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Biomedical subjects

D Putterman

Publications and source records attributed to D Putterman.

6 recordsLinked to original sources
PubMed1996

The spectrum of septic encephalopathy. Definitions, etiologies, and mortalities.

OBJECTIVE: To determine whether the severity of septic encephalopathy is correlated with gram-negative bacteremia and mortality and whether there exists a single or combination of metabolic derangements(s) that cause septic encephalopathy. DESIGN AND SETTING: Prospective case series in an academic medical center. PATIENTS: Fifty patients selected according to clinical and laboratory criteria for severe sepsis. The criteria included temperature, heart rate, respiratory rate, and hypotension and/or signs of systemic hypoperfusion. MAIN OUTCOME MEASURES: A single or combination of metabolic and laboratory derangements and organ failures, three different methods to grade the severity of septic encephalopathy, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, gram-negative bacteremia and infection, and mortality. RESULTS: Encephalopathy was associated with an increase in mortality when graded by the Glasgow Coma Score; a score of 15 had 16% mortality, 13 to 14 had 20%, 9 to 12 had 50%, and 3 to 8 had 63% mortality (P < .05). Bacteremia was associated with encephalopathy; 13% of septic patients without encephalopathy vs 59% of patients with encephalopathy had bacteremia (P < .001) when graded by altered mental status. Septic encephalopathic patients had elevated serum urea nitrogen and bilirubin levels, increased APACHE II scores, and a higher incidence of renal failure. CONCLUSIONS: The severity of septic encephalopathy correlated with mortality, bacteremia, and renal and hepatic dysfunction. The Glasgow Coma Score is a useful tool for characterizing septic encephalopathy. Considerable variations can be found according to different criteria used to classify septic encephalopathy.

APACHE↗
PubMed1994

Pulmonary embolism as the presenting feature of hepatocellular carcinoma.

Primary hepatocellular carcinoma can be revealed by recurrent pulmonary embolism as observed in this case of a 63-year-old woman initially hospitalized for abdominal pain and shortness of breath. The clinical diagnosis was confirmed by laboratory findings, a ventilation perfusion scan and pulmonary angiography which demonstrated peripheral basal artery cut-off and slow filling with delayed washout. The patient was treated with heparin then with nicoumarol and responded well. One month after discharge the patient again complained of shortness of breath and was readmitted. Anticoagulation was adequate as evidenced by a prothrombin time of 1.39 INR and the physical examination and laboratory tests again suggested pulmonary emboli, confirmed by a ventilation perfusion scan. Computed tomography of the chest and abdomen revealed multiple hypodense masses filling half of the liver volume and needle biopsy led to the diagnosis of hepatocellular carcinoma. Hypercoagulability in malignancy is well-known although cases of migratory thrombophlebitis are extremely rare. Pulmonary embolism has not been described as a presenting feature of hepatocellular carcinoma. In this case, there was no evidence of hepatic dysfunction and the pulmonary embolism occurred despite adequate anticoagulation. Clinicians should include occult carcinoma among the possible causes of recurrent pulmonary embolism and when searching for malignancy can include hepatocellular carcinoma among the causes of hypercoagulation.

Carcinoma, Hepatocellular↗
PubMed1990

Ubiquitin in avian leukosis virus particles.

We have identified unconjugated ubiquitin as a component of avian leukosis virus (ALV). Quantitation both by immunoblotting and by protein staining showed that ubiquitin makes up about 0.5% of total viral protein, corresponding to 100 molecules per virion. This level is about fivefold higher than the level of unconjugated ubiquitin in the cytosol, when expressed as a fraction of total protein. Other abundant low molecular weight proteins in the cytosol were not detected in virions, indicating that packaging occurs in a specific manner. A naturally occurring ALV mutant that lacks the env gene was found to package normal levels of ubiquitin, ruling out involvement of the viral glycoproteins as carriers of ubiquitin. We examined disrupted virus particles as well as lysates of infected cells for the presence of gag protein-ubiquitin conjugates. No conjugates could be detected, suggesting that ubiquitin does not enter virions linked to gag protein.

Animals↗