Corneal fleck dystrophy in an English family.
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Aged↗
Biomedical subjects
L Ficker
Publications and source records attributed to L Ficker.
Enterobacter cloacae endophthalmitis: report of four cases.
Members of the genus Enterobacter are commensal organisms of the gastrointestinal tract and are considered pathogenic only for patients with lowered resistance to infection (e.g., chronic infection, cancer, or diabetes mellitus) or those with impaired immunity (congenital, acquired, or impaired immunity secondary to therapy). We report on four cases of endophthalmitis caused by Enterobacter cloacae: two in patients with acute postoperative endophthalmitis, one in a patient with delayed bleb-related endophthalmitis, and one in a patient presenting with presumed posttraumatic endophthalmitis. Each patient presented with severe disease many days after the onset of ocular symptoms, and two patients had systemic risk factors accounting for a reduced resistance to infection. Endophthalmitis caused by gram-negative bacilli is characterized by acute onset, rapid progression, and poor final visual outcome. Each of these patients was treated by a standard protocol with intravitreal, systemic, and topical antibiotics and systemic steroids. Despite treatment, the final visual outcomes for three of these patients was no perception of light, and that for one patient remained perception of hand movements only. In common with endophthalmitis caused by other gram-negative organisms, intraocular infection secondary to Enterobacter cloacae infection is a devastating disease which, despite treatment, results in extensive ocular damage and severe visual loss. Since 1966, only four cases of endophthalmitis secondary to infection with members of this genus have been reported. This report presents four cases which occurred over a period of 14 months and, to the best of our knowledge, the first case of bleb-related endophthalmitis secondary to E. cloacae infection.
Adult↗
Outcome of acanthamoeba keratitis treated with polyhexamethyl biguanide and propamidine.
OBJECTIVE: This study investigates the clinical outcome of Acanthamoeba keratitis treated with polyhexamethyl biguanide (PHMB) and propamidine isethionate (Brolene). DESIGN: A retrospective review of all patients treated for Acanthamoeba keratitis between September 1992 and February 1995 was carried out. All patients were treated with PHMB 0.02% and propamidine 0.1% hourly for 3 days, the frequency reduced to four to six times daily according to clinical response. MAIN OUTCOME MEASURES: Age, gender, result of laboratory investigation, duration of disease before diagnosis, visual acuity (VA) pretreatment and post-treatment, need for keratoplasty, and presence of adverse reaction were measured. RESULTS: One hundred eleven cases were identified in 105 patients (60 male, 45 female; mean age, 32). Ninety-two percent of infections were in contact lens wearers. The clinical diagnosis was confirmed by corneal culture or histopathology in 64 cases (57.7%). The diagnosis was made "early" (within 28 days) in 65 cases (58.6%). Twenty-one (18.9%) were "intermediate" (28 days-2 months) and 20 (18%) were "late" (> 2 months) diagnoses. Overall post-treatment VA was 6/12 or better in the majority (88/111, 79.3%) of cases, and 18 (16.2%) had VA of 6/36 or worse. The VA of > or = 6/12 was achieved by 90.8% of the early, 71.4% of the intermediate, and 65% of the late groups. Clinical relapses occurred in 19 patients on reducing the therapy. Treatment toxicity was never serious and consisted only of stinging or superficial punctate keratopathy. Keratoplasty was indicated in only ten patients, and disease activity was controlled adequately in all patients before grafting. CONCLUSIONS: Combined treatment with PHMB and propamidine is well tolerated, nontoxic, and effective. Typically, visual outcome is favorable and the requirement for keratoplasty reduced markedly.
Acanthamoeba↗
Complementary insulin therapy improves blood glucose and serum lipid parameters in type 2 (non-insulin-dependent) diabetic patients. II. Effects on serum lipids, lipoproteins and apoproteins.
