DR. ING HAS NO FINANCIAL INTERESTS IN ANY OF THE PRODUCTS LISTED BELOW
FL-41 LENS TINT (Possible Sources Greater Toronto Area and Vancouver)
Credit Valley Optical: 2300 EGLINTON AVE W (Mississauga)
Eye Care Optical: 390 STEELES AVE W (Thornhill)
Spectrum Vision Care: 147 CLARENCE ST (Brampton)
Kanda Optical (Etobicoke)
Performance Vision Optometry 1242 Burrard St. (Vancouver)
Luxury Eyewear 415-650 41st Ave W (Vancouver)
“Are All FL-41 Migraine Relief Glasses Created Equal?” (https://www.axonoptics.com/2018/12/are-all-fl-41-migraine-glasses-created-equal/)
? order online and get shipped to Canada (?$15 shipping at Theraspecs).
SCLERAL CONTACT LENS a possible consideration for some patients with extreme dry eyes
- Steve Sanger, East York
- Jennie Khalfan, Mississauga
- KEI Contact Lens Clinic
- Vishakha Thakar, Vaughan
- Jennifer Liao North York
- Barbara Caffery, Shalu Pal downtown TO
- Approximately $250 for fitting consultation and$500-1500 depending on which type of scleral fits best.
REFRACTORY GIANT CELL ARTERITIS
ANISEKONIA TESTS / LENSES
THE MEDICAL USE OF CANNABIS FOR GLAUCOMA
The Canadian Ophthalmological Society does NOT support the medical use of cannabis
for the treatment of glaucoma due to the short duration of action, the incidence of
undesirable psychotropic and other systemic side effects and the absence of scientific
evidence showing a beneficial effect on the course of the disease. This is in contrast to
other more effective and less harmful medical, laser and surgical modalities for the
treatment of glaucoma.
ALPHAEON® Beauty Eyelash Serum formulation Peptide myristoly pentapeptide-17 which is in the, are thought to stimulate the keratin gene in the body; responsible for lash growth (as opposed to the prostaglandin in Latisse)
ERIVEDGE (Vismodegib) from EyeWiki
Vismodegib (Erivedge) is a molecular inhibitor of the Hedgehog signaling pathway. It was developed by Genentech and approved by the FDA in January 2012 for the treatment of metastatic and locally advanced basal cell CA.
The hedgehog signaling cascade, which includes key receptor proteins such as Smoothened (SMO), have been implicated in cancers of the brain, lung, mammary gland, prostate and skin. The discovery of cyclopamine, an endogenous steroidal plant alkaloid that binds to SMO and inhibits downstream gene expression, initiated the quest for the identification of other agents that could inhibit the Hedgehog pathway. Vismodegib was one of the first such molecules to be developed and was originally used for the treatment of medulloblastoma.4 It acts by binding to SMO and preventing the activation of downstream target genes.7 When it was demonstrated in genetically engineered mice that the overactivation of the Hedgehog pathway was implicated in the development of other forms of cancer such as basal-cell carcinoma, investigators applied the Hedgehog inhibitors to halt these disease processes.
Vismodegib inhibits the Hedgehog signaling pathway. The Hedgehog pathway plays a crucial role during embryogenic development but has limited activity in most adult tissues, with the exception of hair, skin and stem cells.7, 9 In more than 90% of BCC, the Hedgehog signaling pathway is abnormally upregulated.5, 10 Mutations in key receptor proteins such as Patched (PTCH) and Smoothened (SMO) result in abnormal transcription of target genes that regulate basal cell growth and proliferation. Vismodegib acts as an SMO antagonist to prevent GLI1 and GLI2 transcription factor activation, blocking the signaling cascade.
Vismodegib is FDA approved ro the treatment of metastatic and locally advanced BCC that cannt be treated with surgery or radiation. The dose of vismodegib is 150 mg orally once a day.
