Adverse Reactions: Retinopathy with changes in pigmentation and visual field defects, can occur following hydroxychloroquine administration, but is rare. In its early form, it appears reversible upon discontinuation of the drug. If allowed to develop however, there may be a risk of progression even after treatment withdrawal.
Corneal changes including edema and opacities have been reported. They are either symptomless or may cause disturbances such as halos, blurring of vision or photophobia. They are reversible upon discontinuation of therapy. Blurring of vision due to a disturbance of accommodation which is dose dependent and reversible may also occur.
Skin rashes sometimes occur; pigmentary changes in skin and mucous membranes, bleaching of hair, and alopecia have also been reported. These usually resolve readily upon cessation of therapy. Isolated cases of exfoliative dermatitis have been reported.
HYDROXYCHLOROQUINE SULFATE | Drug | BNF content published by NICE
Other adverse reactions include gastrointestinal disturbances such as nausea, diarrhea, anorexia, abdominal pain and, rarely, vomiting. These symptoms usually resolve immediately upon reducing the dose or upon stopping the treatment. Less frequently, muscle weakness, vertigo, tinnitus, nerve deafness, headache, nervousness, and emotional lability have been reported with this class of drugs.
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Rarely, there have been reports of bone marrow depression, cardiomyopathy, neuromyopathy, psychosis and convulsions. Isolated cases of abnormal liver function tests have been reported and two cases of fulminant hepatic failure have been published. Symptoms And Treatment Of Overdose: Overdosage with the 4-aminoquinolines is dangerous particularly in infants, as little as 1 to 2 g having proved fatal.
Symptoms: The 4-aminoquinoline compounds are very rapidly and completely absorbed following ingestion and in accidental overdosage toxic symptoms may occur within 30 minutes.
These consist of headache, drowsiness, visual disturbances, cardiovascular collapse, and convulsions, followed by sudden and early respiratory and cardiac arrest. Treatment: Treatment is symptomatic and must be prompt with immediate evacuation of the stomach by emesis at home, before transportation to the hospital , or gastric lavage until the stomach is completely emptied.
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If finely powdered activated charcoal is introduced by the stomach tube, after lavage and within 30 minutes after ingestion of the tablets, it may inhibit further intestinal absorption of the drug. To be effective, the dose of activated charcoal should be at least five times the estimated dose of ingested hydroxychloroquine. Convulsions, if present should be controlled before attempting gastric lavage. If due to cerebral stimulation, cautious administration of an ultrashort-acting barbiturate may be tried but, if due to anoxia, convulsions should be corrected by oxygen administration, artificial respiration or, in shock with hypotension, by vasopressor therapy.
Because of the importance of supporting respiration, tracheal intubation or tracheostomy, followed by gastric lavage, has also been advised. Exchange transfusions have been used to reduce the level of 4-aminoquiolines in the blood. Consideration should be given to administering diazepam parenterally, since studies have reported it beneficial in reversing chloroquine cardiotoxicity.
A patient who survives the acute phase and is asymptomatic should be closely observed for at least 6 hours. Fluids may be forced, and sufficient ammonium chloride may be administered for a few days to acidify the urine to help promote urinary excretion.
Dosage And Administration: The dosages cited below are stated in terms of hydroxychloroquine sulfate. One mg tablet is equivalent to mg base. Each dose should be taken with a meal or a glass of milk. Rheumatoid Arthritis: The compound is cumulative in action and will require several weeks to exert its beneficial therapeutic effects, whereas minor side effects may occur somewhat early.
Several months of therapy may be required before maximum effects can be obtained. If objective improvement such as reduced joint swelling, increased mobility does not occur within 6 months, the drug should be stopped. Safe use of the drug in the treatment of juvenile rheumatoid arthritis has not been established. Initial Dosage: Adults: to mg daily. In a few patients, the side effects may require temporary reduction of the initial dosage. Generally, after 5 to 10 days the dose may be gradually increased to the optimum response level, frequently, without return of side effects.
The incidence of retinopathy has been reported to be higher when the maintenance dose is exceeded. If a relapse occurs after medication is withdrawn, therapy may be resumed or continued on an intermittent schedule if there are no ocular contraindications. Combination Therapy: Hydroxychloroquine may be used safely and effectively in combination with corticosteroids, salicylates, NSAIDS, and methotrexate and other second line therapeutic agents.
