Pharmacotherapy - Science topic

Yes, Nootropics like citicoline and piracetam can be given because these drugs increase oxygen utilization in nerves so nerves can grow better.

Many journals are missing in RG's database. See https://help.researchgate.net/hc/en-us/articles/14293139566353: "Due to resourcing constraints, please understand that we cannot accept requests to manually add journals to our database. Currently, we only import journal data from CrossRef. ..." - When a journal is missing in RG's database, I add the bibliographic data to the abstract field (like in https://www.researchgate.net/publication/268925009 or https://www.researchgate.net/publication/344474227).

See also this help page ("How to add research") for general instructions how to add publications to ResearchGate: https://help.researchgate.net/hc/en-us/articles/14293005132305

Belumosudil (KD025) is a specific inhibitor for ROCK2, which has been used for lung fibrosis and some other diseases. It may also be a potential drug in renal diseases.

What is your outcome variable? is it dichotomous or continuous?

for binary outcomes use qui square and t test (if you have 2 groups only) for continuous regardless of distribution as far as you use randomization to assign patients to treatments.

See Friedman 2015 book on clinical trials. Mohammad Al Qadire

Clinical Pharmacist is an active member of healthcare team providing direct patient care. American College of Clinical Pharmacy describes role of a Clinical Pharmacist as working directly with physicians, other health professionals, and patients to ensure that the medications prescribed for patients contribute to the best possible health outcomes. This role provides opportunity for a Clinical Pharmacist to apply core of pharmacy in patient care.

In addiction is the mesolimbic pathway, also called reward pathway, as a dopaminergic pathway in the brain, involved

Before combining with other antipsychotics, it might be helpful to control serum levels, because particularly in clozapine, non-compliance or only partial compliance is a frequent cause of treatment resistance.

Great discussion. You are all invited to Join PharmaHuF on LinkedIn where we are collecting a lot of the evidence concerning this subject. Just request to join and I can approve. 

You are right. We are conducting this type of study in Europe now. I hope that the results will be positive for patients, GPs and payers. U.S. evidence tell us that this type of coolaborative care should be establish within helath system.

Amisulpride might indeed be very effective in the elderly patients. However, to my experience, the potential of inducing EPS is not that small. I have seen parkinsonism even after very low doses and if dose goes up to 200 mg and a patient is older than 75... Well, the drug becomes problematic. On the other hand, the use as an augmentation in MDD could be bigger. Low doses (usually up to 100 mg/day) are quite effective, particularly in cases with lack of energy / apathy / anhedonia. 

Dear Behailu

I may suggest the following, and you can also see the attached article for more details. check the references in the article to get more ideas. good luck

Management of cancer pain. Pharmacology and principles of management

Morphine and alternative opioids in cancer pain: the EAPC recommendations

I provide discharge counseling to all patients at my 88 bed acute and residential psychiatric children's hospital. Most moderate-large sized hospitals in my region who staff clinical pharmacists also perform this service. Hospitals without adequate pharmacist coverage cannot consistently provide this important service.

Agree with Ian Mcgrane. This is a new market, with Deplin claiming to be superior to Enlyte and visa versa: the representatives are doing their job well, as are the new companies that tout the benefits of MTHR genotyping.  BUT THE SCIENCE IS NOT THERE TO JUSTIFY MAKING THIS STANDARD CLINICAL PRACTICE. And we should not be wasting patient's $ on this without basic and translational research making risks vs benefits clear.

Abstract

Purpose of review The magnitude of placebo response is an important factor in the outcome of clinical trials, in that excessive placebo response can obscure true drug–placebo differences. There is ample evidence of the impact of elevated placebo response in trials of major depression, but less intensive research has been done in the area of schizophrenia. We present a current review of placebo response in clinical trials of schizophrenia.

Recent findings The existing evidence suggests that placebo response in schizophrenia trials may be similar in magnitude, quality, and impact to that observed in depression trials, and has similarly increased over the past several years. We discuss factors influencing excessive placebo response during the conduct of clinical trials and how they may be managed to help minimize placebo response.

Summary There does not appear to be any single major factor contributing to the high levels of placebo response in schizophrenia clinical trials; therefore, a multipronged approach to minimizing excessive placebo response or its impact is recommended.

For more plz read at following link.

Regards

Efectivamente la terapia de compresión y las medidas de higiene venosa son las únicas donde se ha demostrado efecto significativo directo en la insuficiencia venosa crónica; es decir, mejoría en el tono de la pared vascular venosa y por ende, mejoría en la circulación.

