Examining the efficacy of verteporfin photo-dynamic therapy (PDT) at different dose & fluence levels.

OBJECTIVES: Photodynamic therapy (PDT) is a vaso-occlusive treatment for a number of chorioretinal vascular pathologies. We aimed to retrospectively analyse efficiency and safety of PDT for different conditions (central serous retinopathy (CSR), age-related macular degeneration (AMD), macular telangiectasia type 2 and choroidal hemangioma) and with different verteporfin parameters. METHODS: Clinical parameters were ascertained from the medical records of patients undergoing PDT over a 6-year period. This included indications for PDT, dosing regimens of verteporfin PDT (which includes treatment dose of verteporfin and fluence). Response to treatment was measured by best corrected visual acuity (BCVA) and central foveal thickness (CFT) on ocular coherence tomography. Complications and side effects were recorded. RESULTS: 67.4 % (31/46) of PDT treatments performed over the last six years were for CSR. In the CSR cohort, there were significant improvements in BCVA (0.47 ± 0.24 to 0.29 ± 0.27, p < 0.05) and CFT (350.2µm ± 66.9 µm to 286.1µm ± 60.6 µm. In the AMD cohort, there was no change in BCVA (1.08 ± 0.52 to 1.07 ± 0.53, p = 0.96) but significant improvement in CFT (488.2µm ± 164.6 µm to 348.7µm ± 65.7 µm, p < 0.05). There was no significant difference in BCVA or CFT for macular telangiectasia type 2 and choroidal hemangioma. CONCLUSIONS: PDT continues to have a role in the management of medical retina conditions. Our results show PDT is most effective in improving and stabilizing visual acuity in CSR, with earlier intervention resulting in better outcomes.

Skin hyperpigmentation after sclerotherapy with polidocanol: A systematic review.

Skin hyperpigmentation after sclerotherapy with polidocanol-containing sclerosants is a common local side effect. Sclerotherapists should be familiar with factors that trigger hyperpigmentation after sclerotherapy with polidocanol-containing sclerosants. A systematic literature review of works reporting hyperpigmentation after sclerotherapy for telangiectasias, reticular veins, side branches and truncal varices with polidocanol-containing sclerosants was performed. Reported incidence rates, follow-up periods and potentially triggering factors were assessed and analysed. The search yielded 1687 results; of these, 27 reports met the inclusion criteria. The incidence of hyperpigmentation seemed to increase with higher concentrations of polidocanol and was more evident after sclerotherapy for epifascial veins than for intrafascial truncal veins when the polidocanol concentration was more than 0.25%. Regarding sclerotherapy for telangiectasias and reticular veins, the incidence of hyperpigmentation ranged between 2% and 25% for polidocanol 0.25% (liquid and foam), between 12.5% and 67.9% for polidocanol 0.5% (liquid and foam) and between 13% and 73% for polidocanol 1% (liquid and foam). Regarding truncal veins, the incidence ranged from 7% to 45.8% for polidocanol 1% (liquid and foam), from 16% to 17% for polidocanol 2% (foam) and from 7.4% to 32.5% for polidocanol 3% (liquid and foam). Regarding the treatment of side branches, the incidence of hyperpigmentation ranged from 5.6% to 53% for both foam and liquid sclerotherapy. Regarding the duration of hyperpigmentation, there are few data describing reticular veins and telangiectasias. Hyperpigmentation persisting for more than 6 months has been reported to have an incidence of up to 7.5%. Hyperpigmentation persisting for more than 1 year after foam polidocanol 1%-3% treatment for truncal veins has an incidence ranging from 8.1% to 17.5%. Other factors such as higher volumes and compression therapy after treatment seem to have a minor influence. Data regarding hyperpigmentation after polidocanol-related sclerotherapy are poor and should be improved by higher-quality research.

Photodistributed eruptive telangiectasias: an uncommon adverse drug reaction. A retrospective case series.

Drug-induced photodistributed telangiectasia (PT) is a cutaneous adverse effect (AE) resulting from the interaction of ultraviolet radiation with pharmacotherapy. Reports of PT in the literature are scarce. We report 25 cases of drug-induced PT highlighting the potential relationship between the onset of skin lesions, drug intake and photo exposure. We alert practitioners that PT is a possible dermatological phototoxic AE of many drugs.

Ado-trastuzumab emtansine associated spider telangiectasia.

