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Krrista Range of ED pills and its treatment for Erectile Dysfunction and ED treatment

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Introduction:

ED is the inability to keep the penis erect and firm enough for sex. It’s not always a matter of huge concern while experiencing occasional erection problems. However, if erectile dysfunction persists, it may stress the person out, lower his confidence, complicate relationships, etc. Problems in maintaining an erection while having sex can also result in heart disease and a symptom of an underlying medical illness that needs to be treated.

However, erectile problems can be treated. It can be treated by several ED pills such as Sildenafil (Viagra), Tadalafil (Adcirca, Cialis), Vardenafil (Levitra, Staxyn), Avanafil (Stendra). Not only ED pills, but erectile dysfunction can also be treated with several other procedures- alprostadil self-injection, alprostadil urethral suppository, and testosterone replacement. Another treatment involves penis pumps and penile treatments.

1.1 PDE-5 Inhibitor:

A phosphodiesterase type 5 inhibitor is a vasodilator that prevents cyclic GMP degradation by the cGMP-specific phosphodiesterase type 5 (PDE5) in the smooth muscle cells lining the individuals’ blood arteries supplying various tissues. These medications treat erectile dysfunction by widening the penis’s corpora cavernosa, making it easier to get an erection when sexually stimulated.

The first effective oral medication for ED was Sildenafil. PDE5 is also naturally found in the smooth muscle lining the walls of the pulmonary arterioles, which is why Sildenafil and Tadalafil, two PDE5 inhibitors, have received FDA approval to treat pulmonary hypertension. Clinically approved medications for the treatment of erectile dysfunction include Sildenafil (Viagra), Tadalafil (Cialis), and Vardenafil (Levitra).

Tadalafil is also prescribed for treating benign prostatic hyperplasia, while Sildenafil is also prescribed for managing certain subtypes of pulmonary hypertension. In addition, as per recommendations from The European Society for Vascular Medicine, PDE5 inhibitors have been utilized as a second-line treatment in severe cases of Raynaud’s phenomenon when it is linked to systemic sclerosis.

Krrista is another new age medication family that includes the renowned PDE5 inhibitors vardenafil and dapoxetine.

Krrista contains two active ingredients, Vardenafil for erectile dysfunction and Dapoxetine for preterm ejaculation (PE).

Super Krrista 40+60 Mg, Krrista Power 40+60 Mg, and Extra Super Krrista 20+100 Mg are some of the other strengths of Krrista.

Men with erectile dysfunction or premature ejaculation may benefit by using Krista. With ED, also known as Impotence, it is difficult to get or keep an erection during sexual activity.

2. Krrista: A PDE-5 Inhibitor:

Krrista range of medicines treats erectile dysfunction in men. Erectile dysfunction is alarmingly widespread among men and is projected to become a greater concern with time. Over the past few years, the reasons behind erectile dysfunction have shifted enormously from psychological to organic causes.  

The organic causes include diabetes mellitus, hypertension, smoking, peripheral vascular disease, pelvic or abdominal surgery (especially prostate surgery), multiple sclerosis, peripheral neuropathy, and Parkinson’s disease.

Although coadministration has not been associated with alterations in the safety or efficacy of either treatment, there is a possibility for negative drug interactions with other medications that inhibit or stimulate CYP3A4. These medications include HIV protease inhibitors, ketoconazole, and itraconazole. Combining PETN with nitrovasodilators like nitroglycerin is not advised because it could result in potentially fatal hypotension. With other antihypertensive medications, PDE5 inhibitors do not interact synergistically.

3.1 Mechanism of inhibition of Krrista:

Nitric oxide (NO) plays a major role in the physiological process of vasodilation that helps Krrista function. Nitric oxide actively advances the production of cGMP in the penile region- a process significant to developing an erection. 

For instance, during sexual stimulation, significant quantities of NO are released from endothelial cells and penile nerves in the penis. This causes the smooth vasculature of the corpus cavernosum to relax, which results in vasocongestion and a persistent erection. By preventing the body’s natural PDE5 enzyme from degrading cGMP, Krrista extends the effects of this neurotransmitter. 

Krrista helps men develop a lasting erection and boosts sexual satisfaction. However, one must know that the medicine does not work in absence of sexual arousal. 

