Archive December 2018

Systemic Corticosteroid: Uses, Mechanism of Action and Side-effects

<h1>Systemic Corticosteroid: Uses, Mechanism of Action and Side-effects</h1>

Systemic Corticosteroid: Uses, Mechanism of Action and Side-effects

Systemic corticosteroid
Author: Dr Amanda Oakley, Dermatologist, Hamilton, New Zealand, 1997. Updated February 2016.
What is a systemic corticosteroid?
A corticosteroid taken by mouth or given by intramuscular injection is often called a systemic steroid. Systemic steroids are synthetic derivatives of the natural steroid, cortisol, produced by the adrenal glands, and have profound anti-inflammatory effects.
Systemic (cortico)steroids are also called glucocorticoids or cortisones. They include:
Prednisone Prednisolone Methylprednisolone Beclomethasone Betamethasone Dexamethasone Hydrocortisone Triamcinolone. Prednisone and prednisolone are equivalent, and are the most commonly prescribed oral corticosteroids for inflammatory skin diseases. Oral prednisone is the most commonly prescribed systemic steroid in New Zealand.
Fludrocortisone is predominantly a mineralocorticoid and its anti-inflammatory effects are minimal.
What is prednisone used for in dermatology?
Prednisone is used for a few days (short-term) to indefinitely (long-term) in a wide variety of skin conditions including:
Eczema/dermatitis Autoimmune bullous diseases Lupus erythematosus Sarcoidosis Vasculitis Systemic steroids are best avoided in patients with psoriasis.
How does a systemic steroid work?
Systemic steroids work in the same way as natural cortisol. Natural cortisol has important effects in the body, including regulation of:
Protein, carbohydrate, lipid and nucleic acid metabolism Inflammation and immune response Distribution and excretion of water and solutes Secretion of adrenocorticotrophic hormone (ACTH) from the pituitary gland. How do systemic steroids differ?
Systemic steroids differ in dose, mineralocorticoid potency, half-life (duration of action) and how effectively they suppress the hyphothalamic-pituitary-adrenal (HPA) axis (suppression leads to reduced production of natural cortisol).
What is the usual dose of prednisone?
Generally, a higher dose of prednisone, such as 40–60 mg daily, is prescribed at first, to gain control of the skin condition. In 2–4 weeks, the dose is reduced.
Prednisone is best taken as a single dose in the morning, which is thought to reduce steroid-induced suppression of the pituitary-adrenal axis compared to evening dosing.
The maintenance dose should be kept as low as possible to minimise adverse effects.
Steroid dose is commonly characterised as:
Low dose, eg 20mg/day of prednisone, sometimes more than 100 mg/day Treatment for less than one month is considered short-term treatment. Corticosteroids for a few days or weeks are relatively safe when prescribed for acute dermatitis. Treatment continuing for more than 3 months is regarded as long term, and results in the majority of undesirable side effects.
What are the side effects and risks of short-term systemic steroid?
Side effects are rarely serious if a systemic steroid has been prescribed for one month or less. The following problems may arise, particularly when higher doses are taken:
Sleep disturbance Increased appetite Weight gain Increase in postprandial blood sugar Psychological effects, including increased or decreased energy. Rare and potentially serious side effects of a short course of corticosteroid include:
Severe infection Mania, psychosis, delirium, depression with suicidal intent Heart failure Peptic ulceration Diabetes mellitus Avascular necrosis of the hip. The risk of a serious side effect increases with increasing dose.
What are the side effects and risks of long-term systemic steroid?
Nearly everyone on a systemic steroid for more than a month suffers from some adverse effects, depending on daily dose and how long they have been on the drug. The main concerns are infections , hypertension, diabetes, osteoporosis, avascular necrosis, myopathy, cataracts, and glaucoma. The list that follows is incomplete.
Cutaneous adverse effects
Cutaneous adverse effects from long-term systemic steroids may include:
Bacterial infections: cellulitis, wound infection Fungal infections: tinea, candida, pityriasis versicolor Viral infections: herpes zoster Skin thinning, purpura, fragility, telangiectasia and slow wound healing, especially in sun-damaged areas Stretch marks (striae) under the arms and in the groin Steroid acne Hypertrichosis and hair loss. Adverse effects of systemic steroids
Easy bruising
Moon face
Skin thinning
Fragile skin
Acne
Effects on body fat
Redistribution of body fat: moon face, buffalo hump, truncal obesity Weight gain: increased appetite and food intake Effects on the eye
Glaucoma Posterior subcapsular cataracts; children are more susceptible than adults Eyelid oedema and exophthalmos Central serous chorioretinopathy Vascular disease
Hypertension Ischaemic heart disease Stroke and transient ischaemic attack (TIA) The effects of systemic steroids on atherosclerotic vascular disease may be due to complex metabolic changes, including:
Hyperlipidaemia Peripheral insulin resistance and hyperinsulinaemia. Gastrointestinal tract
Dyspepsia, gastritis, peptic ulceration and perforation of the gut, especially in patients also taking non-steroidal anti-inflammatory drugs Acute pancreatitis Fatty liver Fluid balance Sodium and fluid retention cause leg swelling and weight increase Potassium loss causes general weakness Reproductive system
Irregular menstruation Hirsutism Lowered fertility in men and women Possible fetal growth retardation in women taking prolonged courses of steroids during pregnancy Breast feeding can usually continue but infant should be monitored for adrenal suppression if mother on > 40 mg prednisone daily Musculoskeletal system
Bone fracture Osteoporosis Osteonecrosis, especially hip Myopathy affecting shoulders and thighs Tendon rupture Growth restriction in children Osteoporosis is particularly common in smokers, postmenopausal women, the elderly, underweight or immobile, and patients with diabetes or lung problems. Osteoporosis may result in fractures of the spine, ribs or hip joint with minimal trauma. These occur after the first year in 10–20% of patients treated with more than 7.5 mg prednisone daily. It is estimated that up to 50% of patients on long-term prednisone will develop bone fractures. Vertebral fractures are more common in patients on steroids, even in those with normal bone density.
Nervous system
Psychological effects: mood changes, increased energy, excitement, euphoria, agitation Less often: hypomania, psychosis, delirium, memory loss, depression, anxiety, personality change Insomnia and sleep disturbance Shakiness and tremor Headaches Metabolic effects
Transient or persistent diabetes in previously non-diabetic patients Higher blood sugar levels in patients with diabetes mellitus Cushing syndrome Immune response
Raised neutrophil and total white cell count are usual on prednisone Impaired innate and acquired immunity Increased susceptibility to tuberculosis Increased severity of measles, varicella Reduced efficacy and increased risk of vaccines Live vaccines such as polio or MMR (measles, mumps, rubella) should not be given to patients taking ≥ 20 mg prednisone daily. It is safe and advisable to have other routine immunisations, such as annual influenza vaccination.
Risks during intercurrent illness or surgery
Significant intercurrent illness, trauma, or surgical procedure requires a temporary increase in corticosteroid dose, or if already stopped, a temporary re-introduction of corticosteroid treatment for up to twelve months after the steroids are stopped.
Patients who have taken ≥10 mg prednisone daily within 3 months of surgery requiring a general anaesthetic are advised to tell their anaesthetist so that intraoperative intravenous hydrocortisone can be added.
Effects of reducing the dose of systemic steroid
No tapering is necessary if a course of prednisone has been for less than one to two weeks. Steroid should be withdrawn slowly after longer courses, to avoid acute adrenal insufficiency, particularly if the medication has been taken for several months or longer.
Side effects from reducing prednisone may include:
Fever Hypotension Tiredness Headaches Muscle and joint aches Weight loss Depression Rhinitis Conjunctivitis Painful itchy skin nodules. Hypopituitary-pituitary-adrenal (HPA) axis suppression can persist for months or years after steroids are stopped.
Monitoring during steroid treatment
Regular monitoring during treatment with systemic steroid may include:
Blood pressure Body weight Blood sugar Patients on prednisone should be advised to avoid non-steroidal anti-inflammatory drugs and licorice.
Prevention of osteoporosis
Bone density scans should be considered for patients that have taken or are expected to take 7.5 mg or more of prednisone each day for three months or longer. Baseline fracture risk can be estimated from T-scores.
Current recommendations are:
Bisphosphonate therapy (alendronate, etidronate, zolidronic acid) for individuals with femoral T-scores <-2.5. It reduces fracture risk by half. Smoking cessation Balanced diet, aiming for healthy body weight Minimal alcohol Regular weight-bearing exercise Consider risk of falling and its mitigation Calcium, vitamin D and oestrogen are no longer recommended for prophylaxis of osteoporosis, as adverse events outweigh benefit.
Source

