Hi everyone!  Wasn't sure which place to post this, just wanted to share with everyone here my experience so you know in case.  I am going to a new psychiatrist for depression (my last doctor really didn't want to deal with someone who was a challenge because of having a disorder he knew nothing about) and this doc so far seems really nice.  Anyway, he prescribed me selegiline.  The day after, I had a flare up.  I thought coincidence.  The next day, worse, worse, and worse.  I looked it up, and the chemistry behind it is something about cytokines, and interleukins, and being pro-inflammatory.  I really lost it, thinking he would throw in the towel like so many of my other docs did, and would say this is too hard with your "problems."  In fact after many tears and a week of not telling him I stopped it (flare stopped day after), he told me it would never be something he would do.  Could it be???  I've been so emotionally scarred by doctors!  Could he be for real?  He's starting me on emsam (patch form) to hopefully bypass the problem internally, but I thought of this forum, and wanted people here to know.  So few docs know about our "problem" but so many of us are hurting from depression too.  I just wanted everyone here to know about the possibility in case a doc offers it to you.  Good luck to you all!  Cydnie

Cydnie,

I think your doctor needs to have your serotonin levels checked.  A study done by Dr. Dean Metcalfe at the NIH was done in 2008 on mastocytosis patients and our serotonin levels and the disease was found to cause either high levels or way low levels.  Mine are way low.  When I showed this report to my doctors one of them told me that any kind of anti-depressant which is a serotonin reuptake inhibitor is contra-indicated in a patient like me.  

At the time it explained why I had adverse reactions to two medications earlier - one being Revotril and the other Doxepin.  Revotril is a sedating kind of anti-depressant and Doxepin is a tri-cyclic antihistamine/antidepressant.   Both of them make me much sicker!!

I would not be surprised that this might be your case, but you'll only know by having your blood serotonin levels checked in order to see where they are.  By confirming this you will know what anti-depressants you can use.  

I hope this helps!

Lisa

Tricyclic antidepressants also boost norepinephrine and can cause a rise in dopamine neurotransmission, too.  Personally, I think I lack dopamine, but will have tests done before I try anything, to see if anything is deficient.  Sorry about the length of this, but thought someone might be interested.....

This is from Stahl's Essential Psychopharmacology Online:

http://stahlonline.cambridge.org/prescribers_drug.jsf?page=0521683505c25_p147-15...


Doxepin

Brands

   * Sinequan
   * see index for additional brand names

Generic?

   * Yes

Class

   * Tricyclic antidepressant (TCA)
   * Serotonin and norepinephrine/noradrenaline reuptake inhibitor

Commonly Prescribed For

   * (bold for FDA approved)
   * Psychoneurotic patient with depression and/or anxiety
   * Depression and/or anxiety associated with alcoholism
   * Depression and/or anxiety associated with organic disease
   * Psychotic depressive disorders with associated anxiety
   * Involutional depression
   * Manic-depressive disorder
   * Pruritus/itching (topical)
   * Dermatitis, atopic (topical)
   * Lichen simplex chronicus (topical)
   * Anxiety
   * Insomnia
   * Neuropathic pain/chronic pain
   * Treatment-resistant depression

How The Drug Works

At antidepressant doses:

   * Boosts neurotransmitters serotonin and norepinephrine/noradrenaline
   * Blocks serotonin reuptake pump (serotonin transporter), presumably increasing serotonergic neurotransmission
   * Blocks norepinephrine reuptake pump (norepinephrine transporter), presumably increasing noradrenergic neurotransmission
   * Presumably by desensitizes both serotonin 1A receptors and beta adrenergic receptors
   * Since dopamine is inactivated by norepinephrine reuptake in frontal cortex, which largely lacks dopamine transporters, doxepin can thus increase dopamine neurotransmission in this part of the brain
   * May be effective in treating skin conditions because of its strong antihistamine properties

At low doses (1-6 mg/day):

   * Selectively and potently blocks histamine 1 receptors, presumably decreasing wakefulness and thus promoting sleep

How Long Until It Works

   * May have immediate effects in treating insomnia or anxiety
   * Onset of therapeutic actions usually not immediate, but often delayed 2-4 weeks
   * If it is not working within 6-8 weeks for depression, it may require a dosage increase or it may not work at all
   * May continue to work for many years to prevent relapse of symptoms

If It Works

   * The goal of treatment of depression is complete remission of current symptoms as well as prevention of future relapses
   * The goal of treatment of insomnia is to improve quality of sleep, including effects on total wake time and number of nighttime awakenings.
   * The goal of treatment of chronic neuropathic pain is to reduce symptoms as much as possible, especially in combination with other treatments
   * Treatment of depression most often reduces or even eliminates symptoms, but not a cure since symptoms can recur after medicine stopped
   * Treatment of chronic neuropathic pain may reduce symptoms, but rarely eliminates them completely, and is not a cure since symptoms can recur after medicine is stopped
   * Continue treatment of depression until all symptoms are gone (remission)
   * Once symptoms of depression are gone, continue treating for 1 year for the first episode of depression
   * For second and subsequent episodes of depression, treatment may need to be indefinite
   * Use in anxiety disorders, chronic pain, and skin conditions may also need to be indefinite, but long-term treatment is not well studied in these conditions