3. Patient preferences:

Clinical judgments are based on various variables. Some doctors will assert that they only rely on research findings, while others will cite their own clinical experience as the only source of information. 

Doctors now have various oral PDE5 inhibitors, among which Krrista is very effective. It is safe, productive, and available for treating ED in males. Since the outcome of treatment for ED is not dependent on a laboratory finding and cannot be assessed using radiology, it differs from most other areas of medicine in that it relies purely on the patient’s assessment. As a result, only the patients and their partners can truly determine what treatment is “best” for them. 

Other investigations attempted to infer patient preferences through the observation of prescription data. Men who have originally prescribed Sildenafil as a treatment for ED are less likely to switch to another PDE5 inhibitor than men who are initially prescribed Vardenafil or Tadalafil, according to a review of prescription data from 40,000 pharmacies in the US. 38 In a different UK investigation, the prescription information of 2703 patients who started their treatment for ED with a PDE5 inhibitor was examined.

Conclusion:

ED is very common andhas significant health effects. The most common form of ED medication is a PDE5 inhibitor. Additionally, PDE5 inhibitors, such as Krrista tried new ways to formulate the drugs and hence improved their overall efficacy.

An awareness of the various qualities should be the focus of a conversation between the patient and the provider when choosing an oral PDE5 inhibitor medication. This can increase the possibility that the patient will be satisfied.

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CategoriesLifestyle

How to consume the Krrista Range of ED Pills?

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ED Pills and treatment of Erectile dysfunction

Erectile Dysfunction is the inability to get or maintain an erection firm enough for sexual intercourse. Although occasional erection problems can be bothersome, they are not necessarily serious. However, if erectile dysfunction persists, it may cause stress, undermine confidence, and hamper relationships, etc., for the individual.

But the good news is, erectile dysfunction can be managed.

Several ED medications, including Sildenafil (Viagra), Tadalafil (Adcirca, Cialis), Vardenafil (Levitra, Staxyn), and Avanafil are proven to help men build an erection. In addition to ED medications, alternative treatments, such as testosterone replacement, self-injection with alprostadil, and urethral suppositories with alprostadil, can also be used to treat erectile dysfunction.

Out of the pool of ED treatments available in the market, one is the PDE5 inhibitor range of drugs, Krrista. Krrista range of medicines is clinically tested and highly effective medicines that treat erectile dysfunction and premature ejaculation.

Let’s know more about it.

Krrista Range of ED medicines

Krrista range of ED pills is PDE5 inhibitors that work by increasing the flow of blood in the penile region of men.

This range of medicines cannot cure low libido, however, it relaxes muscles and increases blood flow to treat erectile dysfunction.

To enhance blood flow to the penis, Krrista works by relaxing the muscles in blood vessel walls. PDE5 medications prevent phosphodiesterase type-5 (PDE5), a specific enzyme, from functioning too quickly. PDE5 slows down the action of a chemical that relaxes muscles and dilates blood vessels, allowing it to carry out its intended function.

To understand the full mechanism of PDE5 inhibitors, click here.

Krrista only functions as intended when there is sexual stimulation, such as during sexual activity. The medicine does not work like a magic. If it is not working on you, chances are that you are not turned on enough.

Following are the different medicines that have successfully helped men treat their erectile dysfunction-

  • Krrista Strong
  • Krrista Power
  • KrristaPurple Flame
  • Krrista Purple Storm
  • Super Krrista
  • Extra Super Krrista
  • Krrista Pink Flame
  • Krrista Pink Storm
  • Krrista Blue-P
  • Krrista Blue Storm
  • Krrista Force

How to take Krrista for the first time?

When you first start using ED medications, they can be questions. As with any new drug, you may not be sure what to anticipate. Learning how to take Krrista properly to achieve the finest results is critical.

Before taking it, you should consult with your doctor. It is best to discuss whether PDE 5 inhibitors are appropriate for you if you have any of the following medical issues:

  • Hypertension
  • Hypotension
  • Cardiovascular disease
  • Arrhythmias
  • Cardiac arrests
  • Stroke and more.

