Antivirals, Antibiotics and Immune Modulators
Minocyclin
Thread starter glenp
glenp
"and this too shall pass"
Vancouver Canada suburbs
I couldn't find the minocyclin thread. Has anyone had negative affects from minocyclin? I have been taking minocyclin for 6 months and have had much improvement. I've noticed ringing in my ears which really scares me and wonder if anyone has had any bad affects from it. I have had damage from gentamycin so am very cautious now - I just stopped and will call my doctor tomorrow. I really hate to stop - It has improved my migraines and head pain dramatically. I am wondering if the ringing in the ears could be it affecting the inner ear as gentamycin can?? and that is permanent?? I called the pharmassist who said all symptoms disappear after treatment is stopped!!!! ???
aruschima
glenp said:
Hi Glenp,
1.The ringing in the ear sounds like Tinnitus and sounds like a side effect of Minocycline
Minocycline may cause upset stomach, diarrhea, dizziness, unsteadiness, drowsiness, headache and vomiting. Minocycline increases sensitivity to sunlight. It has also been linked to cases of lupus. Minocycline can reduce the effectiveness of oral contraceptives.[8] Prolonged use of minocycline over an extended period of time can lead to blue-gray skin (permanent blue discoloration of gums) or teeth discoloration. Rare but serious side effects include fever, yellowing of the eyes or skin, stomach pain, sore throat, vision changes, and mental changes, including depersonalization.[9][10]
Minocycline, but not other tetracyclines, can cause vestibular disturbances with dizziness, ataxia, vertigo and tinnitus. This side effect is much more common in women than in men, occurring in 50% to 70% of women receiving minocycline. As a result of the frequency of this bothersome side effect, minocycline is rarely used in female patients.[11]
Symptoms of an allergic reaction include rash, itching, swelling, severe dizziness, and trouble breathing.[9] Minocycline has also been reported to cause idiopathic intracranial hypertension (pseudotumor cerebri).
ADVERSE REACTIONS Others: Thyroid cancer has been reported in the post-marketing setting in association with minocycline products. When minocycline therapy is given over prolonged periods, monitoring for signs of thyroid cancer should be considered
http://en.wikipedia.org/wiki/Minocycline
2. Minocycline is known for its bad side effect and can also induce, or activate dormant autoimmune diseases.
I had a long thread on prohealth years ago on
Antibiotics + FM/ME/CFIDS + Adverse Drug Reactions+Autoimmune D.
You can find it here :http://www.prohealth.com/fibromyalgia/blog/boardDetail.cfm?id=1015520&setBoard=FM#1015520
In my opinion: not a good idea to take ABX for patients with ME/CFS, especially those who have autoimmune (like) issues. But if it helped you, you might be able to change to one which has less side effects than Minocycline, if you intend to take ABX for a longer period.
I tried Minocylcine 18-24 months ago for a couple of weeks. It made me very nauseous and I didn't see any other change during that time so I quit. I tried again a couple of months later with the same result, so I gave up on it.
I didn't have any ringing in my ears, though.
FunkOdyssey
Minocycline: inhibiting NF-KappaB in the brain, inhibiting microglial activation, inhibits HIV replication, protects brains of mice from an MLV (close relative of XMRV). Seems like it would at least help via NF-KappaB inhibition, and if we were really lucky might directly inhibit XMRV replication as it does in HIV. The list of studies documenting one or another neuroprotective feature of minocycline is ridiculously long now but I will limit this to what seems most relevant to XMRV:
J Infect Dis. 2010 Apr 15;201(8):1132-40.
Minocycline attenuates HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells.
Szeto GL, Brice AK, Yang HC, Barber SA, Siliciano RF, Clements JE.
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Treatment of human immunodeficiency virus (HIV) infection with highly active antiretroviral therapy (HAART) is effective but can be associated with toxic effects and is expensive. Other options may be useful for long-term therapy. The immunomodulatory antibiotic minocycline could be an effective, low-cost adjunctive treatment to HAART. Minocycline mediated a dose-dependent decrease in single-cycle CXCR4-tropic HIV infection and decreased viral RNA after infection of CD4+ T cells with HIV NL4-3. Reactivation from latency was also decreased in a primary CD4+ T cell-derived model and in resting CD4+ T cells from HIV-infected patients. Minocycline treatment resulted in significant changes in activation marker expression and inhibited proliferation and cytokine secretion of CD4+ T cells in response to activation. This study demonstrates that minocycline reduces HIV replication and reactivation and decreases CD4+ T cell activation. The anti-HIV effects of minocycline are mediated by altering the cellular environment rather than directly targeting virus, placing minocycline in the class of anticellular anti-HIV drugs.