The aim of the present study was to evaluate the effects of complementary insulin therapy, consisting of a single dose of 1 to 8 units of shortacting insulin before each meal (4-6x daily) and sometimes at 02.30 h, on concentrations of serum lipids, lipoproteins and apoproteins in type 2 (non-insulin-dependent) diabetic patients, unsatisfactorily controlled either by oral hypoglycemic agents (OHA) or by longacting insulin 1-2x daily (INS 1-2). Compared means +/- SD. Patients on INS 1-2 (n = 82) had better baseline glycemic control than patients on OHA (n = 68) (HbAlc: 9.33 +/- 1.76% vs. 10.59 +/- 1.83%, p < 0.001 and fructosamine: 3.34 +/- 0.74 mmol/l vs. 3.85 +/- 0.84 mmol/l, p < 0.001) and serum triglyceride concentrations (3.03 +/- 2.05 mmol/l vs. 4.95 +/- 4.48 mmol/l, p < 0.001), in spite of longer duration of diabetes (13.35 +/- 8.07 years vs. 10.1 +/- 6.9 years, p < 0.001). After 8-10 weeks of complementary insulin therapy, OHA patients (n = 33) improved both the glycemic control (HbA1c: 10.5 +/- 1.78% vs. 9.0 +/- 1.75%, p < 0.001) and fructosamine: 4.0 +/- 0.85 mmol/l vs. 3.5 +/- 0.76 mmol/l, p < 0.001) and most of the lipid parameters (decreased serum triglyceride: 5.8 +/- 5.64 mmol/l vs. 3.6 +/- 4.69 mmol/l, p < 0.001, total cholesterol/HDL-cholesterol: 6.8 +/- 3.13 vs. 5.6 +/- 2.23, p < 0.01 and increased HDL-cholesterol: 1.0 +/- 0.30 mmol/l vs. 1.2 +/- 0.30 mmol/l, p < 0.001, apo AI: 1.6 +/- 0.26 g/l vs. 1.8 +/- 0.28 g/l, p < 0.001, LpAI particles: 0.6 +/- 0.1 g/l vs. 0.7 +/- 0.12 g/l, p < 0.001 and LDL-cholesterol/apo B: 2.1 +/- 0.67 vs. 2.7 +/- 0.67, p < 0.001). In patients previously on INS 1-2x (n = 34), complementary insulin therapy with reduced dose of insulin per day (49.6 +/- 22.5 U/d vs. 36.6 +/- 13.3 U/d, p < 0.001) did not further improve glycemic control but improved the number of proatherogenic and antiatherogenic lipoprotein particles (decreased apo B: 1.7 +/- 0.52 g/l vs. 1.5 +/- 0.94 g/l, p < 0.01, apo AI/Lp AI: 2.9 +/- 1.01 vs. 2.3 +/- 0.98, p < 0.01 and increased Lp AI particles: 0.6 +/- 0.10 g/l vs. 0.7 +/- 0.12 g/l, p < 0.0001); BMI also decreased (29.4 +/- 4.28 kg/m2 vs. 28.9 +/- 4.24 kg/m2, p < 0.05). These results demonstrate that complementary insulin therapy probably induces antiatherogenic lipoprotein changes in NIDDM patients previously treated by either OHA or INS 1-2x. Thus, this type of therapy should be used more often and start earlier, and should be preferred to longacting insulins.
Adult↗
[Personal experience with 200mg of micronized fenofibrate (Lipanthyl 200 M) in the treatment of primary dyslipidemias].
Micronized phenofibrate 200 mg was administered in clinical trial to 30 patients with dyslipidaemia. Their average age was 51.9 years (10 with type 2a, 12 with type 2b and 8 with types 4 and 5). After 12 weeks of treatment significant improvement of the whole lipid profile was achieved. The total cholesterol declined in different sub-groups by 16, 17 and 20% resp. LDL cholesterol declined by 20 and 18 per cent in types 2a and 2b, in types 4 and 5 it was not assessed (it was not possible to use Friedewald's equation). Triglycerides declined by 39, 45 and 75%. The HDL concentration increased by 16, 27 and 25%. The atherogenic indexes TCh/HDL-Ch declined by 28, 36 and 32%. LDL-Ch/HDL-Ch dropped by 30 and 34%. The extent of the hypolipidaemic effect depended on the baseline value: the more pathological the baseline value, the more marked the improvement. As to other investigated indicators there was a significant rise of the apolipoprotein AI and Lp AI particle concentration. Apoprotein B declined insignificantly. Uric acid declined significantly by 28%. Fibrinogen dropped significantly only in type 2a. The lipoprotein(a) concentration did not change significantly. The drug was very well tolerated and undesirable effects were minimal. Micronized phenofibrate (Lipanthyl 200 M) due to its comprehensive favourable effect on the entire lipid profile and other risk factors can prove useful in the treatment of all types of dyslipidaemias (with the exception of type I). As compared with Lipanthyl 100, the better pharmacokinetic properties make it possible to reduce the dose from 300 mg/day and it can be administered in a single daily dose.