Before using Krrista for the first time, a patient should consider a few things if your doctor has given the go-ahead and written a prescription:-

Proper Timing is necessary

Krrista should be taken orally between 30 minutes to one hour before sexual activity, although one hour before is best. It will be simpler to use Krrista regularly once you’ve used it for the first time and are more familiar with how it works.

For example, some individuals could find that they must take it one hour before sexual activity, whereas, on the other hand, some might discover that it takes closer to two to three hours for it to begin functioning for them.

Consume the recommended quantity

50 mg is the usual dosage that a person can take with or without food. However, your physician will recommend you the right dosage on the basis of your medical history, fitness and lifestyle.

It is best to consume Krrista range of ED pills on an empty stomach. If you are eating, have a meal with a very low-fat content. This will ensure the highest efficacy of the medicine.

Sexual stimulation is necessary

It’s possible for Krrista to not function for the first time. Making sure you’re sexually stimulated will improve your chances of success. You can anticipate that your erection will last between two and three hours once it begins to function.

What is the right dosage of Krrista?

There are three different dosages for Krrista pills: 25, 50, and 100 mg. A doctor may recommend a different dosage depending on whether a patient plans to use Krrista daily or only when necessary.

Based on a patient’s age and medical history, a doctor may change the dosage of Krrista prescribed to them. For example, men over 65 or those who are suffering from hepatic and renal impairment, for instance, usually start with a dose of 25 mg per day. The maximum suggested dose is 100 mg. However, the effectiveness of Krrista will not improve by taking it more frequently or in more doses than advised. There may be potentially fatal adverse effects from this.

Krrista’s interactions with other drugs

Krrista can cause some drug-drug interactions. It is highly warned to not take the following medicines with Krrista:-

  • Nitroglycerin, isosorbide, and amyl nitrate or any other medicine containing nitrates
  • Drugs like Revatio that treat pulmonary arterial hypertension
  • Vasodilators that relieve chest pain
  • HIV/AIDS medications like saquinavir and ritonavir
  • Antifungal medications such as itraconazole and ketoconazole, certain antibiotics, including erythromycin
  • Additional ED drugs, such as Levitra (vardenafil) and Cialis (tadalafil)

Krrista might also interact with certain foods and medications. For instance, grapefruit is a natural alternative for treating ED since it can raise blood levels. However, combining it with Krista may cause undesirable side effects like low blood pressure, flushing, or headaches. Caffeine might have a comparable impact. According to one study, drinking two to three cups of coffee daily can lower your risk of developing ED.

Caffeine and Krrista don’t interact, but minor adverse effects could still happen. Ask the healthcare professional if you need to avoid certain meals or drinks while taking Krrista.

Krrista side effects

The more severe adverse effects of Krista include allergic reactions, prolonged erections, eyesight and hearing loss, and dangerously low blood pressure. Below given are some common side effects of Krrista when not taken in the right dosage or at the wrong time:

Allergic reactions:-

Individuals consuming Krrista should seek immediate medical assistance if they experience breathing problems, facial or throat swelling, or hives, as these are indications of an allergic reaction.

Prolonged erections:-

It is one of the most well-known side effects of Krrista. If they last too long, they can permanently harm the penis.

Get immediate medical treatment if you experience an erection that lasts more than four hours (priapism). Likewise, if you frequently get extended erections, see your doctor immediately.

Loss of vision: –

Taking medicine occasionally results in a sudden loss of eyesight in one or both eyes. For example, it might be a symptom of non-arteritic anterior ischemic optic neuropathy, a dangerous eye condition (NAION). To prevent potential eye injury or loss of eyesight, people taking Krista should seek medical assistance as soon as they notice any change in their vision.

Heart attack and stroke:–

Heart attacks and strokes are the least common Krrista adverse effects. The risk of heart attack or stroke from using Krrista is highest in people with underlying heart conditions, such as irregular heartbeat. Patients with poor cardiac output conditions or those trying to prevent heart failure are not given Krrista.

However, despite the minimal risk of heart disease, patients with underlying cardiac issues should be cautious. They should discuss their medical history with their doctor and consume Krrista per the doctor’s directions.

