitic involvement appears to precede the onset of clinical hepatitis while the tremor syndrome usually follows the onset of illness. The Guillain-Barré syndrome, peripheral nerve disorders, and behavioral abnormalities may occur at any stage of the disease. Neuropsychological alterations noted during the prodrome of viral hepatitis usually clear without sequelae but abnormalities which follow the onset of jaundice may persist during the convalescent phase for prolonged periods. Neither occurrence, type, nor severity of neuropsychological dysfunction appear to be related to specific hepatitis viruses since both type B and non-B infections have been implicated. Furthermore, neuropsychological dysfunction does not appear to be related to the severity of the hepatitis as assessed by clinical or histological features. Although direct viral invasion of nervous tissue and immune complex-mediated damage have been postulated, the mechanism(s) of neuropsychological abnormalities remains to be determined.

Acute Disease↗
PubMed1978

Peliosis hepatis in hematologic disease. Report of two cases.

Two patients with hematologic disease, one of whom had received androgenic steroids, had liver damage associated with peliosis hepatis. In one patient with spherocytic hemolytic anemia, peliosis hepatis was an incidental postmortem finding. In the other patient, who was treated with androgenic-anabolic steroids for aplastic anemia, hepatic failure associated with peliosis hepatis developed. Splenic involvement by peliosis was present in both patients. Peliosis hepatis should be considered in the differential diagnosis of hepatic disease in patients with hematologic disorders, especially if treatment has included androgenic-anabolic steroids.

Anemia, Aplastic↗
PubMed1978

[Salicylate hepatitis].

Explore the source record for details and available documents.

Chemical and Drug Induced Liver Injury↗
PubMed1978

Type B hepatitis after needle-stick exposure: prevention with hepatitis B immune globulin. Final report of the Veterans Administration Cooperative Study.

Hepatitis B immune globulin (HBIG) and immune serum globulin (ISG) were examined in a randomized, double-blind trial to assess their relative efficacies in preventing type B hepatitis after needle-stick exposure to hepatitis B surface antigen (HBsAG)-positive donors. Clinical hepatitis developed in 1.4% of HBIG and in 5.9% of ISG recipients (P = 0.016), and seroconversion (anti-HBs) occurred in 5.6% and 20.7% of them respectively (P less than 0.001). Mild and transient side-effects were noted in 3.0% of ISG and in 3.2% of HBIG recipients. Available donor sera were examined for DNA polymerase (DNAP) and e antigen and antibody (HBeAg; anti-HBE). Both DNAP and HBeAg showed a highly statistically significant correlation with the infectivity of HBsAg-positive donors. Hepatitis B immune globulin remained significantly superior to ISG in preventing type B hepatitis even when the analysis was confined to these two high-risk subgroups. The efficacy of ISG in preventing type B hepatitis cannot be ascertained because a true placebo group was not included.

Adolescent↗
PubMed1978

Carcinoembryonic antigen levels in benign and malignant pleural effusions.

One hundred ninety-one unselected fluid specimens submitted routinely for cytologic examination were assayed to determine whether the measurement of carcinoembryonic antigen (CEA) levels in pleural effusions is useful in detecting malignancy. The mean +/- SD CEA level of 103 benign effusions was 4.1 +/- 2.9 ng/ml. Only one benign effusion had a level greater than 12 ng/ml (18 ng/ml). Benign inflammatory effusions (pneumonia, empyema) had a higher mean CEA activity (6.2 +/- 3.4) than effusions caused by congestive heart failure (2.9 +/- 1.5) (p less than 0.001). Twenty-four (34%) of 70 malignant effusions had a CEA level greater than 12 ng/ml, and 28 (40%) were "positive" by cytologic study. Thirty-eight (54%) were detected by one or both methods. Ten malignant effusions were positive by CEA (greater than 12 ng/ml) alone. These data suggest that the determination of CEA activity levels, when used in conjunction with other clinical findings, may be useful in detecting malignant pleural effusions.

Carcinoembryonic Antigen↗
PubMed1978

Carcinoembryonic antigen assay of ascites and detection of malignancy.

Levels of carcinoembryonic antigen (CEA) activity were measured in 105 unselected samples of ascitic fluid submitted for routine cytologic analysis to ascertain whether this assay was useful in the detection of malignancy. The highest CEA level found in the 70 specimens of "benign" ascites was 10 ng/ml. Using values greater than 10 ng/ml as indicating a cancerous effusion, CEA assay successfully detected 14 of the 29 malignant ascites studied. Cytology, on the other hand, detected only 12 of these fluids. Combining the two methods increased the yield to 20. The CEA assay alone thus detected more than one fourth of these malignant fluids. The assay was particularly useful in detecting malignant transudates, nearly half of which had elevated CEA levels despite negative cytologic findings. The CEA assay of ascites thus showed promise as an adjunct to cytology in the detection of malignant ascites when used as part of a complete clinical and laboratory assessment.

Ascitic Fluid↗
PubMed1978

Lactic acidosis in oat cell carcinoma with extensive hepatic metastases.