Dosage Forms↗
The histopathology of the iridocorneal-endothelial syndrome.
The iridocorneal-endothelial (ICE) syndrome is characterised clinically by a "hammered-silver" appearance of the corneal endothelium, corneal failure, glaucoma, and iris destruction. Specular photomicroscopic studies of the corneal endothelium have demonstrated a population of abnormal cells termed "ICE cells." The purpose of this study was to define the histological appearances typical of this disease and in particular the ultrastructural morphology of the ICE cell. Thirty-five corneas, 11 trabeculectomy specimens, and 3 failed corneal grafts taken from patients with the ICE syndrome were examined by transmission and scanning electron microscopy. Comparison was made with seven normal corneas. Ten corneas and two trabeculectomy specimens demonstrated a population of well-differentiated cells with epithelial features such as desmosomes, tonofilaments, and microvilli. Other cell types identified were cells that resembled those of normal corneal endothelium, inflammatory cells, and cells with a fibroblast-like morphology. It seems likely that the epithelial cells of our specimens are the histological equivalent of the ICE cell seen by specular photomicroscopy. The other cell types may be either residual normal endothelial cells or else arise from secondary phenomena of various kinds.
Cornea↗
On the pathology of the iridocorneal-endothelial syndrome: the ultrastructural appearances of 'subtotal-ice'.
The iridocorneal-endothelial syndrome (ICE syndrome) is characterised by corneal failure, glaucoma and iris destruction. Specular photomicroscopical and histological studies of the corneal endothelium in this disease show a population of abnormal cells named 'ICE-cells'. In many patients some areas of the endothelium are occupied by ICE-cells and others by normal cells, an appearance described as 'subtotal-ICE'. Specular photomicroscopical observations suggest that ICE-cells and normal endothelial cells may actively interact at the boundary zone where they meet. The purpose of this study was to examine the ultrastructural appearances of the boundary zone to gain insight into the cellular pathology of this region. Thirty-five corneas taken from patients with the ICE syndrome were examined by light, transmission and scanning electron microscopy. The subtotal-ICE appearance was demonstrated in four specimens. The morphology of ICE-cells at the boundary zone suggests that they are non-motile but also implies a general state of high metabolic activity. Many of the normal endothelial cells in this region are damaged, an appearance which may result from a toxic effect from the nearby ICE-cells.
Atrophy↗
Placebo controlled trial of fusidic acid gel and oxytetracycline for recurrent blepharitis and rosacea.
A prospective, randomised, double blind, partial crossover, placebo controlled trial has been conducted to compare the performance of topical fusidic acid gel (Fucithalmic) and oral oxytetracycline as treatment for symptomatic chronic blepharitis. Treatment success was judged both by a reduction in symptoms and clinical examination before and after therapy. Seventy five per cent of patients with blepharitis and associated rosacea were symptomatically improved by fusidic acid gel and 50% by oxytetracycline, but fewer (35%) appeared to benefit from the combination. Patients with chronic blepharitis of other aetiologies did not respond to fusidic acid gel but 25% did benefit from oxytetracycline and 30% from the combination. Our results demonstrate the need to investigate patients with blepharitis for concomitant rosacea as they respond well to targeted therapy.
Blepharitis↗
Refractive results after corneal triple procedures (PK+ECCE+IOL)
We have analysed the refractive results of corneal triple procedures (penetrating keratoplasty with extracapsular cataract extraction and posterior chamber intraocular lens implantation) in 52 eyes of 47 patients with a mean follow-up of 39 months. The patients were predominantly old and female and most received unilateral surgery. The contralateral acuity was 6/24 or worse in more than 50% of cases at the time of surgery. Many of these patients were significantly ametropic pre-operatively. Biometry does not seem to have improved the refractive results in those patients in whom it was attempted. The majority of patients were hypermetropic when their refraction stabilised, with resulting poor uncorrected visual performance. Possible improvements are discussed.
