Thalidomide can prevent menstruation.In addition, very common (reported in more than 10% of people) adverse effects include tremor, dizziness, tingling, numbness, constipation, and peripheral edema.Common adverse effects (reported by 1–10% of people) include confusion, depressed mood, reduced coordination, heart failure, difficulty breathing, interstitial lung disease, lung inflammation, vomiting, dry mouth, rashes, dry skin, fever, weakness, and a sense of unwellness. Interactions
There are no expected pharmacokinetic interactions between thalidomide and other medicines due to its neutral effects on P-glycoprotein and the cytochrome P450 family. It may interact with sedatives due to its sedative action and bradycardic agents, like beta-blockers, due to its bradycardia-inducing effects. The risk of peripheral neuropathy may be increased by concomitant treatment with other agents known to cause peripheral neuropathy. The risk of venous thromboembolisms with thalidomide seems to be increased when patients are treated with oral contraceptives or other cytotoxic agents (including doxorubicin and melphalan) concurrently. Thalidomide may interfere with various contraceptives, and hence it is advised that women of reproductive age use at least two different means of contraception to ensure that no child will be conceived while they are taking thalidomide. Overdose
As of 2013, eighteen cases of overdoses had been reported with doses of up to 14.4 grams, none of them fatal. No specific antidote for overdose exists and treatment is purely supportive. Pharmacology
The precise mechanism of action for thalidomide is not known, although efforts to identify thalidomides teratogenic action generated 2,000 research papers and the proposal of 15 or 16 plausible mechanisms by 2000.
7p22.1 microduplication syndrome (also called Trisomy 7p22.1) is a newly discovered genetic disorder which is characterized by cranial and facial dysmorphisms, intellectual disability, and motor-speech delays. It is caused by a duplication of the p22.1 region of chromosome 7. Signs and symptoms
The symptoms of this syndrome are (but are not limited to) cranio-facial dysmorphisms such as macrocephaly, frontal bossing, low-set ears, hypertelorism, etc., intellectual disabilities, speech and motor delays, and heart, ocular, renal and skeletal defects (such as patent foramen ovale {heart} or brachydactyly type D {skeletal} ). Causes
This condition (as the name implies) is caused by a 430 kB duplication of the p22.1 region of chromosome 7. This mutation is autosomal recessive , meaning that a baby would need 1 copy of a mutated gene from both parents in order to show symptoms of the disorder. Epidemiology
Only 60 cases of 7q22.1 microduplication syndrome have been recorded in medical literature


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