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Not so great report – Ulcerative Colitis

<h1>Not so great report – Ulcerative Colitis</h1>

Not so great report – Ulcerative Colitis

I had a great day on Saturday after seeing a pretty big blood clot on Friday afternoon, but Sunday night things went south pretty dramatically. Lots of bleeding, horror show in the toilet bowl, so I went to my doctor today and had a long talk about what the heck is going on. He did another look and said what he can see looks the same as when I was in on Thursday, but the clots are worrisome. He said if they get worse go to the hospital. Of course he leaves the country for a month on Thursday, but is sending my chart to his on call doctor with notes to see me ASAP if I call.
We established a few things, some I like, some I don’t:
1- this flare up is worse than he thought and perhaps a higher dose to start might have been better, although he is super conservative with prednisone.
2- I have to go up to 30 mg of pred for a week and taper slowly a week at a time so that I am on 15 mg for my scope scheduled for January 8.
3- I was worried that I have become steroid dependent. He said it is too soon to tell, do you guys have any thoughts on this? Every time I hit 15 mg the bleeding comes back, and each time it is worse. My doctor says he has seen this before and I just need to be patient.
4- I asked about not responding to 5ASA’s any more, he said that he thinks this is just a flare up, not to worry. We would know more after my scope and then we can talk about meds again.
5- I asked about moving my care to and IBD center a bit over an hour from my house, he said we should talk after my scope, but that he would be ok sending my info there if things looked bad, but if they didn’t, they wouldn’t take me because they generally only treat the “more difficult” cases.
That being said, my face is huge! I am so sick of pred, I have been on it since November 2, starting at 20 and moving down to 15, only to go higher. It is making me nuts. Any tips on surviving another round of this evil drug? I made an appointment with my eye doctor because my eyes feel really scratchy and irritated, I’m sure this isn’t a good thing. Thanks for your sage advice and support as always.
Current meds because my signature isn’t right: 30 mg of pred, 4 shire generic lialda, VSL #3, culturelle and reuteri.