INTRODUCTION: Breast cancer is the most common cancer in women. Human epidermal growth factor receptor 2 (HER2) positivity rate is 20% and generally has a poor prognosis. Ado-trastuzumab emtansine (T-DM1) is an antibody-drug conjugate consisting of HER2 target monoclonal antibody trastuzumab and microtubule inhibitor emtansine. The most common side effects are fatigue, diarrhea, anemia, and it is generally a safe and tolerable agent. CASE REPORT: In our case, we reported our patient who developed mucosal and cutaneous telangiectasia after T-DM1 treatment and who had a complete response in metastases after skin lesions. MANAGEMENT AND OUTCOME: While no side effects were observed during the use of T-DM1 for HER2 positive disease, nose bleeding and spider telangiectasia on the skin developed in the 9th month of the treatment. In these lesions, which did not require any treatment, no regression was observed during T-DM1 treatment. DISCUSSION: We think that T-DM1, which was detected with a low incidence of skin toxicity in studies, may form telangiectatic lesions due to vascular dilatation through emtansine, and therefore care should be taken in the treatment of T-DM1.

Dermoscopy of topical steroid-dependent or damaged face: A cross-sectional study.

BACKGROUND: Topical corticosteroid (TCS) abuse is rampant and results in steroid addiction labeled as topical steroid-dependent or damaged face (TSDF). Indian market is replete with triple combination creams containing TCS sold as over-the-counter products at low cost, luring people to use them without prescription. The resultant damage if detected late is irreversible and difficult to treat. Dermoscopy can help in the early identification of features of TSDF at a preclinical stage resulting in better prognosis. However, the literature on the same is limited. AIMS: This study is undertaken to characterize dermoscopic features of TSDF and to correlate them with potency and duration of application of the TCS. METHODS: One hundred and thirty-two patients aged 18 years or above, with clinical symptoms and signs suggestive of TSDF and with history of application of TCS on the face for a period of more than one month, were enrolled in the study. Their demographic details, clinical features, and dermoscopy findings were recorded using a predesigned structured format. Comparison of dermoscopic findings with clinical examination, gender, potency of TCS, and duration of TCS use was done using Chi-square test, Fisher's exact test, and one-tailed Z-test. RESULTS: Mean age of the patients was 31.7 ± 8.1 years. Male to female ratio was 2:9. Sixty-nine (52.3%) patients abused TCS for more than one year. Clinical findings noted in the patients were erythema (81.1%), hyperpigmentation (80.3%), and hypertrichosis (68.2%). The most common dermoscopy findings seen were brown globules (96.2%), red diffuse areas (92.4%), vessels (87.1%), white structureless areas (86.4%), and hypertrichosis (80.3%). Red diffuse areas, vessels, brown globules, white structureless areas, and white hair were observed in a statistically higher proportion of cases dermoscopically. Y-shaped vessels and brown globules were seen in significantly higher number of patients, using TCS for more than three months and in those continuing it beyond six months, polygonal vessels were predominant. LIMITATIONS: Lack of histopathological correlation is the limitation of our study. Furthermore, brown globules seen in 96.2% patients of TSDF on dermoscopy may have been over-estimated and not always signify TSDF; instead, it could represent melasma for which patient applied TCS. CONCLUSION: Dermoscopy in TSDF can help dermatologists in a multitude of ways from confirming the diagnosis to differentiating from other causes of red face and predicting the approximate duration of TCS abuse.

Management of cutaneous side effects of inflammatory bowel disease therapy: A dermatologic viewpoint.

Medications used in the treatment of inflammatory bowel disease cause a wide range of dermatologic side effects, and minimal guidance exists on how to manage them. The intention of this review article is to summarize common dermatologic adverse reactions related to inflammatory bowel disease therapy and to provide evidence-based guidance on management. We conducted a scoping review using PubMed and Google Scholar to identify studies reporting clinical information on dermatologic side effects of medications used in the treatment of inflammatory bowel disease. The most commonly reported dermatological adverse effects from inflammatory bowel disease therapy were cutaneous malignancy and cutaneous infections. Thiopurines, methotrexate, tumor necrosis factor (TNF) inhibitors, interleukin (IL)-12/23 inhibitors, and integrin inhibitors can be continued if nonmelanoma skin cancer arises during therapy and the malignancy should be surgically excised. TNF inhibitors and IL-12/23 inhibitors can be continued in the setting of stage I surgically resectable melanoma but should be discontinued in advanced melanoma. For complicated cutaneous bacterial infections, methotrexate and TNF inhibitors should be halted, and IV antibiotics should be administered. Complicated herpes zoster infection warrants discontinuation of TNF inhibitors, whereas IL-12/23 and JAK inhibitors can be continued. Inflammatory bowel disease therapies are associated with several dermatological adverse effects, and management options vary by agent. Certain agents may require discontinuation in the setting of nonmelanoma skin cancer, melanoma, and cutaneous infections. Many other dermatological adverse effects from inflammatory bowel disease therapy require specialized management or referral to dermatology.

