Simultaneous quantitation of polymyxin B1, polymyxin B2 and polymyxin B1-1 in human plasma and treated human urine using solid phase extraction and liquid chromatography-tandem mass spectrometry.

Two liquid chromatographic-tandem mass spectrometric (LC-MS/MS) methods have been developed and validated for the quantitative determination of polymyxin B1, polymyxin B2 and polymyxin B1-1 concentrations in human plasma and treated urine. During method development, technical challenges such as the separation of structural isomers polymyxin B1and polymyxin B1-1 and nonspecific binding in urine samples were encountered and overcome. Two automated solid phase extraction methods were used to extract plasma samples (100μL) and urine samples (200μL) and the resulting extracts were analyzed using reversed phase LC-MS/MS with an electrospray (ESI) interface and selected reaction monitoring (SRM) in the positive ionization mode.

Treatment of periocular infantile hemangiomas with propranolol: case series of 18 children.

Purpose: To study the efficacy of propranolol in the treatment of periocular infantile hemangiomas (IHs).

Design: Retrospective interventional case series.

Participants: Eighteen children presenting periocular IH with occlusion of the pupil, anisometropic astigmatism, proliferating eyelid IH, or cosmetically disfiguring periocular IH.

Morning glory syndrome: clinical, computerized tomographic, and ultrasonographic findings.

Objective: To evaluate the ophthalmic, radiologic, and ultrasonographic findings in morning glory syndrome.

Patients And Methods: Retrospective review of patients' charts.

Results: Twenty-one patients were included.

Novel TIGR/MYOC mutations in families with juvenile onset primary open angle glaucoma.

Mutations in the trabecular meshwork induced glucocorticoid response protein (TIGR) or myocilin (MYOC) has recently been shown to cause juvenile onset primary open angle glaucoma (JOAG). In this study, we identified two new mutations (Asp380Ala and Ser502Pro) in two British families and another (Pro370Leu) in a French-Canadian family. These mutations were not present in a total of 106 normal chromosomes.

Sequence analysis and homology modeling suggest that primary congenital glaucoma on 2p21 results from mutations disrupting either the hinge region or the conserved core structures of cytochrome P4501B1.

We recently reported three truncating mutations of the cytochrome P4501B1 gene (CYP1B1) in five families with primary congenital glaucoma (PCG) linked to the GLC3A locus on chromosome 2p21. This could be the first direct evidence supporting the hypothesis that members of the cytochrome P450 superfamily may control the processes of growth and differentiation. We present a comprehensive sequence analysis of the translated regions of the CYP1B1 gene in 22 PCG families and 100 randomly selected normal individuals.

Pattern electroretinogram and spatial contrast sensitivity in primary congenital glaucoma.

Objective: The authors investigated the temporal and spatial characteristics of pattern electroretinogram (PERG) and spatial contrast sensitivity (CS) in primary congenital glaucoma (PCG) to determine whether the PERG and CS could be useful tools in the diagnosis of childhood glaucoma, especially PCG.

Participants: The PERGs were evaluated in eyes from ten patients with PCG and nine age-matched visually normal subjects.

Intervention: All patients received complete ophthalmologic evaluations including visual field testing.

A second locus (GLC3B) for primary congenital glaucoma (Buphthalmos) maps to the 1p36 region.

Primary congenital glaucoma (gene symbol: GLC3) is an ocular disorder that occurs for 0.01-0.04% of blind people.

On- and off-responses in the photopic electroretinogram in complete-type congenital stationary night blindness.

We examined the on- and off-responses of the photopic electroretinogram in patients with complete congenital stationary night blindness. Standard flash electroretinograms as well as those produced in a ganzfeld modified for long-duration light stimuli (500 msec) permitted the separation of on- and off-responses in four patients and four normal subjects. The amplitude and latency of the elctroretinogram on-response (a- and b-waves) and off-response (d-wave) in addition to the oscillatory potentials of the off-response in normal subjects and patients were compared.

Assignment of a locus (GLC3A) for primary congenital glaucoma (Buphthalmos) to 2p21 and evidence for genetic heterogeneity.

Primary congenital glaucoma (GLC3) is an inherited eye disorder that accounts for 0.01-0.04% of total blindness.

Clinical evaluation of aminocaproic acid for managing traumatic hyphema in children.

Purpose: The purpose of this study is to determine the incidence of secondary hemorrhage after traumatic hyphema in children and to evaluate the efficacy of epsilon aminocaproic acid in reducing this incidence.

Methods: In a prospective, randomized, double-blind study performed between November 1987 and February 1994, 94 children admitted for traumatic hyphema were assigned to receive either aminocaproic acid (n = 48) (100 mg/kg every 4 hours; maximum, 30 g daily) or placebo (n = 46) for 5 days. Patients who had ingested aspirin in the week preceding admission were excluded from the study.

Incidence and prognosis of childhood glaucoma. A study of 63 cases.

Sixty-three consecutive cases (95 eyes) of glaucoma in children were studied. Glaucoma associated with congenital anomalies (group II) formed the largest group in this study. This accounted for 46% of the cases compared to primary congenital glaucoma (group I) that accounted for 22.

[Orbital apex syndrome in a child with Wegener's granulomatosis].

The authors report the case of a 10 year-old child presenting with orbital apex syndrome as the initial manifestation of Wegener's granulomatosis. Orbital apex syndrome is characterized by complete or partial paralysis of the third, fourth and sixth cranial nerves with involvement of the trigeminal nerve's ophthalmic branch. The different mechanisms responsible for ocular complications in Wegener's granulomatosis and the usefulness of computer assisted tomography in this clinical situation are discussed.