OBJECTIVE: To familiarize physicians with the natural history, clinical manifestations, diagnosis, and management of infantile hemangiomas.
METHODS: A Pubmed search was conducted in November 2019 in Clinical Queries using the key term "infantile hemangioma". The search strategy included meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews published within the past 20 years. Only papers published in the English literature were included in this review. The information retrieved from the above search was used in the compilation of the present article.
RESULTS: The majority of infantile hemangiomas are not present at birth. They often appear in the first few weeks of life as areas of pallor, followed by telangiectatic or faint red patches. Then, they grow rapidly in the first 3 to 6 months of life. Superficial lesions are bright red, protuberant, bosselated, or with a smooth surface, and sharply demarcated. Deep lesions are bluish and dome-shaped. Infantile hemangiomas continue to grow until 9 to 12 months of age, at which time the growth rate slows down to parallel the growth of the child. Involution typically begins by the time the child is a year old. Approximately 50% of infantile hemangiomas will show complete involution by the time a child reaches age 5; 70% will have disappeared by age 7; and 95% will have regressed by 10 to 12 years of age. The majority of infantile hemangiomas require no treatment. Treatment options include oral propranolol, topical timolol, and oral corticosteroids. Indications for active intervention include hemorrhage unresponsive to treatment, impending ulceration in areas where serious complications might ensue, interference with vital structures, life- or function-threatening complications, and significant disfigurement.
CONCLUSION: Treatment should be individualized, depending upon the size, rate of growth, morphology, number, and location of the lesion (s), existing or potential complications, benefits and adverse events associated with the treatment, age of the patient, level of parental concern, and the physician's comfort level with the various treatment options. Currently, oral propranolol is the treatment of choice for high-risk and complicated infantile hemangiomas. Topical timolol may be considered for superficial infantile hemangiomas that need to be treated and for complicated infantile hemangiomas in patients at risk for severe adverse events from oral administration of propranolol.
METHODS AND RESULTS: We compared clinical characteristics and treatment approaches between patients with or without a history of COPD, before and after 1:2 propensity matching (for age, sex, geographical region, income level, and ethnic group) in 5232 prospectively recruited patients with HF and reduced ejection fraction (HFrEF, <40%) from 11 Asian regions (Northeast Asia: South Korea, Japan, Taiwan, Hong Kong, and China; South Asia: India; Southeast Asia: Thailand, Malaysia, Philippines, Indonesia, and Singapore). Among the 5232 patients with HFrEF, a history of COPD was present in 8.3% (n = 434), with significant variation in geography (11.0% in Northeast Asia vs. 4.7% in South Asia), regional income level (9.7% in high income vs. 5.8% in low income), and ethnicity (17.0% in Filipinos vs. 5.2% in Indians) (all P
METHODS: From the Malaysian National Neurology Registry, we included hypertensive patients with first ischemic stroke who presented within 48 hours from ictus. Antihypertensive drugs were divided into Ang II increasers (angiotensin-I receptor blockers (ARBs), calcium channel blockers (CCBs) and diuretics) and Ang II suppressors (angiotensin-converting-enzyme inhibitors (ACEIs) and beta blockers). We evaluated stroke severity during admission with the National Institute of Health Stroke Scale (NIHSS). We performed a multivariable logistic regression with the score being dichotomized at 15. Scores of less than 15 were categorized as less severe stroke.
RESULTS: A total of 710 patients were included. ACEIs was the most commonly prescribed antihypertensive drug in patients using Ang II suppressors (74%) and CCBs, in patients prescribed with Ang II increasers at 77%. There was no significant difference in the severity of ischemic stroke between patients who were using Ang II increasers in comparison to patients with Ang II suppressors (OR: 1.32, 95%CI: 0.83-2.10, p = 0.24).
CONCLUSION: In our study, we found that use of antihypertensive drugs that increase Ang II formation was not associated with less severe ischemic stroke as compared to use of antihypertensive drugs that suppress Ang II formation.