Conclusion

An individual can lessen the harshness of ED’s progression by taking Krrista every day. It is also one’s ability to urinate and general quality of life, among other advantages. For instance, the potent medicine Krrista boosts blood flow to the penis, enabling one to get and sustain an erection.

Furthermore, Krrista is an inhibitor of phosphodiesterase type 5 (PDE5). PDE5 is an enzyme that controls specific blood molecules, but its effect on the body might make it more difficult to achieve and maintain an erection. To address erectile dysfunction, utilize Krrista (ED). It aids in maintaining an erection momentarily so that you can engage in sexual activity, but it does not treat ED. It also does not affect arousal.

To have an erection, you still need mental or physical stimulus. Only prescriptions from doctors are accepted for this drug. Make sure to have the right dosage of Krrista as specified by the professional doctor to prevent side effects.

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CategoriesLifestyle

Interactions of PDE5 inhibitors – Other medicines

by admin
  1. Introduction:
    PDE5 is used in the clinical environment to treat erectile dysfunction (ED) and lower pulmonary arterial hypertension (PAH), improve exercise tolerance, and increase arterial oxygenation in patients with secondary PAH.

    There have been significant developments in the pharmacologic management of ED in recent years. PDE5i selectively inhibits the PDE5 enzyme’s catalytic site in cavernosal tissue. For patients with ED, PDE5i are a first-line therapeutic choice.

    There are several potent and selective PDE5s, such as Sildenafil, Vardenafil, Tadalafil, and Avanafil. Both the European Medicine Agency (EMEA) and the US Food and Drug Administration (FDA) have authorized these medications for the treatment of ED. In 1998, sildenafil, the first highly selective oral PDE5i drug to be made commercially available, was introduced.

    The diagnosis and management of ED were revolutionized by sildenafil. Tadalafil and vardenafil are now commonly accessible as well. The FDA officially approved avanafil, and it will go on sale in late 2013.

    To understand the mechanism of related drug interactions, it is crucial to comprehend the biochemical effects of PDE5 inhibitors. Nitric oxide (NO), which is produced by endothelial cells of the vasculature, is released during sexual stimulation by nonadrenergic, noncholinergic neurons in the corpus cavernosum, or erectile body, of the penis.

    Cyclic guanosine monophosphate is produced more frequently as a result of nitric oxide’s activation of the guanylate cyclase enzyme (cGMP). In addition, the smooth muscle cells in the sinusoids and blood vessels of the corpus cavernosum relax as a result of cyclic guanosine monophosphate, increasing blood flow to the penis.

  • Interaction of PDE5 inhibitors: 
    In smooth muscle, nitroglycerin is transformed into nitric oxide (NO), which then activates guanylyl cyclase, raising the concentration of cGMP and relaxing the smooth muscle. Vein dilatation reduces venous return to the heart, which lowers left ventricular volume (reduced preload), and lowers the need for myocardial oxygen. Myocardial oxygen requirements are lowered as a result of artery relaxation because it lowers artery resistance (reduced afterload). Additionally, nitroglycerin widens coronary arteries, which enhances myocardial blood flow.

    Vasodilators like nitrates and nitrate-containing substances are used to treat angina and heart failure. Because phosphodiesterase type 5 inhibitors, which are used to treat erectile dysfunction, are also vasodilators, taking them with nitrates may have synergistic effects that strengthen their hypotensive effects. However, PDE5 inhibitors are modest vasodilators, so patients with baseline hypotension, left ventricular outflow blockage, aortic stenosis, congestive heart failure, low blood volume, and other disorders should use caution when using them.

    2.2 Nitrates with PDE5:
    Organic nitrates interact with PDE5 inhibitors like sildenafil and tadalafil to cause a synergistic reduction in blood pressure (BP). Nitric oxide, which is given off by organic nitrates, stimulates guanylate cyclase and causes it to catalyse the synthesis of cyclic guanosine monophosphate (cGMP). Improved erectile function is brought on by cyclic guanosine monophosphate’s reduction of calcium flow into smooth muscle cells, which causes the arteries, arterioles, and sinusoids of the corpus cavernosum to relax. PDE5 stops cGMP from doing its work. When a PDE5 inhibitor is used with a nitric oxide donor, these effects can include a significant increase in cGMP, pronounced vasodilation, and in some people, frank hypotension. Therefore, using organic nitrates continues to be completely against the advice of using PDE5 inhibitors.