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Corticosteroids and salicylates can generally be decreased gradually in dosage or eliminated after the drug has been used for several weeks. When gradual reduction of steroid dosage is suggested, it may be done by reducing every 4 to 5 days, the dose of cortisone by no more than 5 to 15 mg; of hydrocortisone from 5 to 10 mg; of prednisolone and prednisone from 1 to 2.
No definitive dose combinations have been established. Lupus Erythematosus: Adults: Initially, the average dose is mg once or twice daily. This may be continued for several weeks or months, depending upon the response of the patient.
For prolonged maintenance therapy, a smaller dose, from to mg daily will suffice. The incidence of retinopathy has been reported to be higher when this maintenance dose is exceeded. Suppressive therapy should begin 2 weeks before exposure. Patients had regular clinical evaluation, determination of serum and cerebrospinal fluid angiotensin-converting enzyme level, computed tomography or magnetic resonance imaging, chest radiography, lung function testing, and slit-lamp examination of the eyes. Two patients failed to respond. Cerebrospinal fluid abnormalities, including lymphocytosis, were seen in 3 patients.
Magnetic resonance imaging with gadolinium was most helpful in supporting the diagnosis of sarcoidosis and monitoring the course of the disease.
Ocular toxic effects from chloroquine or hydroxychloroquine were not observed. Although systemic corticosteroids suppress inflammation in many patients, the disease may require unacceptably high doses of the drugs to maintain improvement. These patients had clinical as well as histological evidence of multisystem sarcoidosis. In these patients, corticosteroids were slowly reduced in dosage and then discontinued.
At the same time, hydroxychloroquine sulfate, mg twice daily, or chloroquine phosphate, mg twice daily, was started and was continued for 6 months or more. Two additional patients, who did not wish to take corticosteroids, received hydroxychloroquine. All patients who received chloroquine or hydroxychloroquine had thorough eye evaluation, including a slit-lamp examination, at 3-month intervals by an ophthalmologist experienced in managing ocular sarcoidosis.
Response to treatment was assessed by history, neurological and ocular examination, measurement of serum and cerebrospinal fluid CSF angiotensin-converting enzyme ACE , computed tomography, magnetic resonance MR imaging, and gallium 67 67 Ga scanning. Twelve patients, 6 women and 6 men from 20 to 49 years of age, formed the basis of this study. Seven were of African American origin. The diagnosis of sarcoidosis was based on the presence of noncaseating granulomas in the brain in 3 patients, in the lung in 5, in the lymph nodes in 2, in the nasal mucosa in 1, and in the skin in 1 patient.
The Kveim-Siltzbach test was positive in the 1 patient in whom it was performed. Cerebrospinal fluid lymphocytosis and increased protein level were seen in 3 patients. Electromyographic changes consistent with axonal neuropathy were seen in 4 patients. In 2 patients the disease progressed regardless of the type of therapy.
One of the patients showed evidence of pigmented epithelial retinal deposits without any involvement of macula or fovea. Two had transient localized retro-orbital pain that subsided after discontinuing the drug. These 2 patients received a thorough examination including slit-lamp evaluation and MR imaging of the brain. No evidence of optic neuritis, papilledema, or retinal damage was observed. The pain did not return after the therapy was resumed.
One patient patient 4 developed bleaching of her hair. In , a year-old man developed numbness of his left foot, pain in the left calf muscles associated with diminishing muscle strength, and difficulty walking. He paid little attention to his symptoms. In , because of nonspecific chest symptoms of tightness and cough, a chest x-ray film was obtained. It showed bilateral hilar adenopathy and pulmonary infiltration. A transbronchial lung biopsy showed noncaseating granulomas. Because he was not sufficiently symptomatic, he did not accept any treatment.
In , a repeated chest x-ray film and computed tomograms disclosed the changes seen in His chest tightness, cough, and symptoms of neuropathy were still present but not severe enough for the patient to accept therapy. In , his condition worsened and he agreed to receive treatment. He was given prednisone, 60 mg daily, with instructions to continue treatment for 6 months.
After 2 weeks, the patient developed severe corticosteroid-induced side effects psychosis, insomnia, memory loss, muscle weakness, and weight gain. He discontinued the drug and did not come for a follow-up visit until At that time, he had been receiving no treatment for more than a year. His ataxia had worsened to the degree that he was nearly totally incapacitated.