Aged↗
[Reaven's metabolic syndrome X in the families of individuals with premature cerebrovascular attacks].
In families of subjects with premature ischaemic cerebrovascular attacks (a total of 45 families with 190 members) the authors detected a high incidence of dyslipidaemia, arterial hypertension, impaired glucose tolerance and non-insulin dependent diabetes mellitus, frequently with striking cumulation. The authors investigated therefore the relationship of the insulin level as an indirect reflection of insulin resistance with these risk factors. The fasting insulin levels correlated significantly positively with triglyceride levels, apolipoprotein B, atherogenic indices and negatively with HDL-cholesterol. The probands and siblings with arterial hypertension had significantly higher fasting insulin levels, as compared with subjects without hypertension which was due to a more frequent incidence of overweight. Patients with an impaired glucose tolerance and NIDDM had significantly higher fasting insulin levels and insulin levels after two hours (the latter value was not assessed in diabetes) and unfavourable "atherogenic" lipid and lipoprotein values, as compared with subjects without glucose intolerance and the control group. Overweight (BMI > 26) had an adverse impact on all investigated indicators of lipid and carbohydrate metabolism whereby a W/H ratio > 0.85 as a manifestation of central obesity further accentuated this adverse effect. The authors draw from these results therapeutic conclusions as regards the mentioned risk factors in these families. They emphasize the importance of non-pharmacological intervention of the metabolic X syndrome by weight reduction and more physical activity not only in families of subjects with early atherosclerosis but in the entire population which has a high prevalence of cardiovascular diseases.
Cerebrovascular Disorders↗
[Lipoprotein (a): a genetic risk factor for early ischemic cerebrovascular stroke].
In 45 subjects after a cerebrovascular attack (age less than 55 years) and their first degree relatives -45 siblings, 60 children, 9 parents and 31 partners--lipoprotein (a) levels by the ELISA method as well as some other lipids, lipoproteins and apoproteins were assessed and compared with two control groups (I and II) of healthy subjects with a negative family history of early atherosclerosis. The lipoprotein (a) levels were significantly higher not only in probands, as compared with the control group I (27.4 +/- 30.7 x 16.0 +/- 18.9; p < 0.05, Mann Whitney U-test) but also in their children when compared with control group II (28.1 +/- 31.9 x 12.5 +/- 16.3; p < 0.05). The lipoprotein (a) levels did not correlate with age, there was, however, a significant positive correlation with total cholesterol (r = 0.2244, p < 0.01), LDL-cholesterol (r = 0.2834, p < 0.0001) and apolipoprotein B (r = 0.1759, p < 0.05) when Spearman's correlation coefficient was used. Familial dyslipidaemia Lp (a) defined as lipoprotein (a) higher than 25 mg/dl (or 30 mg/dl resp.) at least in two close relatives in one family was found in 27% (and 21.6%) evaluated families (10/37 and 8/37 resp.). "Risk" levels of lipoprotein (a) > 25-30 mg/dl were found most frequently in combination with other types of hyperlipoproteinaemia--in subjects with types IIa and IIb, in families in combination with familial combined hyperlipidaemia. The results indicate that "risk" levels of lipoprotein (a) are a frequent genetically conditioned metabolic disorder in patients with premature ischaemic cerebrovascular attacks.
Adult↗
The case against thiomersal.
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Blepharitis↗
Role of cell-mediated immunity to staphylococci in blepharitis.
We studied cell-mediated immunity to staphylococcal antigens in 116 patients with chronic blepharitis and eight normal subjects. Antibodies in tears and blood were measured. Enhanced cell-mediated immunity to Staphylococcus aureus was demonstrated in 46 of 116 patients (40%) in the absence of antibodies to teichoic acid but not among normal subjects. Symptoms of grittiness and morning stickiness were more frequent among patients without enhanced responses. Folliculitis occurred more commonly among patients with enhanced immunity. Marginal keratitis occurred equally among patients with and without enhanced systemic immunity, but patients with enhanced response more commonly required topical corticosteroid therapy. Desensitization to staphylococcal antigens could be investigated as a potential therapeutic approach in selected patients.