  • DRUG INTERACTIONS
    PDE5i therapy has helped a lot of men with ED and a growing number of individuals with PH. PDE5i are mostly metabolized by CYP3A and, to a lesser extent, CYP2C9 in the liver. Therefore, the clearance of these agents may change if these enzymes are inhibited or stimulated.

    3.1 Cytochrome P450 3A Inhibitors
    By increasing exposure to medications with a low therapeutic index, inhibitory drug interactions can be fatal. Plasma concentrations of PDE5i are raised by potent CYP450 inhibitors. In addition, CYP3A inhibitor-induced increases in PDE5i plasma concentrations can hasten the onset and severity of additional PDE5i medication interactions. Never take PDE5i when using nitrates. To prevent negative side effects, it’s crucial to be aware of these possible drug interactions. Simultaneous administration of powerful CYP3A inhibitors like ketoconazole and itraconazole, which are antifungal medications, increases the plasma levels of sildenafil.

    3.2 Cytochrome P450 3A Inducers
    The plasma concentrations of PDE5i are reduced, and their clearance is increased by P4503A inducers. Many other CYP3A4 inducers, such as carbamazepine, phenytoin, and phenobarbital, would probably reduce PDE5i plasma levels, even though not all interactions have been researched. Tadalafil levels in plasma were lowered by rifampin by 88%. When PDE5i are used in conjunction with CYP3A4 inducers, their efficacy may be decreased in some people, necessitating a dose adjustment. For patients using rifampin for an extended period of time, tadalafil (Adcirca®) is not advised. When taken alongside sildenafil, the CYP3A and 2C9 inducer bosentan lowers the amount of sildenafil in the blood. Due to the concurrent drop in sildenafil and increase in bosentan concentration, it’s interesting to note that this drug combination can be described as having a mutual pharmacokinetic interaction.

    3.3 Oral hypoglycemic medications:
    Sulfonylureas and benzoic acid derivatives are examples of hypoglycemic medications, while biguanides, -glucosidase inhibitors, and thiazolidinediones are examples of anti-hyperglycemic medications. Vardenafil and glyburide have not been found to interact pharmacologically, and there is currently no further relevant research available. However, the treatment of diabetes mellitus-induced-ED has made substantial use of all 3 PDE5i. Recently, Vardi et al. demonstrated that PDE5i are safe and dramatically improved ED in diabetic males in a meta-analysis of double-blind, placebo-controlled studies.

    3.4 PDE5Is and alpha-Blockers:
    Patients with benign prostatic hypertrophy benefit from “uroselective” -blockers (tamsulosin, alfuzosin), which preferentially inhibit 1A and 1D receptors found largely in the prostate. Because of their higher affinity for 1B receptors, which are widely distributed in the peripheral vasculature, some -blockers, such as doxazosin, are used as third-line medicines for hypertension, whereas other -blockers, such as terazosin, are less selective.

    Every -blocker has the potential to cause orthostatic hypotension and vasodilation, and taking PDE5Is concurrently raises the chance of a clinically significant drop in blood pressure. Different PDE5I and -blocker combinations interact to varying degrees. The medications co-administered, the amount of the -blocker, the timing of delivery, and the length or stability of the -blocker therapy all affect the PDE5I—blocker interaction to varying degrees. Less harm to the cardiovascular system is caused by tadalafil than.

    According to studies, patients already taking calcium antagonists, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, and PDE5 inhibitors may see minor drops in blood pressure.

    These modest, additive blood pressure drops have often not been considered clinically relevant. PDE5 inhibitors continue to be effective in treating ED in individuals with hypertension who are receiving antihypertensive medications. When PDE5 inhibitors are administered to individuals already taking common antihypertensive medications, the side-effect profile does not worsen.

    These recent trials demonstrate that in individuals already o
    n alpha-blockers, vardenafil at doses of 5, 10, and 20 mg is linked with modest mean maximal incremental decreases in SBP (about 4 to 6 mm Hg). There was no dose response in the decreases in standing blood pressure seen with increasing doses of vardenafil, similar to other PDE5 inhibitors on an alpha-blocker background. Compared to prior research using healthy volunteers who had never taken alpha-blockers, there were smaller orthostatic declines in SBP of 85 mm Hg seen in patients in these more recent investigations using vardenafil.

