Plasma immunotherapy in a child with acquired immunodeficiency syndrome.
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Biomedical subjects
Publications and source records attributed to V K Wong.
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Inhibition of rabbit subconjunctival fibroblast attachment and proliferation by the antimetabolites 5-fluorouracil (5-FU) and cytosine arabinoside (ara-C) was determined by radionucleotide uptake, cell counting, and colorimetric assays for the concentration range of 1000 to 0.0001 micrograms/ml over an 11-day period. The mean 50% inhibitory doses (ID50s) against proliferation were calculated for each assay. Rabbit fibroblast attachment was not inhibited at any drug concentration by either 5-FU or ara-C. Ara-C was a 10 to 100 times more potent inhibitor of rabbit fibroblast proliferation than 5-FU. The mean ID50s for rabbit subconjunctival fibroblasts were compared with the mean ID50s from a similar series of experiments conducted in our laboratory on human subconjunctival fibroblasts. Unpaired t-test analysis showed a significant difference between the inhibitory effects of 5-FU on rabbit and human fibroblast proliferation. An ID50 against rabbit fibroblasts was detectable after 24 hours of incubation with 5-FU by the 3H-thymidine uptake assay, whereas the ID50 against human fibroblasts was detectable after 48 hours of incubation. Once inhibition of proliferation occurred, however, human fibroblasts were up to six times more sensitive to the antiproliferative effects of 5-FU than rabbit fibroblasts as measured by the 3H-thymidine uptake assay (p = 0.0005). Unpaired t-test analysis showed no statistical difference between the ID50s of ara-C on rabbit and human fibroblasts. Starting on day 3, however, doses greater than 1 micrograms/ml of ara-C were cytotoxic to rabbit fibroblasts but only cytostatic to human fibroblasts as determined by trypan blue uptake assay microscopically. Rabbit ocular fibroblasts may be useful in modelling the proliferation of human ocular fibroblasts in vitro to a limited degree. This tissue culture system may be useful for predicting optimal drug dosages for in vivo rabbit and human glaucoma filtering surgery.
The safety and efficacy of imipenem/cilastatin were evaluated in 21 children, ages 3 to 48 months, with bacterial meningitis. Eradication of bacteria from the cerebrospinal fluid was demonstrated within 24 hours of antibiotic therapy in all but 2 patients who had Haemophilus influenzae type b meningitis and ultimately achieved bacteriologic cure after 2 to 3 days of imipenem/cilastatin therapy. Cerebrospinal fluid penetrations of imipenem and cilastatin were determined at various times after drug administration with mean cerebrospinal fluid: serum ratios of 14 and 10% for imipenem and cilastatin, respectively. The study was terminated when 7 (33%) patients developed seizure activity after antibiotic therapy was administered. The usefulness of imipenem/cilastatin for the treatment of bacterial meningitis in children may be limited by a possible increased incidence of drug-related seizure activity.
We studied the immunologic responsiveness to Haemophilus influenzae type b capsular polysaccharide-Neisseria meningitidis group b outer membrane protein conjugate vaccine (PRP-NOMP) in children 2 to 42 months of age with vaccine dosages containing 7.5, 15, or 30 micrograms of PRP. Overall, PRP-NOMP was highly immunogenic. Geometric mean titers of anti-PRP antibody increased from 0.09 to 3.3 mg/L and 6.6 mg/L following each dose of vaccine, respectively, in the 2- to 18-month age group. Similarly, anti-PRP antibody geometric mean titers increased from 0.12 to 5.9 mg/L in the older than 18-month age group. However, we noted an apparent inverse relationship between vaccine dosages and immune responses following two doses of PRP-NOMP in 2- to 18-month-old children. Anti-PRP antibody geometric mean titers were 12.0, 6.9, and 3.5 mg/L, respectively, after the second dose of vaccine containing 7.5, 15, or 30 micrograms of PRP. Additional studies are needed to understand the mechanisms responsible for this inverse relationship and also to determine the optimal dosage of PRP-NOMP for young children.