If It Doesn’t Work

   * Many depressed patients only have a partial response where some symptoms are improved but others persist (especially insomnia, fatigue, and problems concentrating)
   * Other depressed patients may be nonresponders, sometimes called treatment-resistant or treatment-refractory
   * Consider increasing dose, switching to another agent or adding an appropriate augmenting agent
   * Consider psychotherapy
   * Consider evaluation for another diagnosis or for a comorbid condition (e.g., medical illness, substance abuse, etc.)
   * Some patients may experience apparent lack of consistent efficacy due to activation of latent or underlying bipolar disorder, and require antidepressant discontinuation and a switch to a mood stabilizer
   * If Insomnia does not improve after 7-10 days, it may be a manifestation of a primary psychiatric or physical illness such as obstructive sleep apnea or restless leg syndrome, which requires independent evaluation

Best Augmenting Combos for Partial Response or Treatment-Resistance

   * Lithium, buspirone, thyroid hormone (for depression)
   * Trazodone, GABA-ergic sedative hypnotics (for insomnia)
   * Gabapentin, tiagabine, other anticonvulsants, even opiates if done by experts while monitoring carefully in difficult cases (for chronic pain)

Tests

   * None for healthy individuals
   * Since tricyclic and tetracyclic antidepressants are frequently associated with weight gain, before starting treatment, weigh all patients and determine if the patient is already overweight (BMI 25.0–29.9) or obese (BMI ≥30)
   * Before giving a drug that can cause weight gain to an overweight or obese patient, consider determining whether the patient already has pre-diabetes (fasting plasma glucose 100–125 mg/dL), diabetes (fasting plasma glucose >126 mg/dl), or dyslipidemia (increased total cholesterol, LDL cholesterol and triglycerides; decreased HDL cholesterol), and treat or refer such patients for treatment including nutrition and weight management, physical activity counseling, smoking cessation, and medical management
   * Monitor weight and BMI during treatment
   * While giving a drug to a patient who has gained >5% of initial weight, consider evaluating for the presence of pre-diabetes, diabetes, or dyslipidemia, or consider switching to a different antidepressant
   * EKGs may be useful for selected patients (e.g., those with personal or family history of QTc prolongation; cardiac arrhythmia; recent myocardial infarction; uncompensated heart failure; or taking agents that prolong QTc interval such as pimozide, thioridazine, selected antiarrhythmics, moxifloxacin, sparfloxacin, etc.)
   * Patients at risk for electrolyte disturbances (e.g., patients on diuretic therapy) should have baseline and periodic serum potassium and magnesium measurements

Cyndie ,

I have had to work hard to trust new doctors . Of the 5 that stand out from the crowd , only 2 do for bad reasons .3 for very good reasons . One , young doctor did not stress when i didnt fit a box . he treated what he saw and asked me how I was coping when I was at my lowest ebb .

I had had a close call ( short of epi pen ) on the saturday , then the following wednesday ,  a CT contrast reaction - 7 doses of adrenaline , steriods , piriton IV and nebulisers  ( before I got here ) . Which was the worst day of my life so far . 3 weeks later another  2 Epi Pen level reaction . So it was then he met me -  i was a mess . he took time to ask me , not make assumptions and take my answers and not read into them .

By this point I had been through 8 months of 3 weekly reactions and an april with 4 , 2in one week .

I was being served poorly by an immunologist , who wouldn't consider triggers - sulphites as a cause of my reactions , which had distressed me greatly . i was getting to london , on a train and taxi to see him , with my partner using a wheelchair . When i tried to discuss anesthetic as I ahd an upcoming procedure  - his response was - dont tell them you are having reactions otherwise they will not do it - not useful .

So I have had expierences which mean I should hold most doctors in very little regard . But I have also had some which mean I know many doctors would be horrified at how I have been treated. Like your experience they would never disregard my condition (s). As a nurse I learnt that it is not having a medical licence that makes you a doctor it is the person and their humanity .  

The listening open doctor helped a lot in my attitude . I felt able to give them a chance .

I next met him the following january , he was now working in ED . Again he cared for me , treating what he saw , despite still not knowing what was wrong .

The not good immunologist binned me to St Thomas' , were the best UK masto docs are .

In the UK we have General practioners who see you and one is available 24/7 . They then refer us to specialists . My GP in my new area my GP is happy that I understand my condition and am helping myself . He also warned me to be vigilant about medications to ensure my preperations are safe.

My last one took a good year to really get how this illness affects me and that i am determined with a capital D .

Your reaction to the drug may also have been the effect on your serotonin levels . As some masto / mcas patients dont do well with having even low serotonin messed with . So SSRI's are not advised either . MOAI's and traditional benzodizapines are safer and looking in those categories may be the best for you . Are you a patient of one of the masto specalists ?? if not your doc can contact them for general advice on drugs . As I fully appreciate depression is unbearable . I ahve been depressed in the past so I understand

I hope this helps ,

Josie