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<h1></h1>

naturalcurl said…
Is it possible to achieve symptom-free long lasting remission just from pred and the usual mild maintenance drugs? I have been thinking of steroids as a temporary rescue.
Yes it is possible. But in the end, it really comes down to:
1.) “Is this a run-of-the-mill-flare?”
or
2.) “Is this disease progression in extent or severity?”.
A short course of pred will solve scenario #1, but NOT #2. In scenario #2, you end up regressing to a flare during a taper due to a stronger maintenance dosage/meds being needed to kick the pred to the curb.
The idea on #1, is that if you can cease the immune attack for approximately 2 months via prednisone, that seems to shut off the immune attack mode, and put it back into a quiescent/quiet/remission state. And you can continue with a remission without the pred. If you’re not sure whether you’re a scenario #1 or #2, then a short course of pred and taper can answer it definitively.
If you’re on the fence about humira, then asking for endoscopy (that is a colonoscopy or a flexible-sigmoidoscopy) beforehand can help justify whether it is necessary or not.
When deciding whether to take pred, I always ask which is worse the pred side effects or my UC side effects? The times I’ve taken pred I was near incontinent, going 24+ times a day, and in pain. Taking pred then was a no-brainer, and I took it with a smile on my face. If you’re 3-4 bms a day with minor inconvenience from your UC, pred is likely a firm no (I’d consider steroid enemas or Uceris pills/foam before going the pred route in this scenario). Pred is like the biggest weapon in your arsenal, as you use it cautiously only when nothing else works, things are FUBAR, and there’s no other way out of that situation.

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Recombinant Human Endostatin Market Potential Growth By Leading Companies Pfizer Inc., Novus Biologicals, Biocon, Thermo Fisher Scientific, Yantai Medgenn Ltd., FUJIFILM KYOWA KIRIN BIOLOGICS Co.

<h1>Recombinant Human Endostatin Market Potential Growth By Leading Companies Pfizer Inc., Novus Biologicals, Biocon, Thermo Fisher Scientific, Yantai Medgenn Ltd., FUJIFILM KYOWA KIRIN BIOLOGICS Co.</h1>

Recombinant Human Endostatin Market Potential Growth By Leading Companies Pfizer Inc., Novus Biologicals, Biocon, Thermo Fisher Scientific, Yantai Medgenn Ltd., FUJIFILM KYOWA KIRIN BIOLOGICS Co.

Press release from: Coherent Market Insights Recombinant Human Endostatin Market Increasing research and development activities for identifying potential uses of recombinant human endostatin is expected to propel growth of the market. For instance, according to a paper published in the journal Nature, September 2015, a study was conducted to evaluate effects of recombinant human endostatin in combination with radiotherapy for treating esophageal squamous cell carcinoma and to discover its potential mechanisms. These findings suggested that recombinant human endostatin is a potential anti-angiogenic agent in esophageal squamous cell carcinoma mainly when combined with radiotherapy.Download PDF Brochure of Research Report @ www.coherentmarketinsights.com/insight/request-pdf/2262 Furthermore, according to National Center for Biotechnology Information (NCBI) January 2017, recombinant human endostatin in combination with Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone (CHOP) may aid in treatment of Angioimmunoblastic T Cell Lymphoma (AITL), a form of Peripheral T Cell Lymphoma (PTCL). Such novel therapies for PTCL treatment are immediately desired to improve the outcomes of patients with this disease. These factors are expected to propel growth of the recombinant human endostatin market.Endostatin is a protein located in most Basement Membranes (BMs) in the body such as vascular basement membranes. A number of clinical studies have validated the significant survival benefits of recombinant human endostatin in treating late stage Non-Small-Cell Lung Carcinoma (NSCLC). Therefore, recombinant human endostatin (Endostar) was approved by the State Food and Drug Administration of China (CFDA) in September 2005, for the treatment of NSCLC. Endostatin is expressed in various organs, with the highest levels in liver, lung, and kidney.Market DriversGovernment initiatives to reduce prices of anticancer drugs is expected to drive growth of the recombinant human endostatin market during the forecast period. For instance, in August 2018, Government of China took initiatives to reduce prices of anticancer drugs by 44%. Chinese National Health and Family Planning Commission organized a national-wide drug price and reimbursement drug list negotiation, in which a total of 39 products have been successfully added including recombinant human endostatin.Market RestraintIncreasing challenges in significant production of recombinant human endostatin is expected to hinder the market growth. For instance, in April 2017, according to a National Center for Biotechnology Information (NCBI) report, tumor treatment needs large quantities of biologically active recombinant human endostatin, which in turn requires production of large quantities of recombinant human endostatin. This process is difficult as it based on recombinant DNA technology and also have low success rates for the treatment of cancer. Furthermore, the cost of recombinant human endostatin is high and it has short half-life. Endostatin is unstable since, endostatin-purification process may denature its structure and the resultant yields may be low.The major players operating in the recombinant human endostatin market include;* Pfizer Inc.,

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Dexamethasone Intravitreal Implant (Ozurdex) for Long-Term Macular Edema after Epiretinal Membrane Peeling Surgery

