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Biomedical subjects

R Jaffe

Publications and source records attributed to R Jaffe.

At least 271 records · Page 15Linked to original sources
PubMedDate not supplied

Onychomycosis: recognition, diagnosis, and management.

About 20% of the US population between the ages of 40 and 60 years have fungal nail disease, or onychomycosis. The incidence of this infection is increasing worldwide. Most cases of onychomycosis in the United States are caused by dermatophytes, but nondermatophyte fungi (molds or yeasts) may also be causative agents. To confirm the diagnosis of onychomycosis, a potassium hydroxide examination should be performed. A culture is necessary to determine the fungal pathogen and to aid in selecting appropriate therapy. Worldwide, fluconazole (not yet approved in the United States for onychomycosis), itraconazole, and oral terbinafine have superseded griseofulvin and ketoconazole as the agents of choice in treating onychomycosis. These newer systemic compounds have higher cure rates and cause fewer side effects than traditional agents. Intermittent dosing with itraconazole (3 or 4 one-week pulses of 200 or 400 mg daily) is the latest advance in the treatment of onychomycosis. This regimen has been found to be at least as safe and effective as short-term continuous therapy, yet more flexible, convenient, and economical.

Antifungal Agents↗
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Adenoviral infections in pediatric liver transplant recipients.

Over a 5 1/2-year period, 22 of 262 children receiving liver transplants developed adenoviral infections. Five had adenoviral hepatitis in the allograft, caused by serotype 5. All five were treated for rejection, either just before or at the time of infection. Liver biopsy specimens had characteristic histological appearance, and diagnosis of adenoviral infection was confirmed with monoclonal antiadenoviral antibodies, electron microscopy, and by culture of liver tissue. In the remaining 17 patients, adenovirus was isolated from urine, stool, throat secretions, and/or blood samples, but none had any detectable visceral infection. Serotypes 1 and 2 predominated, similar to children not receiving transplants during the same time period. Three of the patients with hepatitis are alive and well; two died of liver failure. Adenoviral hepatitis did not recur in the second allograft of a patient who underwent retransplantation for combined rejection and adenoviral hepatitis, and appears, therefore, not to be a contraindication to retransplantation when liver failure ensues.

Adenoviridae Infections↗
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Echovirus hepatic failure in infancy: report of four cases with speculation on the pathogenesis.

Disseminated echovirus infection with fulminant hepatic failure occurs almost exclusively in newborns. Although a relatively uncommon condition, it is on occasion associated with neonatal death accompanied by diffuse and extensive hemorrhagic necrosis of the liver and adrenals as the defining finding. We report four cases of severe systemic neonatal echovirus infection and present histologic and clinical evidence to demonstrate the two histologic patterns of liver involvement; intravascular coagulation in the early clinical course and a veno-occlusive component in later stages of the disease. Viral damage to vascular endothelium and hepatic venous endothelium by a "hit-and-run" process in the early viremic phase rather than direct hepatocyte injury is postulated to be a mechanism.

Disseminated Intravascular Coagulation↗
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Enteric adenovirus infection in pediatric small bowel transplant recipients.

Three of 70 small bowel transplant recipients were diagnosed with adenovirus enteritis. The biopsies were performed for surveillance in one patient at 2.7 years after transplantation and in two symptomatic children 1.5 years and 4.5 months after transplantation. In all three patients the characteristic epithelial changes were not noted by the primary observers. Two biopsies had been called "suggestive of acute rejection" and both patients had been so treated. One biopsy had been diagnosed as "regenerative". Once the epithelial changes were recognized as being viral, confirmation was possible by stool culture in one patient, immunohistochemistry in two patients, or by lift technique of the H&E sections for electron microscopy. The immune suppression was reduced and none of the patients developed disseminated infection. As in other transplanted organs, such as lung and liver, adenovirus infection may be limited largely to the allograft but can be destructive. Early recognition of the characteristic changes that are illustrated can lead to confirmation of the virus and appropriate reduction of immune suppression. A mistaken diagnosis of rejection and augmentation of immune suppression can lead to viral dissemination and potential fatality.

Adenovirus Infections, Human↗
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Fascin and the differential diagnosis of childhood histiocytic lesions.