    According to current labeling, vardenafil should be started at the lowest starting dose, and patients should wait until they are stable on their -blocker dose before beginning PDE5 inhibitor medication. On the other hand, individuals already taking a PDE5 inhibitor at the recommended dosage should take alpha-blockers at the lowest possible dose.

    3.5 Anticoagulant agents
    Initial studies showed that sildenafil increases the inhibitory effects of nitric oxide donors on adenosine diphosphate-dependent platelet aggregation. As a result, PDE3 and PDE5 activities are prominent in platelets. This observation was subsequently verified. On the other hand, in vivo interaction investigations show no discernible interaction between PDE5i and the CYP2C9 substrate warfarin.

    There hasn’t been any evidence of a higher risk of clinically significant bleeding episodes after PDE5i in the trials published thus far or in the current recommendations. However, the potential implications of reduced platelet aggregation under the influence of PDE5i should be considered for the high-risk cardiovascular patient frequently taking various anti-thrombotic regimens or warfarin for systemic anticoagulation. Sildenafil administration to individuals with coagulopathies or active peptic ulcer disorders is also not supported by any safety data.

  • Future Perspective: 
    The success of different PDE5i in treating males with ED of varied syndromes depends on their metabolic characteristics. Sildenafil, tadalafil, and vardenafil are metabolized mostly in the liver by CYP3A, with CYP2C9 serving as a minor metabolic pathway. Some of the most important PDE5i-related medication interactions are caused by this enzyme pathway. Additionally, it is advised to exercise caution when taking strong CYP3A inhibitors like antibiotics with the macrolid class, azole antifungals, or antiviral protease inhibitors. To prevent overdose, therapeutic drug monitoring of PDE5i response must be carried out during new drug therapy.

    There is yet to be long-term safety data for all PDE5i. Studies on how avanafil interacts with CYP3A inducers and inhibitors are also necessary. Other CYP3A inducers, such as carbamazepine, phenytoin, and phenobarbital, may decrease PDE5i plasma levels even if not all interactions have been studied. Some negative effects can be decreased by altering selectivity and pharmacokinetics factors.

    Conclusion:
    As people get older, ED is more prevalent. The higher likelihood of additional comorbidities and chronic disorders coexisting complicates ED in the elderly. Compared to younger patients, older adults typically consume nearly three times as many prescription medicines, averaging over ten each year. Physicians should be aware that various medications and even non-medical products can interact with PDE5i metabolism, absorption, or mechanism of action in this group of patients, and the younger ones.

    We have a summary of these interactions in this review. The three PDE5i are sufficiently safe overall. The primary contraindication for all 3 continues to be the usage of nitrates.  Vardenafil is likewise not advised for use in individuals who are using type 1A or type 3 antiarrhythmics, while tadalafil and sildenafil have not been associated with any additional significant side effects. If -blockers are being used concurrently when there are strong CYP3A inhibitors present, such as azole antifungals, antiretroviral protease inhibitors, or macrolid antibiotics, caution rather than contraindication is advised. On the other hand, testosterone and statins (but only in hypogonadal patients) appear to work in concert to affect PDE5i results.

    More research is needed on possible interactions between PDE5i and other medicines. It is crucial to titrate doses carefully based on efficacy and the prevalence of hypotension. Pharmacodynamic studies will be necessary for the follow-up analysis to ascertain the ideal exposure window and target medication concentration.

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CategoriesCompany Updates

Clinical Trials in Erectile Dysfunction – A Complete Guide

by admin

Abstract

In this article, we have tried to analyze different methodologies through which health issues such as erectile dysfunction can be treated and cured. We have discussed the clinical trials involved in this and the root causes and symptoms of the disease. We have also discussed the ongoing research that may come up with revolutionizing cures for health issues such as erectile dysfunction.