<h1>Dexamethasone Intravitreal Implant (Ozurdex) for Long-Term Macular Edema after Epiretinal Membrane Peeling Surgery</h1>

Dexamethasone Intravitreal Implant (Ozurdex) for Long-Term Macular Edema after Epiretinal Membrane Peeling Surgery

Research Article Dexamethasone Intravitreal Implant (Ozurdex) for Long-Term Macular Edema after Epiretinal Membrane Peeling Surgery
1 Department of Ophthalmology, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan 2 Department of Ophthalmology, School of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan 3 Department of Ophthalmology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan 4 Department of Ophthalmology, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung 81267, Taiwan
Correspondence should be addressed to Wen-Chuan Wu ;
Received 17 June 2018; Revised 7 November 2018; Accepted 15 November 2018; Published 10 December 2018
Academic Editor: Elad Moisseiev
Copyright © 2018 Yo-Chen Chang et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract
Purpose . To investigate the functional and anatomical outcome of the 0.7 mg dexamethasone (Ozurdex) intravitreal implant (IVD) in eyes with long-term macular edema after macular epiretinal membrane removal. Methods . We enrolled 40 eyes with persistent macular edema at least 12 months after epiretinal membrane removal. Twenty eyes in the IVD group received IVD and the other 20 eyes were in the control group. The main outcome measures were change in best-corrected visual acuity (BCVA) and central foveal thickness (CFT). Results . For eyes in the IVD group, the mean BCVA improved by 3.45 lines to 0.47 logMAR one month after IVD. However, the mean BCVA improved by only 0.14 lines to 0.74 logMAR at the same time in eyes in the control group. Six months later, the mean BCVA improved to 0.31 and 0.74 logMAR in the IVD and control groups, respectively. In the IVD group, the mean CFT decreased rapidly by 116.8  μ m to 333.9  μ m one month after IVD. Thereafter the CFT decreased at a slower pace. In the control group, the CFT remained static during the follow-up period. However, in the IVD group, 6 months after IVD, the CFT seemed to have a tendency to increase. Conclusions . Single IVD could significantly decrease macular edema and improve visual outcome for eyes with persistent long-term macular edema after macular ERM removal and the effect can be sustained as long as 6 months after the initial injection. However, in order to maintain the visual and anatomical outcome, repeat IVD might be considered if macular edema recurs. 1. Introduction
Idiopathic epiretinal membrane (ERM) is a degenerative disorder occurring in the vitreomacular interface that usually affects the central vision in the affected eye [ 1 ]. The manifestation of an ERM can range from asymptomatic to photopsia, metamorphopsia, macropsia or micropsia, decreased visual acuity (VA), and even central vision loss. In 1978, Dr. Machemer first described pars plana vitrectomy (PPV) with membrane peeling for ERM. Since then this surgery has become a well-established method for the removal of ERM with good results [ 2 ]. Surgical removal of the membrane in patients with significant symptoms can improve visual acuity and reduce metamorphopsia in approximately 70% of cases [ 3 – 5 ]. However, persistent residual intraretinal edema is sometimes still present, limiting the possibilities of complete visual function recovery [ 6 , 7 ]. From our previous study, stable vision is usually achieved approximately 9 months after PPV, and intravitreal injection of bevacizumab cannot further improve the final visual and anatomical outcome [ 8 ]. Therefore, vascular endothelial growth factor (VEGF) might play a minor role in the pathogenesis of persistent macular edema after ERM peeling. In addition to VEGF, inflammatory trauma by mechanical membrane peeling might be associated with postoperative macular edema [ 9 , 10 ]. To further reduce macular edema, intravitreal injection of triamcinolone acetonide (IVTA) after the removal of the ERM has been shown to facilitate fluid absorption and may speed up improvement of the anatomic and functional outcome in short-term follow-up [ 11 ]. The possible reason for the short-term effect of intraoperative IVTA might be explained by the relatively rapid clearance in vitrectomized eyes, which may abate its effect for macular edema [ 12 , 13 ]. Therefore, there may be a rationale for using a sustained-release device to improve this condition. The dexamethasone intravitreal implant (IVD) (Ozurdex; Allergan, Irvine, CA) provides a slow release and stable dose of steroid [ 14 ]. IVD has been widely used for treating noninfectious posterior uveitis, macular edema secondary to retinal vascular occlusion (RVO), diabetic macular edema (DME), and cystoid ME (CME) after cataract surgery [ 15 – 17 ]. Therefore, in our present study, we tried to determine the efficacy of the 0.7 mg dexamethasone intravitreal implant to treat long-term persistent macular edema (no tendency to resolve at least 12 months after surgery) after removal of idiopathic ERM. 2. Patients and Methods