Brain Res. 2009 Aug 25;1286:174-84. Epub 2009 Jun 11.
Attenuation of oxidative stress, inflammation and apoptosis by minocycline prevents retrovirus-induced neurodegeneration in mice.
Kuang X, Scofield VL, Yan M, Stoica G, Liu N, Wong PK.
Department of Carcinogenesis, University of Texas, M.D. Anderson Cancer Center, Science Park-Research Division
The ts1 mutant of the Moloney murine leukemia virus (MoMuLV) causes neurodegeneration in infected mice that resembles HIV-associated dementia. We have shown previously that ts1 infects glial cells in the brain, but not neurons. The most likely mechanism for ts1-mediated neurodegeneration is loss of glial redox support and glial cell toxicity to neurons. Minocycline has been shown to have neuroprotective effects in various models of neurodegeneration. This study was designed to determine whether and how minocycline prevents paralysis and death in ts1-infected mice. We show here that minocycline delays neurodegeneration in ts1-infected mice, and that it prevents death of cultured astrocytes infected by ts1 through attenuating oxidative stress, inflammation and apoptosis. Although minocycline reduces virus titers in the CNS of infected mice, it does not affect virus titers in infected mice thymi, spleens or infected C1 astrocytes. In addition, minocycline prevents death of primary neurons when they are cocultured with ts1-infected astrocytes, through mechanisms involving both inhibition of oxidative stress and upregulation of the transcription factor NF-E2-related factor 2 (Nrf2), which controls cellular antioxidant defenses. We conclude that minocycline delays retrovirus ts1-induced neurodegeneration involving antioxidant, anti-inflammation and anti-apoptotic mechanisms.
J Neurovirol. 2008 Oct;14(5):376-88. Epub 2008 Nov 12.
Mechanisms of minocycline-induced suppression of simian immunodeficiency virus encephalitis: inhibition of apoptosis signal-regulating kinase 1.
Follstaedt SC, Barber SA, Zink MC.
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Human immunodeficiency virus (HIV) infection of the central nervous system (CNS) can lead to cognitive dysfunction, even in individuals treated with highly active antiretroviral therapy. Using an established simian immunodeficiency virus (SIV)/macaque model of HIV CNS disease, we previously reported that infection shifts the balance of activation of mitogen-activated protein kinase (MAPK) signaling pathways in the brain, resulting in increased activation of the neurodegenerative MAPKs p38 and JNK. Minocycline treatment of SIV-infected macaques reduced the incidence and severity of SIV encephalitis in this model, and suppressed the activation of p38 in the brain. The purpose of this study was to further examine the effects of minocycline on neurodegenerative MAPK signaling. We first demonstrated that minocycline also decreases JNK activation in the brain and levels of the inflammatory mediator nitric oxide (NO). We next used NO to activate these MAPK pathways in vitro, and demonstrated that minocycline suppresses p38 and c-Jun N-terminal kinase (JNK) activation by reducing intracellular levels, and hence, activation of apoptosis signal-regulating kinase 1 (ASK1), a MAPK kinase capable of selectively activating both pathways. We then demonstrated that ASK1 activation in the brain during SIV infection is suppressed by minocycline. By suppressing p38 and JNK activation pathways, which are important for the production of and responses to inflammatory mediators, minocycline may interrupt the vicious cycle of inflammation that both results from, and promotes, virus replication in SIV and HIV CNS disease.
Bioinformatics. 2007 Oct 15;23(20):2797-9. Epub 2007 Sep 5.
Identification of potential HIV-1 targets of minocycline.
Jenwitheesuk E, Samudrala R.
National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency
Minocycline, a broad spectrum antibiotic, has been discovered to have inhibitory activity against HIV-1 in vitro, but the targets inhibited are unknown. We used a docking with dynamics protocol developed by us to predict the binding affinities of minocycline against seven active sites of five HIV-1 proteins to putatively identify the potential target(s) of minocycline. The results indicate that minocycline has the highest predicted binding affinity against HIV-1 integrase.
PLoS One. 2010 May 7;5(5):e10523.
Proton magnetic resonance spectroscopy reveals neuroprotection by oral minocycline in a nonhuman primate model of accelerated NeuroAIDS.
Ratai EM, Bombardier JP, Joo CG, Annamalai L, Burdo TH, Campbell J, Fell R, Hakimelahi R, He J, Autissier P, Lentz MR, Halpern EF, Masliah E, Williams KC, Westmoreland SV, Gonzlez RG.