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One hundred children with meningococcal infection diagnosed from January 1, 1985, to February 29, 1988, were reviewed. Clinical manifestations ranged from fever alone to fulminant septic shock with purpura fulminans. Twenty-nine percent of the children presented without skin lesions. Of the 55 patients with meningitis, 6 lacked cerebrospinal fluid abnormalities on initial lumbar puncture but cerebrospinal fluid cultures were positive. An overall case fatality rate of 10% was noted with the following poor prognostic indicators identified: hypothermia; seizures or shock on presentation; a total peripheral white blood cell count less than 5000/mm3; a platelet count less than 100,000/mm3; and the development of purpura fulminans. Meningococcal infections remain an important cause of morbidity and mortality in children. Infections caused by Neisseria meningitidis (including meningitis) should be considered even in the absence of skin lesions or cerebrospinal fluid abnormalities.
In Los Angeles, a substantial increase in the number of infections due to Neisseria meningitidis has been noted. More alarming has been an associated mortality rate of 21%. The prompt recognition of meningococcal disease based on a high index of suspicion and the early institution of effective antibiotic treatment are essential for preventing complications and reducing mortality.
The clinical manifestations of patients with group A beta-hemolytic streptococcal (GAS) bacteremia presenting to an urban children's hospital were reviewed. Group A beta-hemolytic streptococci were isolated from blood cultures from 17 children over a three-year period. Systemic illnesses that may have predisposed these children to GAS bacteremia were identified in seven patients: preceding varicella infection (four patients) or malignant neoplasm/immunosuppressive therapy (three patients). Possible sources of GAS included compromised integument (seven patients), the oropharynx (six patients), or the lower respiratory tract (two patients). The clinical manifestations of GAS sepsis included the following: fever (15 patients); arthritis or arthralgias (four patients); cellulitis (three patients); maculopapular eruption (one patient); petechial or pustular exanthems (three patients); osteomyelitis (two patients); cervical adenitis (one patient); empyema (one patient); and meningitis with multiple brain abscesses (one patient). Two patients died of apparent overwhelming GAS sepsis while at home. Group A beta-hemolytic streptococcal bacteremia can present with a wide range of clinical manifestations and cause mild to fulminant disease in children.
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Branhamella catarrhalis was isolated in blood culture from a 6-month-old infant with AIDS. The child had a nasopharyngeal infection with respiratory syncytial virus and pneumonitis with Pneumocystis carinii. Commensal organisms such as B. catarrhalis may be potential pathogens in infants with AIDS.
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Kluyvera cryocrescens was isolated from a blood culture drawn from a patient with a Broviac catheter-related infection. K. cryocrescens has been considered an opportunistic pathogen but has not previously been associated with central venous catheter infections.
Intracranial venous thrombosis has been described in newborns, but there have been no reports of intractable neonatal seizures due to this condition. We report cortical venous sinus thrombosis in two term neonates who presented with seizures in the first 24 hours of life. The diagnosis was made by cranial computed tomography and was confirmed by cerebral angiography. Both patients improved clinically after the intracranial venous thrombosis resolved. These patients demonstrate that intracranial venous thrombosis should be considered in the differential diagnosis of neonatal seizures.
On exposure to UV light at 254 nm in a borosilicate glass actinometer, vitamin k1 decomposed rapidly with a degradation rate constant of 7.63 day-1. Under UV irradiation, DL methionine and sodium metabisulphite were found to have some photostabilizing effect for vitamin k1 formulations. The degradation rates were reduced by 43.4% and 60.4% in the presence of 0.1% w/v of DL methionine and 0.2% w/v of sodium metabisuphite, respectively. When vitamin k1 formulations were stored at room temperature in clear glass bottles and exposed to the weaker light source of both room fluorescent light and natural daylight, vitamin k1 decomposed at a much slower degradation rate constant of 0.31 day-1. Despite the slower degradation rate, DL methionine and sodium metabisuphite failed to protect vitamin k1 from degradation on exposure to this weaker light source. When vitamin k1 was stored in white plastic bottles under the same testing conditions, the photo-protective effect of these photostabilizers reappeared. The protection provided extended the shelf-life from one day to 2.5 days. When amber glass bottles replaced white plastic bottles as storage containers, vitamin k1 was found stable on an open bench for at least 30 days. Such stability was also observed when vitamin k1 was stored in a refrigerator in either white plastic bottles or amber bottles. Findings in this study showed that package and storage conditions that shield the products from light are still the most efficient ways to maintain the photostability of vitamin k1. However, photostabilizers such as DL methionine and sodium metabisulphite may provide additional protection to vitamin k1 when it is stored in less effective light-resistant containers.