This is a retrospective, nonrandomized study including patients who were diagnosed with idiopathic ERM between January 2014 and June 2015. This study followed the tenets of the Declaration of Helsinki in 1964. All operations were performed by the same physician (W. C. W.) who is a retinal specialist experienced in vitreoretinal and cataract surgery as well as intravitreal injection. The surgical procedure and postoperative medication were using the methods as described previously [ 8 ]. All patients previously underwent standard three-port transconjunctival 25-gauge PPV assisted with triamcinolone for membrane peeling and indocyanine green (ICG) for internal limiting membrane (ILM) peeling using high-magnification viewing lens and intraocular forceps. PVD was induced with active suction of ocutome over the optic disc if the PVD was not already present. Concomitant cataract surgery was performed on phakic patients. At the end of surgery, all patients received a subconjunctival injection of 2 mg Rinderon (betamethasone 4 mg/mL). After surgery, Tobradex eye drops (0.3% tobramycin and 0.1% dexamethasone) 4 times daily, Acular eye drops (ketorolac 0.4%) 3 times daily, and Mydriacyl (0.5% tropicamide) 3 times daily were administered to all patients for 2 weeks. Then, the Tobradex eye drops were switched with Sinomin eye drops (4% sulfamethoxazole) and 0.1% fluorometholone 4 times daily during the follow-up period. In addition, Acular eye drops (ketorolac 0.4%) three times daily were prescribed for patients who had macular edema during the follow-up period. There were no significant complications such as rupture of posterior capsule, retinal detachment, iatrogenic macular hole, postoperative vitreous hemorrhage, or endophthalmitis that affected visual outcome during or after surgery.
At least twelve months after PPV, patients who met the following criteria were selected for intravitreal injection of dexamethasone (IVD) treatment: (1) presence of macular edema ≥300  μ m as detected by optical coherence tomography (OCT) and (2) best-corrected visual acuity (BCVA) of 20/40 or less after surgery [ 8 ].
Patients with preexisting ocular diseases (i.e., chronic inflammatory or neoplastic disorders, retinal vascular occlusion glaucoma, or high myopia) were excluded, as well as those with systemic diseases (uncontrolled hypertension or diabetes).
After a complete discussion of the benefits, risks, and alternative treatment, the decision to treat with IVD was made by the eligible patients themselves. If the patient decided to proceed with IVD, a consent form had to be signed by the patient before treatment. In the IVD group, each patient received an intravitreal injection of the 0.7 mg dexamethasone intravitreal implant at least 12 months after PPV. Postoperatively, gentamycin eye drops were administered 4 times daily for 1 week. Meanwhile, those eligible patients who refused IVD were enrolled in the control group.
In order to compare the parameters between the IVD group and the control group, we defined “baseline” as the time point of (1) receiving IVD that was at least 12 months after PPV for patients in the IVD group and (2) the patient deciding not to receive IVD (at least 12 months after PPV for patients in the control group). The treated patients in the IVD group were seen at 1 week after baseline for check-up of injection wound and intraocular pressure. To evaluate the effects and safety of treatment, all recruited patients in both groups underwent comprehensive ophthalmic examinations including visual acuity by Snellen charts, slit-lamp biomicroscopy, Goldmann applanation tonometry, and ophthalmoscopy at 1, 2, 3, and 6 months after baseline. Measurements of macular thickness were performed using the spectral-domain-OCT (SD-OCT [Heidelberg Retina Angiograph 2, Heidelberg Engineering, Heidelberg, Germany]). In all measurements, the central foveal thickness (CFT) was assessed within a 1 mm diameter circle in the central macula. For better comparison of visual acuity between the groups, the visual acuity by Snellen chart was converted to the logarithm of the minimum angle of resolution (logMAR) at baseline and each follow-up visit. 2.1. Statistical Analysis
All data were statistically analyzed by Student’s t -test or the χ 2 test using SPSS statistical software (version 24.0; SPSS Inc., Chicago, Ill., USA). A value of <0.05 was considered statistically significant. 3. Results 3.1. Baseline Demographic Data
During the period of one and half years, we reviewed a total of 400 eyes of 360 patients with idiopathic ERM who underwent PPV and ERM peeling (Table 1 ). There were 40 eyes of 40 patients who met the inclusion criteria. Table 1 shows the baseline demographics of these 40 patients. Both the IVD group and the control group consisted of twenty eyes. Patients in both groups were followed-up for at least 12 months after baseline. The mean interval from PPV to IVD was 58.8 ± 4.0 weeks (range: 53 to 66 weeks) in the IVD group and the mean interval from PPV to baseline was 57.7 ± 4.0 weeks (range: 52 to 66 weeks). The mean BCVA before PPV was 0.81 ± 0.30 in the IVD group and 0.75 ± 0.38 logMAR in the control group. Combined phacoemulsification with intraocular lens implantation, PPV, and membrane peeling were performed for 8 eyes in the IVD group and 10 eyes in the control group. The remaining 12 pseudophakic eyes in the IVD group and 10 pseudophakic eyes in the control group received PPV and membrane peeling only. At baseline, the SD-OCT measured mean CFT was 450.7 ± 72.4  μ m in the IVD group and 466.2 ± 82.8  μ m in the control group. Table 1: Patient demographics at baseline. 3.2. Temporal Change of CFT