A Phase I clinical trial by Von Hoff et al. (2009)1 studied the effect of vismodegib in three doses in 33 patients with metastatic or locally advanced basal-cell carcinoma: 150mg per day (17 patients), 270mg per day (15 patients) and 540mg per day (1 patient). Of the 33 patients, 18 had an objective response (2 complete, 16 partial), 11 had stable disease, and 4 had progressive disease. The median duration of response was 8.8 months. Molecular analysis of biopsy samples in 26 patients demonstrated over-expression of GLI1 mRNA expression in 25 patients. In a pharmacokinetic analysis, the median time to steady state was 14 days (range 7 to 22 days), and increasing the dose did not result in higher steady-state plasma levels. In 10 of 13 patients, there was a decrease in GLI1 expression by more than a factor of two in biopsy samples of treated patients compared with pretreatment biopsy-sample analysis. These findings confirmed the importance of the hedgehog pathway in basal-cell carcinoma and suggested the inhibitors of this pathway can be useful in treatment of these inoperable tumors.
A Phase II multicenter, international, two-cohort, nonrandomized study by Sekulic et al. (2012) studied the effect of vismodegib on patients with metastatic and locally advanced BCC.7 Participants were deemed inappropriate surgical candidates based on multiple recurrences or substantial anticipated morbidity. All patients received once daily 150mg of oral vismodegib. In 33 patients with metastatic BCC, the response rate was 30% (95% confidence interval (CI), 16 to 48; P=0.001). In 63 patients with locally advanced BCC, the response rate was 43% (95% CI, 35 to 56; P<0.001) with complete responses in 13 patients (21%). The median duration for response was 7.6 months (range 1.0-12.9 months; 95% CI, 5.7-9.7).
A randomized, double-blind placebo-controlled trial by Tang et al. (2012) studied the effect of vismodegib on patients with the basal-cell nevus syndrome.11 In 41 patients over a mean follow-up of 8 months, there was reduced per-patient rate of new surgically eligible BCC in the group treated with vismodegib than with placebo (2 vs. 29 cases per group per year, P<0.001). The size of existing BCC also showed significant reduction in the vismodegib group (-65% vs. -11%, P=0.003). The study also demonstrated a reduction of the hedgehog target gene expression by BCC by 90% (P<0.001) and diminished tumor-cell proliferation by analysis of the levels of messenger RNA encoding the hedgehog target gene glioma-associated oncogene homolog 1 (GLI1) in skin-shave biopsy samples of BCC taken at baseline and at 1 month after the start of vismodegib treatment.
In the Phase I clinical trial1, there were 35 adverse events reported in total, of which 23 were grade 3 adverse events over a median follow-up time of 9.8 months. These included fatigue, hyponatremia, muscle spasm and atrial fibrillation. No dose-limiting toxic effects or grade 5 events were observed during the study period.
In the Phase II clinical trial7, adverse events occurred in more than 30% of patients with metastatic and locally advanced BCC, including muscle spasms, alopecia, dysgeusia (taste disturbance), weight loss and fatigue.
In Tang et al’s study11, 54% of patients with basal-cell nevus syndrome (14 of 26) discontinued drug treatment due to adverse events. Patients receiving vismodegib were significantly more likely to experience adverse events compared to placebo, including hair loss, weight loss >5%, muscle cramps, and taste disturbance. Most adverse events were mild or moderate in severity, and no grade 5 events were observed.
Because of the importance of the Hedgehog pathway in embryogenesis and organ development, vismodegib is contraindicated in pregnancy. Vismodegib has been demonstrated to be teratogenic in rat studies and can result in craniofacial abnormalities, open perineum, retardation in normal growth, and absence or fusion of digits.8 Patients of reproductive age should be counseled regarding the use of effective contraception while using this drug.
Other Hedgehog Inhibitors:
There have been other Hedgehog pathway inhibitors that have been developed for treatment of BCC besides Vismodegib. There are five other agents (BMS-833923 LDE224, LEQ506, IPI926 and TAK-441) that have shown promise in animal studies and early clinical trials.9 For example, LDE225 is another selective antagonist of SMO protein. In a double-blind, randomized, vehicle-controlled study, twice daily topical treatment with 0.75% LDE25 cream in patients with the basal cell nevus syndrome resulted in partial responses in 9, complete responses in 3, and no clinical response in 1 out of 13 BCCs treated.12
The use of Vismodegib is an example of selected, targeted molecular biology to treat aggressive basal cell carcinoma. The addition of this drug to the therapeutic armamentarium for recurrent, invasive or metastatic basal cell carcinoma is exciting. Anticipated are even more effective, selective drugs.