Los datos clínicos asociados a la insuficiencia venosa crónica, como es la alteración de la piel cercana al estancamiento de la sangre venosa, flebitis y ulceración (sequedad, prurito, alteraciones de la sensibilidad, enrojecimiento, inflamación, infección y la formación de trombos e hiperpigmentación), si llegan a mejorar con farmacoterapia sistémica y local (antisépticos, antibióticos, antiplaquetarios, hemorreológicos, analgésicos antiinflamatorios y estimulantes de la cicatrización), pero no son resultado del efecto directo de los medicamentos llamados flebotónicos en el tono de la pared vascular del territorio venoso.

Saludos cordiales

Atentamente

Dr. José Luis García Vigil

PD: Envío versión en Español e Inglés para evitar problemas de interpretación, semánticos y de comunicación, inherentes a la traducción,

Indeed compression therapy and venous hygiene measures are the only ones that have shown significant direct effect on chronic venous insufficiency; that is, improvement in the tone of the venous vascular wall and hence, improvement in circulation.

Clinical data associated with chronic venous insufficiency, such as the alteration of the skin near the stagnation of venous blood, phlebitis and ulceration (dryness, itching, abnormal sensitivity, redness, swelling, infection, thrombus formation and hyperpigmentation), if they improve with systemic and local pharmacotherapy (antiseptics, antibiotics, anti-platelet, hemorheologic, anti-inflammatory and stimulating painkillers healing), but they are not a result of the direct effect of drugs called phlebotonics in the tone of the vascular wall of the venous territory.

Best regards

Sincerely

Dr. Jose Luis Garcia Vigil

PD: Shipping version in Spanish and English to avoid problems of interpretation, semantic and communication inherent in the translation,

There is a dearth of outcome data for all treatment modalities for all substance use disorders.  That said, the general consensus of clinicians IN THE UNITED STATES is against substitution (medication) therapy for stimulants (cocaine, methamphetamine, methylphenidate, d-amphetimine, a-amphetimine, dextroamphetamine, e.g. all DOPAMINE upregulators).  [In response to Dr. Rich's comment, I think the original question was aimed at stopping individuals from using methamphetamine using non-medicinal means.  Yes methamphetamine can induce psychosis, but clinicians can stop this not by treating psychosis directly but by trying to get meth users to stop using it.]  So, for clinicians wanting to take an abstinence-based approach, it seems that "talk therapy" like CBT and support-group therapy like 12-step programs (NA, AA, CA, etc) have shown success - but only anecdotally - we don't really know how effective these modalities are and for which patients they work, and how well they work, in achieving long-term remission from methamphetamine (stimulant) use disorders.  I think that, like with all substance use disorders, the best results will be obtained by keeping patients in long-term outpatient treatment following intensive residential treatment.  As Dr. Buttfield said "support" is the key, whatever the particular structure of a pt's aftercare plan.  Given how little real outcome data we have, the best strategy is probably to apply all available treatment modalities and hope that something helps.  But the *anecdotal* results so far are not terribly encouraging; most pts with stimulant use disorders have great difficulty achieving remission for any meaningful period of time.  In other words, the average Px for a pt presenting with stimulant use disorder is not terribly auspicious.  

For now, it seems that the only two viable non-medicinal treatments are direct therapy (CBT or otherwise) and mutual support therapy (12 step or other group therapy approaches).  I really hope that more treatment modalities will be developed for patients suffering from stimulant use disorder.  Remember also that most SUD patients have high comorbidity with other psychiatric disorders (which contribute to the difficulty of achieving absence/remission) -- it is important to Dx and Tx these as well as SUD itself.  

A final comment on the Karila et al article cited above, which reviews medicinal/pharmacological Tx (Rx) treatments.  There are really three types of strategies in medication, and I think it is important to categorize potential medications as such (1) "blockers" - e.g. medications that stop the stimulant from acting, such as naltrexone.  The problem with naltrexone, which works very well with both opioids and alcohol and has shown promise with stimulants, is PATIENT NON-COMPLIANCE.  Patients may take the medication during a study, but often will stop in conjunction with resuming use.  As such, it is not really a treatment, except in long-acting forms such as the monthly IV injection of naltrexone (Vivitrol in the US, manufactured by Alkermes).  The problem with this, again, is that patients will often decline to take medication that blocks the psychoactive effects of the substance they want to use.  Blocking strategies have had weak results so far EXCEPT in conjunction with rigorous aftercare programs, such as those required of physicians in recovery and pharmacists in recovery.