All patients in the IVD group received single IVD. Compared to baseline, the mean CFT at 1 month after IVD decreased rapidly by 116.8 ± 49.7 to 333.9 ± 50.9  μ m for the IVD group and by only −1.3 ± 10.6 to 464.9 ± 76.8  μ m for the control group ( between the IVD and control groups) (Figure 1 ). Thereafter, the CFT in the IVD group decreased at a slower rate. The CFT in the control group remained static during the follow-up period. At 6 months, the mean CFT decreased by 110.7 ± 54.1 to 340.0 ± 53.1  μ m for the IVD group and by only 0.85 ± 8.2 to 467.0 ± 79.8  μ m for the control group ( between the IVD and control groups). The mean reduction in CFT differed significantly between the IVD and control groups at 1, 2, 3, and 6 months after baseline ( ). However, 6 months after baseline, the CFT in the IVD group seemed to have a tendency to increase. For eyes that received combined surgery (8 eyes in the IVD group and 10 eyes in the control group), the mean CFT in the IVD group improved from 442.3 ± 40.6  μ m at baseline to 343.0 ± 59.2  μ m at 6 months ( ). However, the mean CFT in the control group was 478.2 ± 97.8 at baseline and 480.5 ± 93.0 at 6 months ( ). Preoperative pseudophakic eyes that received PPV and membrane peeling (12 eyes in the IVD group and 10 eyes in the control group), the mean CFT in the IVD group improved from 456.1 ± 89.0  μ m at baseline to 337.9 ± 51.2  μ m at 6 months ( ). However, the mean CFT in the control group was 454.1 ± 67.8 at baseline and 453.5 ± 66.2 at 6 months ( ). Figure 1: Temporal change of central foveal thickness (CFT) after IVD. Compared to baseline, the mean CFT at 1 month after IVD decreased rapidly by 116.8 ± 49.7 to 333.9 ± 50.9  μ m for the treatment group and by only −1.3 ± 10.6 to 464.9 ± 76.8  μ m for the control group ( between the IVD and control groups). Thereafter, the CFT in the IVD group decreased at a slower rate. The CFT in the control group remained static during the follow-up period. At 6 months, the mean CFT decreased by 110.7 ± 54.1 to 340.0 ± 53.1  μ m for the treatment group and by only 0.85 ± 8.2 to 467.0 ± 79.8  μ m for the control group ( between the IVD and control groups). compared to baseline. 3.3. Temporal Change of Visual Acuity
At baseline, the mean BCVA was 0.81 ± 0.30 and 0.75 ± 0.38 logMAR in the IVD and control groups, respectively ( ) (Figure 2 ). In the IVD group, the BCVA improved significantly after baseline. At 1 month, the mean BCVA had increased dramatically by 3.45 ± 2.29 and only 0.14 ± 0.66 lines from baseline in the IVD and control groups, respectively ( ). Thereafter, the BCVA in the IVD group continued to improve at a slower rate compared to stable BCVA in the control group. At 6 months, the mean BCVA had increased by 5.0 ± 2.77 lines to 0.31 ± 0.22 logMAR and only 0.14 ± 0.66 lines to 0.74 ± 0.36 logMAR from baseline in the treatment and control groups, respectively ( ). After baseline, the logMAR BCVAs and line improvement were significantly better in the IVD group than in the control group and differed significantly at each follow-up. For eyes that received combined surgery (8 eyes in the IVD group and 10 eyes in the control group), the mean BCVA in the IVD group improved from 0.74 ± 0.27 logMAR at baseline to 0.23 ± 0.22 logMAR at 6 months ( ). However, the mean BCVA in the control group was 0.70 ± 0.27 at baseline and 0.68 ± 0.24 at 6 months ( ). For preoperative pseudophakic eyes that received PPV and membrane peeling (12 eyes in the IVD group and 10 eyes in the control group), the mean BCVA in the IVD group improved from 0.86 ± 0.31 logMAR at baseline to 0.36 ± 0.22 logMAR at 6 months ( ). However, the mean BCVA in the control group was 0.80 ± 0.47 at baseline and 0.79 ± 0.46 at 6 months ( ). Figure 2: Temporal change of BCVA by line and mean BCVA after IVD. At 1 month after IVD, the mean BCVA had improved dramatically by 3.45 ± 2.29 and only 0.14 ± 0.66 lines from baseline in the IVD and control groups, respectively ( , IVD vs. control). Thereafter, the BCVA in the IVD group continued to improve at a slower rate compared to stable BCVA in the control group. At 6 months after IVD, the mean BCVA had increased by 5.0 ± 2.77 lines to 0.31 ± 0.22 logMAR and only 0.14 ± 0.66 lines to 0.74 ± 0.36 logMAR from baseline in the IVD and control groups, respectively ( ). The logMAR BCVAs and line improvement differed significantly at 1, 2, 3, and 6 months after treatment between the two groups. compared to baseline. 3.4. Intraocular Pressure
In the IVD group, three patients (15%) experienced IOP elevations of 10 mm Hg or more from baseline at 1 month postoperatively. These three patients receiving single topical anti-glaucoma medication and no IOP elevation were noted at the 2-, 3-, or 6-month follow-up visits. No new IOP-lowering medication was required in any patients at the time of the latest follow-up. In the control group, none of the patients experienced IOP elevations of 10 mm Hg or more from baseline at any follow-up visit. 3.5. Case Presentation
Figure 3 represents OCT images of the pre- and postoperative course of the eye that suffered from long-term persistent macular edema after ERM and ILM peeling. The preoperative OCT image showed prominent ERM overlying the macular surface, the CFT was 436  μ m and the BCVA was 20/100 (Figure 3(a) ). Thirteen months after operation, no ERM was noted, but the BCVA was still 20/100 with the CFT of 449  μ m (Figure 3(b) ). One month after IVD, the CFT decreased to 350  μ m and the BCVA improved to 20/30 (Figure 3(c) ). Three months after IVD, the CFT further decreased to 290  μ m and the BCVA improved to 20/22 (Figure 3(d) ). Six months after IVD, the CFT was 306  μ m and the BCVA maintained at 20/22 (Figure 3(e) ). Figure 4 represents OCT images of the pre- and postoperative course of the eye that suffered from more long-term persistent macular edema after ERM and ILM peeling. The preoperative OCT image showed prominent ERM overlying the macular surface, the CFT was 656  μ m and the BCVA was 20/400 (Figure 4(a) ).Thirty-six months after operation, no ERM was noted, but the BCVA only improved to 20/200 with the CFT of 422  μ m (Figure 4(b) ). One month after IVD, the CFT decreased to 407  μ m and the BCVA improved