Keywords: Erectile Dysfunction; Clinical Trials

  1. Introduction The foundation of all medical advancements in clinical research involves clinical trials. Clinical trials examine novel approaches to avert, diagnose, or cure illness. Researchers also use clinical trials to examine various facets of treatment, such as enhancing the quality of life for those with chronic diseases.Clinical trial execution, however, requires a meticulous strategy that incorporates scientific, analytical, ethical, and legal concerns. Therefore, to preserve a relationship with both patients and industry in search of the safest, most effective, and most efficient remedies, healthcare professionals must comprehend the principles on which well-conducted clinical trials hinge.1.1 Background of Clinical PracticeFor more than 275 years, clinical trials have provided doctors with the means to discover effective cures for various diseases. There have been struggles but also victories along the road. The industry is where it is now because of the clinical studies conducted decades or even centuries ago.

    Clinical trials are a type of test used in medicine, medical research, and drug development to determine the safety and effectiveness of health interventions by gathering data on adverse medication reactions and side effects of other therapies (e.g., drugs, diagnostics, devices, therapy protocols).

    Prior guidelines: The medicine must be devoid of any additional unintentional characteristics. It must be used for a single disease, not a group of diseases. The medicine must be tested on two dissimilar illness types, as sometimes a treatment can treat one disease by its primary properties while treating another by chance. The drug’s quality must match the strength of the sickness. The timing of action must be noted to distinguish between effect and accident. Finally, the drug’s impact must be observed.

    1.2 Phases of Clinical Research
    Pre-clinical research includes analyses of medication manufacture and purity and animal trials. In addition, the medicine’s safety at dosages that roughly correspond to human exposures is investigated in animal trials, together with its pharmacodynamics (i.e., mechanisms of action) and pharmacokinetics (i.e., drug levels and clinical response) components (i.e., drug absorption, distribution, metabolism, excretion, and potential drug-drug interactions). If the medicine is to be further investigated in human subjects, this information must be submitted for IND approval.

    1.3 Clinical practice in Sexual Dysfunction A complicated bio-psycho-social process, sexual functioning is regulated by the endocrine, vascular, and neurological systems. In addition to biological elements, psychosocial factors such as societal and religious beliefs, health status, personal experience, ethnicity, and sociodemographic situations, as well as the psychological status of the individual or couple, are crucial for a person to have healthy sexual functioning. Sexual activity also involves interpersonal interactions, with each partner bringing their attitudes, needs, and reactions to the partnership. Sexual dysfunction may result from a breakdown in any of these areas.

    Sexual dysfunction is common in the general population. According to estimates, 31% of men and 43% of women experience some form of sexual dysfunction. The most prevalent male sexual disorder is early ejaculation.

  2. Erectile Dysfunction Erectile dysfunction (ED), premature ejaculation, delayed or absent ejaculation, lack of libido, hypogonadism, and Peyronie’s disease are all covered under the general term “male sexual dysfunction” [1]. However, the great bulk of evidence derived from the literature has grown since the introduction of pharmaceutical treatments for ED in the middle of the 1990s, which completely changed how male sexual dysfunction is managed. When you cannot get or maintain an erection that is hard enough to allow for satisfying sexual activity, you are said to have erectile dysfunction (ED). ED can be a temporary or permanent issue. The major symptoms of this dysfunction:
  • You can occasionally have an erection, but not every time you want sex.
  • Can occasionally get an erection, but it does not stay long enough to have satisfying or gratifying sex.
  • Are never able to acquire an erection
    2.1 Principle of Erection: Cause and SymptomsDuring sexual stimulation, nerves release chemicals that enhance blood flow to the penis. Two soft muscular penis chambers (the corpus cavernosum) receive blood in flow. The corpus cavernosum’s chambers are solid. During an erection, the elastic tissues become loose and entrap blood. The penis becomes rigid as a result of the pressure generated by blood.

    During an orgasm, the second set of nerve impulses that reach the penis causes the contraction of tissues, which releases the entrapped blood back to the body, which in turn causes the erection to reverse.

    Men with erectile dysfunction have trouble getting and keeping an erection for sexual enjoyment. Male impotence, or ED, is another name for it. Heart disease, diabetes, a pharmaceutical side effect, or a potassium deficit are a few potential underlying conditions that might contribute to erectile dysfunction. It can also be brought on by several neurogenic conditions, including Parkinson’s disease and spine traumas. In certain instances, the cause is psychological since the male is self-conscious. In addition to disease, age is a deciding factor.

