Certain types of malaria, resistant strains, and complicated cases require different or additional medication.It is widely used to treat primary Sjögren syndrome but does not appear to be effective. Hydroxychloroquine is widely used in the treatment of post-Lyme arthritis. It may have both an anti-spirochete activity and an anti-inflammatory activity, similar to the treatment of rheumatoid arthritis. Contraindications
The drug label advises that hydroxychloroquine should not be prescribed to individuals with known hypersensitivity to 4-aminoquinoline compounds. There are several other contraindications, and caution is required if the person considered for treatment has certain heart conditions, diabetes, or psoriasis. Adverse effects
Hydroxychloroquine has a narrow therapeutic index, meaning there is little difference between toxic and therapeutic doses. The most common adverse effects are nausea, stomach cramps, and diarrhea. Other common adverse effects include itching and headache. The most serious adverse effects affect the eye, with dose-related retinopathy as a concern even after hydroxychloroquine use is discontinued. Serious reported neuropsychiatric adverse effects of hydroxychloroquine use include agitation, mania, difficulty sleeping, hallucinations, psychosis, catatonia, paranoia, depression, and suicidal thoughts. In rare situations, hydroxychloroquine has been implicated in cases of serious skin reactions such as Stevens–Johnson syndrome, toxic epidermal necrolysis, and Drug reaction with eosinophilia and systemic symptoms. Reported blood abnormalities with its use include lymphopenia, eosinophilia, and atypical lymphocytosis.For short-term treatment of acute malaria, adverse effects can include abdominal cramps, diarrhea, heart problems, reduced appetite, headache, nausea and vomiting. Other adverse effects noted with short-term use of Hydroxychloroquine include low blood sugar and QT interval prolongation.
Type 3 is a more severe presentation of type 1 and is caused by a mutation in the same gene, while type 4 is most often caused by a mutation in SOX10. Mutations in other genes can also cause the different types, and some of these have been given their own lettered subtypes. Most types are autosomal dominant. The estimated prevalence of Waardenburg syndrome is 1 in 42,000. Types 1 and 2 are the most common, comprising approximately half and a third of cases, respectively, while type 4 comprises a fifth and type 3 less than 2% of cases. An estimated 2–5% of congenitally deaf people have Waardenburg syndrome. Descriptions of the syndrome date back to at least the first half of the 20th century, however it is named after Dutch ophthalmologist and geneticist Petrus Johannes Waardenburg, who described it in 1951. Its subtypes were progressively discovered in the following decades and had genes attributed to them mostly in the 1990s and 2000s. Signs and symptoms
Waardenburg syndrome has multiple different types with some variations in symptoms, and symptoms can vary among those with the same type. The two features consistent across all types of Waardenburg syndrome are some degree of congenital sensorineural hearing loss and some degree of pigmentation deficiencies, most consistently in the eyes.