to 20/22 (Figure 4(c) ). Three months after IVD, the CFT slightly decreased to 398  μ m and the BCVA maintained at 20/22 (Figure 4(d) ). Six months after IVD, the CFT was 385  μ m and the BCVA further improved to 20/20 (Figure 4(e) ). Figure 3: Pre- and postoperative OCT findings in a patient with long-term persistent macular edema after membrane peeling and internal limiting membrane peeling. Preoperative image shows an ERM overlying the macula. The CFT and BCVA were 436  μ m and 20/100, respectively (a). Thirteen months after operation, no ERM or ILM was noted but the BCVA was still 20/100 with the CFT of 449  μ m (b). At one month after IVD, the CFT decreased to 350  μ m and the BCVA improved to 20/30 (c). At three months after IVD, the CFT decreased to 290  μ m and the BCVA improved to 20/22 (d). Six months after IVD, the CFT was 306  μ m and the BCVA maintained at 20/22 (e). Figure 4: Pre- and postoperative OCT findings in a patient with more long-term persistent macular edema after membrane peeling and internal limiting membrane peeling. The preoperative OCT image showed prominent ERM overlying the macular surface, the CFT was 656  μ m and the BCVA was 20/400 (a). Thirty-six months after operation, no ERM was noted, but the BCVA had only improved to 20/200 with the CFT of 422  μ m (b). One month after IVD, the CFT decreased to 407  μ m and the BCVA improved to 20/22 (c). Three months after IVD, the CFT slightly decreased to 398  μ m and the BCVA maintained at 20/22 (d). Six months after IVD, the CFT was 385  μ m and the BCVA further improved to 20/20 (e). 4. Discussion
Pars plana vitrectomy with membrane peeling is a useful technique for patients with symptomatic ERM, and most patients will have a favorable outcome [ 2 – 6 ]. However, visual recovery may take several months to as long as 1 year as the retinal morphology normalizes slowly [ 8 , 18 ]. However, persistent residual intraretinal edema is sometimes still present, limiting the possibility of a complete visual function recovery [ 6 , 7 ]. To date, the mechanism of macular edema in idiopathic ERM has not been fully studied. Ahn et al. hypothesized that the thickening macula in eyes with ERM might be due to traction-induced distortion of the neurosensory retina or macular edema from breakdown of the blood-retinal barrier [ 19 ]. Mandelcorn et al. demonstrated that positive immunostain for VEGF and transforming growth factor-beta (TGF-beta2) were present in 85% of idiopathic ERM specimens [ 20 ]. However, in our previous study, for patients with persistent macular edema after ERM peeling, there were no significant differences of final visual and anatomical outcome between patients with or without bevacizumab injection [ 8 ]. Therefore, bevacizumab might somewhat reduce macular edema by acting as an anti-VEGF agent which is believed to play a minor role in the pathogenesis of postoperative macular thickening [ 11 ].
Harada et al. hypothesized that the release of inflammatory cytokines and growth factors may contribute to ERM proliferation as well as accompanying macular edema in many cases [ 21 ]. Vinores et al. suggested that postoperative macular edema is in part due to breakdown of the blood-retinal barrier, then release of inflammatory cytokines from preoperative mechanical traction, and intraoperative manipulation [ 22 ]. Corticosteroids are very potent anti-inflammatory agents that can block several pathological processes which are thought to be involved in the development of macular edema in several ways: inhibiting the synthesis of VEGF, prostaglandins, and many proinflammatory cytokines, reducing fibrin deposition, preventing leukocyte migration, and stabilizing endothelial cell tight junctions [ 23 ]. However, the type of corticosteroid and administrating route may affect the efficacy to specific diseases. Systemic corticosteroids might cause certain adverse events such as adrenal suppression, Cushingoid state, osteoporosis, and exacerbation of diabetes [ 24 – 27 ]. Topical or local administration usually leads to a suboptimal drug level in the vitreous and may be associated with relatively high systemic concentrations [ 28 – 30 ]. Therefore, direct intravitreal injection of corticosteroids seems to be the better way to achieve optimal drug level in the vitreous.
Dexamethasone is the most water-soluble and also a potent synthetic glucocorticoid. The anti-inflammatory and immunosuppressant activity of dexamethasone is 30 times more than cortisol [ 31 ] and 12.5 times more than triamcinolone [ 32 ]. In addition, the half-life of dexamethasone is the shortest among other steroids and is less likely to aggregate in the trabecular meshwork and therefore cause elevation of intraocular pressure [ 33 ].
The reason for corticosteroids being effective treatment for long-term persistent macular edema after ERM and ILM peeling in the present study remains unclear. The possible explanation may be due to the effects on Müller cells during ERM and ILM peeling. Müller cells, the major type of glial cells in the retina, are responsible for the homeostatic and metabolic support of retinal neurons. While their cell bodies are located in the inner nuclear layer of the retina, they span across the entire retina [ 34 ]. They have been further identified as fundamental to the transmission of light through the vertebrate retina due to their unique funnel shape [ 35 ]. Under certain conditions, a subset of Müller cells may differentiate to neural progenitor/stem cells which regenerate lost photoreceptors and neurons [ 36 ]. During ILM peeling, the Müller cell footplates which build up the outer portions of the ILM might suffer from mechanical damage [ 37 ]. The initial mechanical damage of the retinal surface might be associated with secondary biochemical pathways involving different cytokines and growth factors, which may contribute to the development of diffuse retinal thickening visible on SD-OCT. Therefore, corticosteroids may be able to antagonize the secondary inflammatory effects triggered by the mechanical distortion and thus accelerate the resolution of macular edema, helping the restoration of physiologic function of Müller cells and therefore improving visual function.
