This condition may also be due to the change in the chromosome affecting the transcription of genes. Other hypertrichosis patterns
Porphyria cutanea tarda may manifest in some patients as hypertrichosis on the face (mainly on top of the cheeks). Medical conditions
Acquired hypertrichosis lanuginosa is commonly present with cancer. This condition is also linked to metabolic disorders, such as anorexia, hormone imbalances, such as hyperthyroidism, or as a side effect of certain drugs.Acquired generalized hypertrichosis may be caused by cancer. The resulting hair growth is known as malignant down. The mechanism behind cancer induced hypertrichosis is unknown. Oral and topical minoxidil treatments are also known to cause acquired generalized hypertrichosis. Medications
Several medications can cause generalized or localized acquired hypertrichosis including:

Anticonvulsants: phenytoin
Immunosuppressants: cyclosporine
Vasodilators: diazoxide and minoxidil
Antibiotics: streptomycin
Diuretics: acetazolamide
Photosensitizers: PsoralenThe acquired hypertrichosis is usually reversible once these medications are discontinued. Other
Unknown causes
The exact genetic mutation that causes congenital circumscribed, localized, and nevoid hypertrichosis is unknown. Pathophysiology
A number of mechanisms can lead to hypertrichosis. One cause involves areas of the skin that are transforming from the small vellus type to the larger terminal type. This change normally occurs during adolescence, when vellus hair follicles in the underarms and groin grow into terminal hair follicles. Hypertrichosis involves this same type of switching, but in areas that do not normally produce terminal hair. The mechanisms for this switch are poorly understood.Another mechanism involves a change in the hair cycle.
The current drug-based treatments of psychotic depression are reasonably effective but can cause side effects, such as nausea, headaches, dizziness, and weight gain. Electroconvulsive therapy (ECT)
In modern practice of ECT a therapeutic clonic seizure is induced by electric current via electrodes placed on a person under general anesthesia. Despite much research the exact mechanism of action of ECT is still not known. ECT carries the risk of temporary cognitive deficits (e.g., confusion, memory problems), in addition to the burden of repeated exposures to general anesthesia. Research
Efforts are made to find a treatment which targets the proposed specific underlying pathophysiology of psychotic depression. A promising candidate was mifepristone, which by competitively blocking certain neuro-receptors, renders cortisol less able to directly act on the brain and was thought to therefore correct an overactive HPA axis. However, a Phase III clinical trial, which investigated the use of mifepristone in PMD, was terminated early due to lack of efficacy.Transcranial magnetic stimulation (TMS) is being investigated as an alternative to ECT in the treatment of depression. TMS involves the administration of a focused electromagnetic field to the cortex to stimulate specific nerve pathways. Research has shown that psychotic depression differs from non-psychotic depression in a number of ways: potential precipitating factors, underlying biology, symptomatology beyond psychotic symptoms, long-term prognosis, and responsiveness to psychopharmacological treatment and ECT. Prognosis
The long-term outcome for psychotic depression is generally poorer than for non-psychotic depression. == References ==