AA Martinos Center for Biomedical Imaging and Neuroradiology Division, Massachusetts General Hospital
BACKGROUND: Despite the advent of highly active anti-retroviral therapy (HAART), HIV-associated neurocognitive disorders continue to be a significant problem. In efforts to understand and alleviate neurocognitive deficits associated with HIV, we used an accelerated simian immunodeficiency virus (SIV) macaque model of NeuroAIDS to test whether minocycline is neuroprotective against lentiviral-induced neuronal injury.
METHODOLOGY/PRINCIPAL FINDINGS: Eleven rhesus macaques were infected with SIV, depleted of CD8+ lymphocytes, and studied until eight weeks post inoculation (wpi). Seven animals received daily minocycline orally beginning at 4 wpi. Neuronal integrity was monitored in vivo by proton magnetic resonance spectroscopy and post-mortem by immunohistochemistry for synaptophysin (SYN), microtubule-associated protein 2 (MAP2), and neuronal counts. Astrogliosis and microglial activation were quantified by measuring glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (IBA-1), respectively. SIV infection followed by CD8+ cell depletion induced a progressive decline in neuronal integrity evidenced by declining N-acetylaspartate/creatine (NAA/Cr), which was arrested with minocycline treatment. The recovery of this ratio was due to increases in NAA, indicating neuronal recovery, and decreases in Cr, likely reflecting downregulation of glial cell activation. SYN, MAP2, and neuronal counts were found to be higher in minocycline-treated animals compared to untreated animals while GFAP and IBA-1 expression were decreased compared to controls. CSF and plasma viral loads were lower in MN-treated animals.
CONCLUSIONS/SIGNIFICANCE: In conclusion, oral minocycline alleviates neuronal damage induced by the AIDS virus.
A novel use for an old drug: the potential for minocycline as anti-HIV adjuvant therapy.
Copeland KF, Brooks JI.
J Infect Dis. 2010 Apr 15;201(8):1115-7. No abstract available. PMID: 20205572
JAMA. 2005 Apr 27;293(16):2003-11.
Neuroprotective and anti-human immunodeficiency virus activity of minocycline.
Zink MC, Uhrlaub J, DeWitt J, Voelker T, Bullock B, Mankowski J, Tarwater P, Clements J, Barber S.
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, Md 21205, USA. mczink@jhmi.edu
CONTEXT: The prevalence of human immunodeficiency virus (HIV) central nervous system (CNS) disease has not decreased despite highly active antiretroviral therapy. Current antiretroviral drugs are expensive, have significant adverse effects including neurotoxicity, and few cross the blood-brain barrier.
OBJECTIVE: To examine the ability of minocycline, an antibiotic with potent anti-inflammatory and neuroprotective properties, to protect against encephalitis and neurodegeneration using a rapid, high viral load simian immunodeficiency virus (SIV) model of HIV-associated CNS disease that constitutes a rigorous in vivo test for potential therapeutics.
DESIGN AND SUBJECTS: Five SIV-infected pigtailed macaques were treated with 4 mg/kg per day of minocycline beginning at early asymptomatic infection (21 days after inoculation). Another 6 macaques were inoculated with SIV but remained untreated. Blood and cerebrospinal fluid (CSF) samples were taken on days 7, 10, 14, 21, 28, 35, 43, 56, 70, 77, and 84, and all macaques were humanely killed at 84 days after inoculation, a time that corresponds to late-stage infection in HIV-infected individuals.
MAIN OUTCOME MEASURES: Blood and CSF samples were tested for viral load by real-time reverse transcription-polymerase chain reaction and levels of monocyte chemoattractant protein 1 were quantitated by enzyme-linked immunosorbent assay. The presence and severity of encephalitis was determined by microscopic examination of tissues. Central nervous system inflammation was further assessed by measuring infiltration and activation of macrophages, activation of p38 mitogen-activated protein kinase and expression of amyloid precursor protein by quantitative immunohistochemistry.
RESULTS: Minocycline-treated macaques had less severe encephalitis (P = .02), reduced CNS expression of neuroinflammatory markers (major histocompatibility complex class II, P = .03; macrophage marker CD68 , P = .07; T-cell intracytoplasmic antigen 1, P = .03; CSF monocyte chemoattractant protein 1, P = .001), reduced activation of p38 mitogen-activated protein kinase (P<.001), less axonal degeneration (beta-amyloid precursor protein, P = .03), and lower CNS virus replication (viral RNA, P = .04; viral antigen, P = .04). In in vitro analysis, minocycline suppression of HIV and SIV replication in cultured primary macrophages did not correlate with suppression of activation of p38-mitogen-activated protein kinase pathways, whereas suppression in primary lymphocytes correlated with suppression of p38 activation.