From literature review, there were several reports with inconsistent results regarding the effect of the 0.7 mg dexamethasone intravitreal implant of macular edema after ERM peeling surgery [ 38 – 42 ]. Furino et al. reported a single injection of the 0.7 mg dexamethasone intravitreal implant was effective in the treatment of at least 2 months duration of macular edema secondary to combined cataract extraction and vitrectomy for macular pucker removal allowing a stable visual acuity recovery in a small retrospective series of 8 eyes [ 38 ]. Taney et al. reported that four of five eyes showed reduction in macular thickness and visual acuity improved by one or more Snellen lines after dexamethasone intravitreal implant in a small retrospective series of 5 eyes suffering from persistent macular edema after vitrectomy for ERM [ 39 ]. However, both studies were limited by a relatively small sample size and lack of control group. Yonekawa et al. reported that both dexamethasone intravitreal implant and triamcinolone acetonide are effective in improving central macular thickness and visual acuity while the intraoperative dexamethasone intravitreal implant or triamcinolone acetonide is used after vitrectomy and membrane peeling [ 40 ]. However, recently, Guidi et al. reported that the intraoperative sustained-release dexamethasone implant did not result in a significant change in macular thickness and volume compared with the vitrectomy alone without dexamethasone implant at 6-month follow-up [ 42 ]. The possible explanation for their negative results may be due to the timing of intervention. According to our previous study, for patients with idiopathic ERM, stable vision is usually achieved approximately 9 months after PPV and membrane peeling [ 8 ]. Therefore, it is reasonable to hold the IVD until the macular thickening persists at least 9 months postoperatively.
In our present study, compared to patients in the control group, in patients with long-term persistent macular edema after ERM peeling surgery, IVD can both significantly reduce CFT and improve visual acuity after injection, and the effect can last as long as 6 months. There were three patients (15%) among the IVD group experiencing IOP elevations of 10 mm Hg or more from baseline at 1 month postoperatively. The IOP in these 3 patients can be well-controlled by single topical anti-glaucoma medication and no new IOP-lowering medication was required in any patients at the time of latest follow-up.
In summary, the present study showed a single injection of the 0.7 mg dexamethasone intravitreal implant may be effective to improve visual function of patients with long-term (longer than 12 months) persistent macular edema secondary to vitrectomy with membrane and ILM peeling for idiopathic ERM. However, there are some limitations of this study including its retrospective nature and relatively small number of patients. Therefore, these results need to be confirmed by a large prospective and randomized trial. Data Availability
The data used to support the findings of this study are available from the corresponding author upon request. Conflicts of Interest
None of the authors have proprietary interest in any material used in this study. Acknowledgments
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I lived on a high daily dose of Prednisone initial 400mg a day for a week, then tapered to 80mg a day for almost a year, then weaned 100% over 2 and a half months.
It was no picnic, but I will attest to the ability of it to help put a can of whoop-ass in side and make you the Hulk inside, while David Banner becomes a 16 year old girl on the outside.
I also have become “anti-biotic tolerant” (well, the bugs what get me, are given “free-fire ROE” against me due to over-prescribed in my youth), and that left me with an over reactive immune system that goes off scale if I get sick. (here comes the irony)I rarely get sick, but/and when I do, I get really bad sick, and my body goes apeshit crazy reacting and fighting it.
I think, that what happens is I kick the puny stuff to the side, no sniffle, no “low grade fevers” nothing for years, then “wham”, the mega monster bug hits me and my body reacts to try and kill it, but brings the burn Danger Close and then it starts losing ground, and I always end up needing steroids and the double antibiotic treatments like Augmentin and other 2 punch antibiotics.
Last two times I have been sick were once in 2005 (the big one) and once in 2012 (the flu, and my brain did the “12 Monkeys” trip, went on a bug hunt and left my body behind for almost 4 days, that left me with Hotel California memories).
So, before you dismiss with wave of hand, the ability of the drugs used, remember, that badass you became on the outside when demanding implements of destruction without a second thought to the mayhem you could produce, that was the whiny 16 year old, and the “Hulk” was one the inside showing all the “Loki” germs and shits what a puny god looks like when in the Swiffer mode.
Hope you get all better and stay gooder longer!

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