Lactic acidosis has been described in patients with leukemia and lymphoma, but its occurrence in other malignant diseases is not documented. We treated two patients with oat cell carcinoma of the lung and extensive liver metastases in whom lactic acidosis developed. Tumor-induced hepatic dysfunction appeared to be a major factor in the pathogenesis of the lactic acidosis observed in these patients.

Acidosis↗
PubMed1977

Ascites following renal transplantation.

Idiopathic ascites has been described in patients on maintenance peritoneal dialysis and hemodialysis. The mechanism responsible for ascites formation in these patients is unknown, and therapy has been generaly unsuccessful. However, renal transplantation has been associated with resolution of this form of ascites. We describe a patient who was free of ascites during maintenance dialysis, in whom ascites developed following renal transplantation associated with transient impairment of renal function. No specific cause of the ascites was found. Resolution of ascited occurred as renal function improved. This experience extends the spectrum of idiopathic ascites in uremic patients to the transplant recipient.

Ascites↗
PubMed1977

Contagiousness of acute hepatitis B. Secondary attack rates in household contacts.

In order to define the hazard of household exposure to patients with acute hepatitis B, in the absence of persistent hepatitis B surface antigen (HBSAg), 98 household contacts of 42 patients with the acute disease were interviewed and tested for HBSAg, antibody to HBSAg (anti-HBS), and serum transaminases shortly after identification and at 3-month intervals for at least 12 months. Most of the index cases with acute hepatitis B were young men and many had used illicit drugs parenterally before the onset of illness. Three of the household contacts had HBSAg detected on initial testing, and 2 of these were carriers with elevated serum transaminase levels. The 3rd HBSAg-positive contact developed acute hepatitis within 2 weeks. This appeared to represent a coprimary infection. Fourteen contacts had anti-HBS on initial evaluation and were considered immune as a result of prior experience with hepatitis B. Of 81 susceptible contacts (neither HBSAg nor anti-HBS on initial screening), 13 were spouses or sexual partners and 2 of these developed acute hepatitis B at 4 and 6 months after the onset of illness in their respective index cases; another developed anti-HBS at 6 months. Thus, 3 (23%) of 13 exposed spouses or sexual partners developed evidence of hepatitis B infection during the surveillance period. In contrast, no evidence of hepatitis B infection related to household exposure was found in 68 parents, siblings, and other domestic contacts. These data confirm the contagiousness of hepatitis B for household contacts of acute cases and suggest that the risk is confined to spouses and sexual partners. These persons appear to be prime candidates for prophylaxis with hepatitis B immune globulin.

Acute Disease↗
PubMed1977

Serum lipids, insulin, and glucagon after portacaval shunt in cirrhosis.

The cholesterol-lowering effect of portacaval anastomosis in homozygous familial hypercholesterolemia suggested a study of lipid metabolism in cirrhotic patients after portasystemic anastomoses. Fasting serum cholesterol, triglycerides, insulin, and glucagon levels were obtained in 20 patients with alcoholic cirrhosis and portacaval anastomosis, and in 21 nonshunted subjects with cirrhosis. After 100 g of glucose, given orally, insulin and glucagon levels were measured. In the shunted patients serum cholesterol was higher than in the nonshunted subjects, 240 +/- 15 mg per 100 ml (mean +/- 1 SEM) versus 180 +/- 13 mg per 100 ml, P less than 0.01. Triglycerides were normal in both groups. Fasting insulin was elevated to a greater extent in the shunted patients with cirrhosis (36 +/- 5 muU per ml) than in the nonshunted patients (22 +/- 4 muU per ml), P less than 0.05. Two hours after glucose, insulin levels were also elevated to a greater extent in the shunted subjects (304 +/- 50 muU per ml) than in the nonshunted subjects (167 +/- 29 muU per ml), P less than 0.03. Fasting glucagon (corrected for interference factor) was elevated to a greater extent in the shunted subjects (204 +/- 35 pg per ml) than in the nonshunted subjects (80 +/- 19 pg per ml), P less than 0.01. The explanation for serum cholesterol elevation after surgical shunting in cirrhotics is unknown. Two possible hypotheses--the differential action of insulin and glucagon on cholesterol metabolism and the effects of shunting on the cirrhotic liver--are discussed.

Alcoholism↗
PubMed1977

Salicylate hepatitis.

Two patients developed acute hepatic injury as a result of salicylate therapy. In each patient serum salicylate levels were below 25 mg per 100 ml during the development of hepatic dysfunction. Liver biopsies, obtained a few days after the peak abnormalities in serum transaminases, revealed nonspecific acute hepatitis. Normal liver tissue was found before the beginning of salicylate treatment in 1 patient, who had systemic lupus erythematosus and drug rechallenge was not attempted. In the other patient, who had rheumatoid arthritis, rechallenge with salicylate evoked hepatic dysfunction and recurrent symptoms. Salicylate-induced liver injury should be considered in the differential diagnosis of hepatic disease occurring in patients receiving high dose salicylate therapy, regardless of serum salicylate levels.

Adult↗