White Blood Cell Counts, Alcoholism, and Cirrhosis in Pneumococcal Pneumonia

Abstract Background An elevated white blood cell (WBC) count is a characteristic finding in pneumococcal pneumonia. Very low WBC counts, occurring in some cases, are often associated with overwhelming pneumonia and have been attributed to alcohol-induced suppression of bone marrow. However, a systematic study of neutropenia, leukocytosis, alcohol ingestion, and cirrhosis in pneumococcal pneumonia has not been previously reported. Methods Using a database of patients with pneumococcal pneumonia at our medical center, we extracted data on WBC counts at admission, differential counts, alcohol ingestion, and cirrhosis, and we related these to 7-day and 30-day mortality. Results White blood cell counts were <6000/mm3 in 49 of 481 patients (10.2%) with pneumococcal pneumonia and >25000/mm3 in 40 (8.3%). Mortality at 7 days was 18.4% and 12.5%, respectively, 5-fold and 3-fold greater in patients with WBC <6000 or >25000 than in those with WBC counts between 6000 and 25000 (P < .001). Increased band forms were not associated with a worse outcome (P = .12). Alcohol use and cirrhosis were not associated with WBC counts <6000 (P = .63 and P = .41, respectively). Conclusions In a large series of cases of pneumococcal pneumonia, WBC counts <6000 or >25000 correlated significantly with increased 7-day mortality. More than 10% band forms was not associated with a poor outcome. Alcohol abuse was not associated with low WBC or increased mortality. Our findings suggest that greater consideration be given to more intense care for patients with bacterial pneumonia who have very high or very low WBC counts at the time of hospital admission.

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GMA161 Treatment of Refractory ITP: Efficacy of Fcγ-RIII Blockade.

Blood ◽

10.1182/blood.v108.11.1074.1074 ◽

2006 ◽

Vol 108 (11) ◽

pp. 1074-1074 ◽

Cited By ~ 3

Author(s):

James B. Bussel ◽

Vivek Patel ◽

Cynthia Dunbar ◽

Stephen Lemery ◽

Krista Tibbs ◽

...

Keyword(s):

Blood Cell ◽

White Blood Cell ◽

Platelet Counts ◽

Cell Counts ◽

Blood Cell Counts ◽

White Blood Cell Counts ◽

Repeated Dosing ◽

Wbc Count ◽

Moderate Nausea ◽

Refractory Itp

Abstract Background: GMA161 is a humanized version of a monoclonal anti-Fcγ-RIII antibody, 3G8, that was in clinical trial in the second half of the 1980s. Infusion of 25 mg of 3G8 (0.25–0.5mg/kg) resulted in transient but dramatic responses in approximately 50% of refractory ITP patients who did not respond to IVIG. It was unclear why certain patients did not respond. Since 3G8 is a mouse monoclonal antibody, it could not be reinfused because of the development of HAMA. Furthermore, there was marked neutropenia and depletion of NK cells (the CD16-expressing leukocytes) and there were significant fever-chill-vomiting reactions that were triggered by the antibody-Fcγ-RIII interaction. Preventing the reactions required a cocktail of methylprednisolone, diphenhydramine, acetaminophen and metaclopramide. GMA161, in addition to being humanized, has the Fc portion denuded of carbohydrates to reduce the binding of its Fc portion to Fc receptors. Methods: The first cohort of 4 patients with chronic ITP (table) and platelet counts < 30,000/ul each received a single infusion of 0.1 mg/kg of GMA161 over 30 minutes. Results: Two of the 4 patients responded with peak platelet counts of 108,000/ul (from 27,000/ul) and 45,000/ul (from 11,000/ul) [figure 1]. Both had had ITP for > 20 years, failed splenectomy and also failed multiple previous therapies including rituximab, cyclophosphamide, steroids, danazol, and IVIg among others. The responses to GMA161 were short-lived, lasting between 7 and 10 days and, as shown in figure 1, the platelet counts peaked at slightly different times. Figure 2 illustrates the dramatic decrease in the WBC count occurring immediately after infusion but then rapidly returning to baseline; this decrease was apparent in all types of white cells, not just neutrophils. The first patient had marked chills, fever, and vomiting 2 hours after infusion; this was reminscent of reactions to 3G8. She received IV methylprednisolone with resolution. The second patient had mild-moderate nausea. The third and fourth patients received acetaminophen, diphenhydramine and ondansetron premedication and had no adverse events. Conclusions: The findings are exciting because this cohort received the starting (lowest) dose of GMA161, 0.1mg/kg, and yet had reasonable activity. The toxicity was minimal with appropriate premedication. In the next cohort, better responses may be anticipated since they will be receiving 0.3 mg/kg. The hope would be that repeated dosing might have a more lasting effect, in at least a subset of patients. GMA161: Cohort #1 Patient ID Age (yrs) Sex Splenectomy Duration of Disease (ITP) Months Major Bleeding Major Diagnoses Previous Treatments #1 29 Female Yes 90 No Anemia 7 #2 32 Female Yes No #3 70 Male Yes 300 No Diabetes 4 #4 59 Female Yes 120 Yes (ICH) Stroke/Asthma 6 Figure 1: Platelet counts of Responders to GMA 161 treatment Figure 1:. Platelet counts of Responders to GMA 161 treatment Figure 2: Mean White Blood Cell Counts of patients treated with GMA 161 Figure 2:. Mean White Blood Cell Counts of patients treated with GMA 161

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An Alternative Elastase-mediated Degradation of Fibrinogen and Fibrin Observed in a Patient with Herpes Simplex Encephalitis and Pneumonia

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650550 ◽

1996 ◽

Vol 76 (02) ◽

pp. 184-186 ◽

Cited By ~ 2

Author(s):

Kenji lijima ◽

Fumiyo Murakami ◽

Yasushi Horie ◽

Katsumi Nakamura ◽

Shiro Ikawa ◽

...

Keyword(s):

Herpes Simplex ◽

Blood Cell ◽

White Blood Cell ◽

Herpes Simplex Encephalitis ◽

Pmn Elastase ◽

Cell Counts ◽

Blood Cell Counts ◽

Sds Page ◽

White Blood Cell Counts ◽

Pmn Élastase

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.

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