It is also present in many patients with Parkinsons disease or Lewy body dementia resulting from sympathetic denervation of the heart or as a side effect of dopaminomimetic therapy. This rarely leads to fainting unless the person has developed true autonomic failure or has an unrelated heart problem.Another disease, dopamine beta hydroxylase deficiency, also thought to be underdiagnosed, causes loss of sympathetic noradrenergic function and is characterized by low or extremely low levels of norepinephrine, but an excess of dopamine.Quadriplegics and paraplegics also might experience these symptoms due to multiple systems inability to maintain normal blood pressure and blood flow to the upper part of the body. Causes
Some causes of orthostatic hypotension include neurodegenerative disorders, low blood volume (e.g. caused by dehydration, bleeding, or the use of diuretics), drugs that cause vasodilation, other types of drugs (notably, narcotics and marijuana), discontinuation of vasoconstrictors, prolonged bed rest (immobility), significant recent weight loss,  anemia, vitamin B12 deficiency, or recent bariatric surgery. Medication
Orthostatic hypotension can be a side effect of certain antidepressants, such as tricyclics or monoamine oxidase inhibitors (MAOIs). Marijuana and tetrahydrocannabinol can on occasion produce marked orthostatic hypotension. Alcohol can potentiate orthostatic hypotension to the point of syncope. Orthostatic hypotension can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers inhibit vasoconstriction normally initiated by the baroreceptor reflex upon postural change and the subsequent drop in pressure. Other factors
Patients prone to orthostatic hypotension are the elderly, post partum mothers, and those having been on bed rest.
According to the US Food and Drug Administration, the drug may cause rare and possibly fatal skin reactions such as Stevens–Johnson syndrome and toxic epidermal necrolysis, although an analysis of the French Pharmacovigilance Database indicated no obvious risk of these reactions.In clinical trials for osteoarthritis, the number of participants reporting adverse effects were similar for those on paracetamol and on placebo. However, the abnormal liver function tests (meaning there was some inflammation or damage to the liver) were almost four times more likely in those on paracetamol, although the clinical importance of this effect is uncertain. After 13 weeks of paracetamol therapy for knee pain, a drop in hemoglobin level indicating gastrointestinal bleeding was observed in 20% of participants, this rate being similar to ibuprofen group.Due to the absence of controlled studies, most of the information about the long-term safety of paracetamol comes from observational studies. These indicate a consistent pattern of increased mortality as well as cardiovascular (stroke, myocardial infarction), gastrointestinal (ulcers, bleeding) and renal adverse effects with increased dose of paracetamol. Use of paracetamol is associated with 1.9 times higher risk of peptic ulcer. Those who take it regularly at a higher dose (more than 2–3 g daily) are at much higher risk (3.6–3.7 times) of gastrointestinal bleeding and other bleeding events. Meta-analyses suggest that paracetamol may increase the risk of kidney impairment by 23% and kidney cancer by 28%.