ALDARA Imiquimod cream activates your body’s own immune system via a molecule called toll-like receptor 7 (TLR7), which in turn activates interferon-alpha to fight the cancerous cells.
Aldara Cream should be applied 5 times per week for a full 6 weeks to a biopsy-confirmed superficial basal cell carcinoma. An example of a 5 times per week application schedule is to apply Aldara Cream, once per day, Monday through Friday. Aldara Cream should be applied prior to normal sleeping hours and left on the skin for approximately 8 hours, after which time the cream should be removed by washing the area with mild soap and water.
IWash your hands before and after applying Aldara Cream. Wash the treatment area with mild soap and water before applying the cream, and allow the area to dry thoroughly.
Sufficient cream should be applied to cover the treatment area, including 1 centimeter of skin surrounding the tumor, but do NOT put Aldara near the eye. Aldara Cream should be rubbed into the treatment area until the cream is no longer visible. Avoid contact with eyes, and lips.
Local skin reactions in the treatment area are common. A rest period of several days may be taken if required by the patient’s discomfort or severity of the local skin reaction.
Early clinical clearance cannot be adequately assessed until resolution of local skin reactions (e.g. 12 weeks post-treatment). Local skin reactions or other findings (e.g. infection) may require that a patient be seen sooner than the post-treatment assessment for clinical clearance. If there is clinical evidence of persistent tumor at the post-treatment assessment for clinical clearance, a biopsy or other alternative intervention should be considered. Lesions that do not respond to therapy should be carefully re-evaluated and management reconsidered; the safety and efficacy of a repeat course of Aldara Cream treatment have not been established. If any suspicious lesion arises in the treatment area at any time after a determination of clinical clearance, the patient should seek a medical evaluation
Aldara Cream is packaged in single-use packets, with 12 packets supplied per box. Patients should be prescribed no more than 36 packets for the 6-week treatment period. Unused packets should be discarded. Partially-used packets should be discarded and not reused.
RITUXIMAB (see webpage above)
Each 1 mL of clear, greenish-yellow solution contains brimonidine tartrate 2 mg (0.2%).
Each 1 mL of ophthalmic solution, 0.15% .
Who should NOT take Apo-Brimonidine?
Anyone who is using monoamine oxidase inhibitors (phenelzine, tranylcypromine)
MYASTHENIA GRAVIS BLOOD TESTS: LRP4, MUSK, Acetylcholine recpetor antibodies
NEUROMYELITIS OPTICA: anti-aquaporin4 (AQP4) IgG antibody test. NMO may have severe bilateral vision loss, poor visual recovery, relapses, and may not show myelitis at onset. ?plasmapheresis (interferon, natalizumab and fingolimod may exacerbate disease course)
MEDICAL CALCULATOR e.g. Steroids, BMI
ANTIBIOTICS (Cleveland Clinic Formulary)
Mucor & Aspergillosis suspected: amphotericin B
Invasive aspergillosis: voriconazole
ALTERNATIVES TO ACETAZOLAMIDE FOR IIH and KIDNEY STONES
Bendroflumethiazide (? 10 mg is very high dose)
Bendroflumethiazide is a very weak carbonic anhydrase inhibitor (does not affect urine ph as do acetazolamide and topiramate)
Analzye the stones. Acetazolamide usually causes calcium phosphate or struvite stones.
2016 Revised AAO guideline
Excess is > 5 mg HCQ/kg actual body weight
VISUAL SNOW dysfunctional sensory processing
Do OCT, MRI (SWI&DWI), EEG, ERG&VEP
Lamotrigine build slowly to 200 mg bid, and determine effect after a month on full dose
Acetazolamide 250 bid to maximum 1g.