CONCLUSIONS: In this experimental SIV model of HIV CNS disease, minocycline reduced the severity of encephalitis, suppressed viral load in the brain, and decreased the expression of CNS inflammatory markers. In vitro, minocycline inhibited SIV and HIV replication. These findings suggest that minocycline, a safe, inexpensive, and readily available antibiotic should be investigated as an anti-HIV therapeutic.
Has anyone tried Minocycline for XMRV?
Ty for your replies
It has really helped me for the 6 months I have been on it ---- helps my head. I hated to stop but am terrified of the buzzing ears - thinking back to when I took gentamycin and got permanent damage - idk if it could cause permanent inner ear damage or not? It really has helped -- migraines, soar head, smells that aren't there, and also soar throat
pine108kell
I always a little surprised when I read that people with CFS can tolerate minocycline for long periods. The die off for me is horrenduous and turns me into a basket case in less than a week. It makes me feel better for a few days because of the anti-inflammatory properties then the die off response becomes unbearable. I definitely have more signifigant bacterial infections (seem to have lyme) or a very different immune system.
I wonder if the benefits you are recieving are from killing organisms or the anti-inflammatory response? If it is the latter, maybe something else will help--I wish I knew what would give the benefits of the powerful anti-inflammatory response relevant to CFS without the die off or long term abx use.
dwy904
Did your ear ringing go away ?
I had minocycline for 1 month and 9 days. After I felt the ringing in ear I stopped right away. The ringing decrease a lot during these four weeks. But I can still hear a little bit. Will it go away ? I am scared.
AlmostEasy
pine108kell said:
If you receive that sort of die off that sounds clearly like a herx reaction as you're aware of. If the OP received benefit immediately, as I do, then it's almost certainly from it's anti inflammatory properties. I benefit from it almost immediately but taking it twice daily makes me feel incredibly strange and once daily isn't quite enough to eliminate my inflammation. I might play with it more.
I don't know the OP's story but I would recommend treating the cause of the inflammation in the first place rather than to continually use an antibiotic long term. I don't think that is a good strategy unless you've gone through extreme measures for years on end without finding any type of solution or reason for your dysfunction. With how much these drugs can alter your microbiome it's a bit frightening when you hear of someone using these long term.
Using potentially just as powerful natural remedies might afford you similar benefits without the potential of tinnitus and turning your skin permanently blue. I would read through the thread I linked and see if you can find any relief with those if you don't know the root cause of your disorder.
The Lederle minocin cure my FMS over 15 years ago. I took it ever day for two years. I had no negative effects except plaque build up on teeth. The generic minocycline didn't work. The best low cost minocycline is Teva and Ranbaxy. The original minocin was time release pellets and the price has skyrocketed where only bill gates can afford it. The way it helps is by helping the immune system. Except for amoxicillin, I say away from all other antibiotics. They can wipe out your intestinal flora. Cipro has been deadly to a lot of people. Everyone responds to antibiotics differently so people can have very negative reaction to the drug. Some people are told that a bad reaction to antibiotics is just the die off. That's debatable. Well, when I had that so called die off with other antibiotics, I just stopped taking it after 2 days.
I have had ringing in ears for the last 40 years. I have ignored it since I am buried with more important symptoms. I still have good hearing.
prioris said:
I only had minocycline for 1 month and 9 days and the ringing sound decrease a lot during following four weeks but it has not completely gone yet. I am so worried.
Roughly 10 percent of the adult population of the United States has experienced tinnitus lasting at least five minutes in the past year. This amounts to nearly 25 million Americans.
If it is decreasing then it's getting better. the fact that you are headed in the right direction is a positive sign. You will have to research the serious consequences for certain situations. my ringing gets better then get worse then gets better then gets worse ... i never had time to pay much attention to it. when i try to take b12 or folate the ringing gets worse. use your intuition to tell you what to do.
For the first and second week, it was like motor sound. During the third week the sound reduced so much and the sound was like 'si si si si' and the motor sound was gone. During the fourth week, the sound is still 'si si si si' but it seems like it increase a little bit these day which is the end of the fourth week. I really have no idea how it will end up. T_T
That is interesting, I don't know much about FMS.
Did you take the Lederle minocin initally? How long did it take to help? Did symptoms come back when you tried the generic minocycline? Are you saying that the Teva and Ranbaxy minocycline helped during these 2 years or in subsequent years have you just researched and found them to be effective compared to generic?
That is true some of the side effects are similar to a herxheimer reaction. Having a confirmation for Lyme might help in the decision to push through or quit.
Do you have ME/CFS issues now that you tried to treat with antibiotics that gave you poor reaction?