 (2) "Mitigating medications".  In my opinion, these show the most promise.  Bupropion, for example, is a very WEAK stimulant (and antidepressant and anxiolytic in some patients) - and if it can provide enough dopamine/norepinephrine/adrenaline upregulation that a patient will resist the urge to use a much stronger stimulant, then it is BY FAR a better alternative 

(3) substitution (harm reduction).  As Karila et al note, substitution with d-amphetamine, a STRONG stimulant, logically shows promise.  However, as with any substitution strategy, the patient remains dependent on a substitute stimulant with dangerous morbidity - but which may arguably be substantially less harmful than dependence on methamphetamine.  The Karila review, written in 2010, concludes "Despite the lack of success in most studies to date, increasing efforts are being made to develop medications for the treatment of methamphetamine dependence and several promising agents are targets of further research."  I am unaware of any such compounds emerging as likely candidates for medicinal treatment in the past several years.  

Furthermore, LONG-TERM COMPLIANCE is something that is rarely studied in the RCTs cited by Karila.  Unfortunately, there seems to be an inverse relationship between the effectiveness (measured in terms of pt quality of life) and pt compliance on medication.  With a blocking strategy, you get LOW LONG TERM COMPLIANCE, and with a strong-substitution strategy, you get much higher compliance (naturally) but then you are really just switching the patient from methamphetamine to a stimulant with less deleterious effects, while you try to keep the dose at a steady level (very difficult given rapid tolerance and relatively flat dose-response curves of many stimulant-substitution alternatives).  I am personally (subjectively) much more optimistic about opioid substitution therapy than I am about stimulant substation therapy for that reason -- but I have no data to  back up this conjecture.  

Dear Chen-Chia,

DEPENDS -- on the "cause" . . . Several years (decades) ago, my wife and I were invited to present at a symposium for elderly patients at a major psychiatric hospital. As we were both giving keynote addresses, we were invited on grand rounds. 

One of the patients we encountered was an elderly man, a grandfather, who although he had developed Alzheimer's was reasonably well adjusted and living at home with his son's family. Everyone loved and helped care for "grandpa" until he started making unwarranted sexual comments and advances towards his two grand-daughters. Subsequently, several weeks before we met him, he was transferred to the long-term psychogeriatric ward of the hospital -- for permanent stay.

Given his history, symptomatology, and the fact that we were both lecturing on the effects of medication use among the elderly, we suggested that his inappropriate behaviour might be due to a cyanocobalamin (vitamin B12) deficiency. A Shillings test revealed that his B12 level of extremely below normal. Subsequent daily injectable doses of 1000 mcg per day resulted in significant improvement in his mental status by the end of several weeks AND after several months, he was happily reunited with his family.

A true story, with a happy ending, that we also reported on as a case history at that time in the medical literature (see my list of publications for the exact reference). This response does NOT detract from the excellent advice that our other 2 colleagues have already provided you with. BUT, it should ADD to that advice and be a reminder to all of us clinicians that the first and most common response is not always the best for a particular individual patient . . .

I hope that this response is of some assistance.

Sincerely,

Lou

for a complete literature overview of Alzheimer drosophila model: 468 papers.

Dear friend thank u so much for the care!!!!! Big hug, Vinícius

Beatrice and Justin,

Thank you for your responses. Since my work focuses on the Roman army, and the Roman army was composed exclusively of male soldiers, I am gender-bound in my research. Please consider this factor in your responses. Beatrice has convinced me to conduct a second, future study involving female soldiers.

Val.

I also published on effect of systemic calcium blockade on intraocular pressure some time ago

Kelly SP, Walley TJ. Effect of the calcium antagonist nifedipine on intraocular pressure in normal subjects. Br J Ophthalmol 1988; 72: 216–8.

From my practical Experience, I did formulate Ciprofloxacin taste masking granules for suspension. It was really a fantastic job that I did in my career. I coated the powder with Eudragit L30D.It was 100% taste mask even when disperse with water. The granules size below #20.I also formulate Zn dispersible tablet with super disintegrant.

My view here, you can try these two combination effort to get a high dose load antibiotic dispersible tablet.

I am not sure where you are citing your findings regarding "Patients with cannabis dependence have high rates of co-occurring ADHD" as cannabis dependence is very different than an actual narcotic chemical dependance, especially given that cannabis is not a narcotic. While my research and specialty is with PTSD and cannabis, I have not seen any sustainable research that shows cannabis increases ADHD. I have argued in my findings that with the correct dose of cannabis, patients with PTSD suffer fewer PTSD-related side effects (ie flashbacks, nightmares, anxiety, etc) and are more present for psychotherapy to have a lasting affect. I also compare current psychotropics side-effects to cannabis side-effect, including overdose. This may assist with your question and may not, but I thought I would offer. Best of luck with your research and ongoing studies.

Frequently, clinical studies on antibiotics efficacy use two parameters for the study: clinical improvement/clinical cure, which means improvement or resolution of symptoms, and microbiological cure, which means disappearance of the microorganism.