Adult↗
Microbial keratitis--the false negative.
The investigation of presumed microbial keratitis includes microscopy and culture of corneal specimens obtained by scraping the infiltrated cornea. Routine microscopy fails to identify the infecting organism in about 15% of cases. We discuss the problems presented by 20 such eyes which required further investigation. We present a diagnostic algorithm aimed at reducing the delay in identifying the pathogen and increasing the rate of positive culture. This is important since unusual pathogens may require treatment with drugs other than the 'first line' broad spectrum combination of an aminoglycoside and a cephalosporin. The algorithm allows sequential restaining and reculturing of specimens for more thorough investigation. In addition to the use of special stains and culture conditions, it presents indications for further corneal scrapes and biopsies. Uncontrolled infection resulted in five perforations and penetrating keratoplasty was indicated in 11 cases. The visual outcome for these patients was poor with fewer than 30% achieving 6/12 acuity. The delay in diagnosis increases morbidity and this should be significantly reduced by adopting the algorithm we propose.
Adult↗
Cefazolin levels after intravitreal injection. Effects of inflammation and surgery.
Cefazolin (2.25 mg) was injected into the vitreous cavity of phakic, aphakic, and aphakic/vitrectomized rabbits; inflamed eyes were compared to controls. Vitreous levels of cefazolin were determined at selected times from 2 to 48 hr, and the half-life was calculated. The effect of inflammation was to increase the half-life or to reduce the rate of elimination of cefazolin from the vitreous cavity. The drug was cleared substantially faster from aphakic/vitrectomized eyes than from phakic or aphakic eyes. Vitreous levels of cefazolin were above the MIC for most common gram-positive organisms causing endophthalmitis in all study groups at 24 hr, but in only the phakic inflamed eyes and in the aphakic eyes with intact vitreous at 48 hr.
Animals↗
Role of staphylococcal toxin production in blepharitis.
Lid isolates of Staphylococcus aureus and coagulase-negative staphylococci (CNS) from controls (12 S. aureus and 110 CNS) and from patients with blepharitis (17 S. aureus and 171 CNS) were tested for production of alpha, beta, delta, epsilon, and previously undescribed hemolytic toxins, because toxin production has been implicated as a cause of blepharoconjunctivitis. The electrolyte content of agar media required for toxin production was first investigated. Alpha-lysin was found to be produced by all isolates of S. aureus colonizing lids of normal controls and patients with blepharitis, but by none of 281 CNS isolates. A new toxin was identified, having low molecular weight (5 kd), produced by one CNS strain isolated from a blepharitic lid. It was produced on basic nutrient agar that lacked sodium but contained glucose, which inhibited production of alpha-lysin. It hemolyzed rabbit and sheep erythrocytes and, surprisingly, was neutralized by polyclonal antiserum to alpha-lysin. This may explain occasional reports of alpha-lysin production by CNS. The overall results do not support a hypothesis of hemolytic toxin production by staphylococci as a general cause of blepharitis.
Bacterial Toxins↗
Acanthamoeba keratitis--resistance to medical therapy.
Successful medical therapy of Acanthamoeba keratitis has been reported with combination therapy; topical Brolene and neomycin. Resistance has not so far been identified as a problem, but was the basis for recurrent disease observed in a patient with bilateral infection. Eradication of amoebae was finally achieved following prolonged topical therapy and two corneal grafts in each eye. Topical anti-amoebic therapy with paromomycin, benzethonium chloride, clotrimazole and R11/29 (a phenanthridinium compound), was continued for three months post-operatively. No further recurrences occurred during 14 months' follow-up. Drug sensitivities were performed for three isolates of Acanthamoeba sp (group II) which demonstrated the development of resistance to Brolene and arsenic. In addition, the resistant isolates were temperature-sensitive mutants which would not grow at temperatures above 30 degrees C. This could explain 'culture-negative' results in some cases of clinical recurrence when incubation of laboratory samples had only been performed at 37 degrees C.
Acanthamoeba Keratitis↗