This is a descriptive screening of 46 examples of childhood histiocytic lesions and some of their look-alikes using a monoclonal antibody, p55, to fascin. Fascin, an actin-bundling protein, identifies dendritic cells in the blood and in tissues. Our aim was to test the diagnostic utility of the antibody in various lesions at different sites and to see whether the staining patterns give insight into the cell types involved. Fascin intensely stained the cells of juvenile xanthogranulomas (JXG), Rosai-Dorfman lesions, and soft tissue dendrocytomas. Normal Langerhans' cells and the cells of Langerhans' cell histiocytosis were unreactive. Their lack of fascin staining may be relevant to fascin being maturation as well as lineage related. Epithelioid and palisading granulomas were unstained, though an example of Kikuchi lymphadenitis had large numbers of dendritic-type cells that stained strongly. A reticulohistiocytoma of the skin was also unstained and look-alike lesions, Spitz nevi, and mast cell lesions did not stain. Two of three large-cell lymphomas (both CD30+) also had fascin reactivity. Even though fascin is not specific to dendritic cells, staining other cell types as well (false positive), and not entirely sensitive, dendritic cells such as tissue Langerhans' cells are unstained (false negative), there seems to be a consistency of staining in childhood histiocytic lesions. This may be of diagnostic use when read in the context of the tissue differential diagnosis. Whether fascin can serve as a marker for the dendritic cell lineage, or at least for some phases of dendritic cell lifecycle, is not answered by this survey.

Antibodies, Monoclonal↗
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Hemophagocytic syndrome presenting as acute hepatic failure in two infants: clinical overlap with neonatal hemochromatosis.

Two patients with hemophagocytic lymphohistiocytosis who presented with acute liver failure are reported. Both presented with fever, hepatosplenomegaly, markedly elevated liver function tests, abnormal coagulation profiles, and an increase in serum ferritin. Both infants were diagnosed with neonatal hemochromatosis based on a clinical picture of hepatic insufficiency with hyperferritinemia and were referred for liver transplantation. The first patient died of liver failure and septicemia before transplantation. Review of autopsy material revealed a hepatitis-like pattern and extensive infiltration of liver and other organs including bone marrow by histiocytes, some of which were hemophagocytic. The second patient underwent liver transplantation but died 44 days thereafter from progressive hemophagocytic lymphohistiocytosis. Examination of the resected liver demonstrated a hepatitis-like pattern, proliferation of histiocytes, and hemophagocytosis, and the bone marrow revealed hemophagocytic histiocytosis. Hemophagocytosis recurred in the allograft. Hepatic manifestations are common in hemophagocytic lymphohistiocytosis and overt hepatic failure may occur, but initial presentation as fulminant hepatic failure is not well recognized. Elevated serum ferritin can make the distinction from neonatal hemochromatosis and other forms of neonatal liver failure difficult. Hemophagocytic lymphohistiocytosis should be considered in the differential diagnosis of neonatal liver disease, especially when it is accompanied by cytopenias.

Antigens, CD↗
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Diagnosis of hirschsprung disease using the rectal biopsy: multi-institutional survey.

Diagnostic pathologists remain uncomfortable with the diagnosis of Hirschsprung disease (HD) via rectal (mucosal/submucosal) biopsy and with performance and interpretation of the associated acetylcholinesterase (AChE) assay. This report details the different diagnostic approaches taken by four major pediatric institutions-Children's Hospital, Columbus, OH; Children's Hospital Medical Center, Cincinnati, OH; Children's Hospital, Pittsburgh, PA; Children's Hospital, Los Angeles, CA-in confirming or excluding the presence of HD. The Columbus approach emphasizes serial morphologic examination of rectal biopsies, while Cincinnati emphasizes the primary diagnostic utility of the AChE stain. Pittsburgh and Los Angeles emphasize a detailed gross and microscopic analysis of rectal biopsies to detect both conventional HD and its more rare subtypes. The diagnostic approaches of these four institutions can be used on a complementary basis to the advantage of the general diagnostic pathologist, especially in HD cases with subtle clinical presentations. The need for careful and continual communication between the clinician and pathologist in diagnosing or excluding the presence of HD is imperative.

Acetylcholinesterase↗
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Characteristics of receptors and enzymes in brains of human alcoholics.

Acute and chronic ethanol administration to animals has been shown to produce changes in the turnover of numerous neurotransmitters, as well as to change the characteristics of certain neurotransmitter receptors. In the present study, brains obtained from human alcoholics and matched control subjects were examined for similar changes. In frontal cortex, the affinity of opiate receptors for dihydromorphine was significantly reduced in brains of alcoholics. Judging from animal studies, this change may reflect alterations in opiate receptor-effector coupling processes. No changes were observed in muscarinic cholinergic or beta-adrenergic receptors in humans, in contrast to animals, possibly because of the protracted abstention from alcohol among the alcoholic patients prior to death. Similarly, no changes in the activities of choline acetyltransferase, tyrosine hydroxylase or MAO-B were observed in brains of alcoholics as compared to the control population. Our studies suggest that many of the alterations witnessed during alcohol intoxication and withdrawal in animals may be more subtle in humans, or may be reversible with abstinence.

Alcoholism↗