    Because there are many possible reasons for ED, a doctor will frequently order blood tests and ask many questions. These examinations can look for various conditions, including diabetes, low testosterone, and cardiac issues. Additionally, the doctor will perform a physical examination that includes a genital exam. Finally, a doctor will conduct additional research after establishing a medical history. If the cause is physical rather than psychological, a test is known as the “postage stamp test” can help. Most nights, men experience 3 to 5 erections. By observing whether postage stamps placed around the penis before bed have fallen off throughout the night, this test looks for the occurrence of erections at night. The Poten test and Snap-Gauge test are two further tests for nocturnal erection.

    2.2 Treatment of Erectile dysfunction ED is frequently treated by medical specialists, including urologists and primary care doctors. Despite being quite prevalent, ED is not a typical aspect of aging. If you have any ED symptoms, see a medical practitioner. ED could be a symptom of a more serious medical condition. Non-invasive treatments are often tried first. Most of the best-known treatments for ED work well and are safe.

    Men should be encouraged to make the required adjustments for their sexual function and general health, as is true for many medical disorders, since lifestyle changes, considered first-line therapy, can positively impact ED management. However, despite the advantages of behavior change, men who come with ED desire the doctor’s assistance with solutions that can make a difference immediately.

    Men with mild erectile dysfunction (score of 22–25 on the erectile function domain of the International Index of Erectile Function) do not typically seek treatment. Healthcare professionals frequently disregard their complaints of mild ED as unimportant and do not properly assess such patients. There does not seem to be any published epidemiological data on the prevalence or risk for such diseases in populations of men with moderate ED, even though
    ED relates to an increased prevalence of age-related disorders, including diabetes and cardiovascular disease. A deeper comprehension of this population’s inherent risk for ED-related disorders may emphasize the value of early detection and treatment.

    2.3 Future of Clinical Research in ED Differentiating between psychogenic and biological erectile dysfunction is a crucial component of erectile dysfunction assessment. Therefore, psychogenic or mixed erectile dysfunction patients should also receive non-pharmacological and pharmaceutical treatments.

    Melanocortin activators: These are medications that seem to work by the nervous system (for example, the brain). Animal studies have demonstrated that they can cause an erection. Intranasal medication administration (PT-141) to males with mild to moderate ED and non-medical (psychological/emotional) as opposed to physical reasons of ED may be beneficial, according to preliminary human research. However, larger studies will be required to prove these medications’ safety and efficacy.

    Gene therapy: In this cutting-edge treatment, genes that generate goods or proteins that may not be operating correctly in the penile tissue of men with ED are delivered. The function of the erectile organ may be enhanced by replacing these proteins. Gene therapy has been shown to improve erectile function in experimental animal models. Studies on humans may also show that this treatment is effective. However, it can take a while for the public and regulatory agencies to approve gene therapy.

  1. Conclusion Inflammatory arthritis patients frequently experience sexual dysfunction, raising morbidity risk. Therefore, we advise HCPs to include a sexual health assessment and the application of methods to improve sexual health as a crucial component of their management in long-term care.

Reference:

  1. Sharon Van Doornum, Ilana N. Ackerman & Andrew M. Briggs (2019) Sexual dysfunction: an often-overlooked concern for people with inflammatory arthritis, Expert Review of Clinical Immunology, 15:12, 1235-1237, DOI: 10.1080/1744666X.2020.1686356
  2. Yafi, F., Jenkins, L., Albersen, M. et al. Erectile dysfunction. Nat Rev Dis Primers 2, 16003 (2016). https://doi.org/10.1038/nrdp.2016.3
  3. Avasthi A, Grover S, Sathyanarayana Rao TS. Clinical Practice Guidelines for Management of Sexual Dysfunction. Indian J Psychiatry. 2017 Jan;59(Suppl 1): S91-S115. DOI: 10.4103/0019-5545.196977. PMID: 28216788; PMCID: PMC5310110.

Nunes KP, Labazi H, Webb RC. New insights into hypertension-associated erectile dysfunction. Current Opinion in Nephrology and Hypertension. 2012;21(2):163–170.

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