This is a correct way of evaluation, provided that the definition of clinical cure and improvement is based on criteria objective enough.

Most patients under the age of 30 with a history of GAD from childhood typically don't require medication. If they do, a small dose of Paxil or Prozac for 3 to 6 months is sufficient. How therapy is conducted is far more important. There are multiple reasons that CBT has become the treatment of choice; however, a closer look reveals other methods are more effective. CBT treats thoughts and emotions as malleable and reward-able. They aren't and they are different from behavior. Patients gain valuable information from their emotions, likely linked to their anxiety. Further, to meet criteria for GAD, patients typically possess a high IQ. This is the key to treatment. These patients process information by linking topics, remembering details and being rewarded either in school or at work. In my professional opinion, it is detrimental to attempt to reverse a conditioning history from youth. It is also nearly impossible and often leads to depression. I have seen many patients benefit from learning how they process information, and gradually carving out quiet time when their mind is not busy. They necessary to succeed, they don't fight a relatively automatic process and of themselves and others as unique. They will remain thinkers for the rest of their lives, but will function at a much higher level and they will most likely not develop depression.

As a clinical researcher who participated in the clinical trials for pregabalin for GAD, it certainly does work but in higher doses (300mg +), when the risk of weight gain increases

According to the fact that only bacterial meningitis and meningoencephalitis can induce confusion, and the lack of interest for the diagnosis of Kernig's sign, nuchal rigidity, and headache, improvement of the mental and hemodynamic status are the BEST and alone scale for evaluating the clinical response of meningitis. Do not forget that a second lumbar puncture is usefull within the three-four days of treatment in case of doubt.

You may look at our paper published in Intensice care Medecine ( 2005) concerning the "Accuracy of clinical presentation for diffrentiating bacterial from viral meningitis ..."; (full on my contributions-publications).

Therapy of MAC infections of non-HIV patients is difficult (1). When you have across the board resistance as your question indicates, any current therapy is probably ineffective. When all else has failed and there is nothing available, one can treat the patient under compassionate basis that will improve quality of life and perhaps, bring about some relieve, if not a cure. We have shown that the use the old neuroleotic thiordazine will improve the quality of life of XDR TB patients and has been recommended as a salvage drug (2). In vitro, small quantities of thioridazine will render MAC strains susceptible to many second line drugs to which the strain was initially resistant (3). The positive in vitro responses are opined to be the result of inhibition of over-expressed efflux pumps which extrude the antibiotics before they reach their intended target (4). I suggest these cited papers for more complete info.

1. Ramirez J, Mason C, Ali J, Lopez FA. Mycobacterium avium complex pulmonary

disease: management options in HIV-negative patients. J La State Med Soc. 2008

Sep-Oct;160(5):248-54; quiz 254, 293. PubMed PMID: 19048978.

2a. Amaral L, Udwadia Z, Abbate E, van Soolingen D. The added effect of

thioridazine in the treatment of drug-resistant tuberculosis. Int J Tuberc Lung

Dis. 2012 Dec;16(12):1706-8; author reply 1708-9. doi: 10.5588/ijtld.12.0616.

PubMed PMID: 23131273.

2b. Amaral L, Boeree MJ, Gillespie SH, Udwadia ZF, van Soolingen D. Thioridazine

cures extensively drug-resistant tuberculosis (XDR-TB) and the need for global

trials is now! Int J Antimicrob Agents. 2010 Jun;35(6):524-6. doi:

10.1016/j.ijantimicag.2009.12.019. Epub 2010 Feb 25. Review. PubMed PMID:

20188526.

3. Viveiros M, Martins M, Couto I, Kristiansen JE, Molnar J, Amaral L. The in

vitro activity of phenothiazines against Mycobacterium avium: potential of

thioridazine for therapy of the co-infected AIDS patient. In Vivo. 2005

Jul-Aug;19(4):733-6. PubMed PMID: 15999542.

4a. Viveiros M, Martins M, Rodrigues L, Machado D, Couto I, Ainsa J, Amaral L.

Inhibitors of mycobacterial efflux pumps as potential boosters for

anti-tubercular drugs. Expert Rev Anti Infect Ther. 2012 Sep;10(9):983-98. doi:

10.1586/eri.12.89. Review. PubMed PMID: 23106274.

4b. Machado D, Couto I, Perdigão J, Rodrigues L, Portugal I, Baptista P, Veigas B,

Amaral L, Viveiros M. Contribution of efflux to the emergence of isoniazid and

multidrug resistance in Mycobacterium tuberculosis. PLoS One. 2012;7(4):e34538.

doi: 10.1371/journal.pone.0034538. Epub 2012 Apr 6. PubMed PMID: 22493700; PubMed Central PMCID: PMC3321020.