Proteomic profiling reveals the differential toxic responses of gills of common carp exposed to nanosilver and silver nitrate.

Although the toxic effects of silver nanoparticles (AgNPs) on fish gills have been reported, the underlying mechanism of toxicity remains unclear. The present study aimed to elucidate the mechanism of toxicity in the gills of common carp following exposure to AgNPs and silver nitrate (AgNO3) using histopathology and proteomics. Histopathological findings revealed that both AgNPs and AgNO3 caused telangiectasia and epithelial cell hyperplasia in fish gills; however, the pathological features and location of lesions caused by the two forms of silver were markedly different. Proteomics revealed that AgNPs and AgNO3 induced 139 and 185 differential expression proteins (DEPs) in gills, respectively, and the two forms of silver induced only 42 shared proteins. AgNPs specifically induced 87 DEPs which mainly involved signaling mechanisms, cytoskeleton, and the arachidonic acid metabolism processes. AgNO3 specifically induced 125 DEPs that were mainly clustered in the glutathione metabolism and protease processes. These results suggested that the toxic effects of AgNPs and AgNO3 were dramatically different in terms of protein expression in fish gills, which may provide novel perspectives for understanding the toxicity mechanism of silver nanoparticles in fish gills.

Linear atrophy and vascular fragility following ultrasoundguided triamcinolone injection for DeQuervain tendonitis.

A 64 year-old woman presented with a one-yearhistory of purpuric, atrophic, linear patches alongthe left lateral forearm. The patient had receivedtwo ultrasound-guided triamcinolone injectionsone year earlier into her left extensor pollicis brevisand abductor pollicis longus tendon sheathsfor DeQuervain tendonitis. In the seven monthsfollowing the second injection, the patient developedatrophy, purpura, and telangiectasias starting at thesite of injection and extending proximally, followingthe course of her left cephalic vein. The patient wastreated initially with amlactin and moisturizing creamcontaining alpha-hydroxy acid cream to aid in dermalrepair. Despite treatment, she continued to haveproximal progression of the atrophy and purpura.A 4mm punch biopsy revealed a normal-appearingepidermis overlying horizontal dermal fibrosis, alongwith atrophic-appearing adipocytes with accentuatedcapillaries in the subcutaneous fat, consistent witha diagnosis of corticosteroid atrophy. These grossand microscopic changes presumably resulted fromlymphatic uptake and spread of the corticosteroidfollowing the injections for tendonitis. Although localatrophy and vascular fragility are well-documentedside effects of corticosteroid injections, linear spreadof these symptoms is rarely reported, and to this pointhas not been demonstrated in the literature followingultrasound-guided steroid injection for DeQuervaintendonitis.

Telangiectasias fotodistribuidas asociadas a amlodipino / Amlodipine-associated photodistributed telangiectasia

No disponible

Telangiectasia and Pulmonary Arterial Hypertension Following Treatment With Trastuzumab Emtansine: A Case Report.

Trastuzumab emtansine (T-DM1) is a Food and Drug Administration-approved novel agent for the treatment of HER-2 positive advanced breast cancer. We report a case of pulmonary arterial hypertension (PAH) that we attribute to the use of T-DM1. A 43-year-old woman with stage IV breast cancer presented with dyspnea on exertion. After excluding other secondary causes of pulmonary hypertension, a diagnosis of moderately severe PAH was made based on right heart catheterization. History revealed that the patient had been on T-DM1 before presentation. During T-DM1 treatment, the patient experienced hereditary hemorrhagic telangiectasia-like symptoms consisting of spider angiomata-skin lesions, epistaxis, and hematochezia, which resolved with discontinuation of T-DM1. Temporal associations of T-DM1 use with the development of PAH in the patient, and the reported association between hereditary hemorrhagic telangiectasia and PAH via genetic linkage, led us to suspect T-DM1 as the cause of PAH.