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PDE5 Inhibitors and treatment of Erectile Dysfunction

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Abstract

The present article discusses several aspects of erectile dysfunction (ED), especially what role PDE5 inhibitors can play in enhancing erectile performance and treating the symptoms of ED with much more efficacy and efficiency. Further discussions about the mechanisms of PDE5 inhibitors have occurred in this article, including the various types of PDE5 inhibitors, the results of PDE5 clinical testing, and the proposed methodologies that can be used for future research opportunities on erectile dysfunction.

1. Introduction

The inability to obtain or sustain an erection strong enough for satisfying sexual performance is known as erectile dysfunction (ED), and it can be chronic or recurrent. The severity of erectile dysfunction might vary. Some men with ED may find it impossible or extremely difficult to have an erection at any time.

Currently, PDE5 inhibitors are regarded as the gold standard for treating erectile dysfunction. They generally start acting quickly, have a brief lifespan of up to a day, are highly potent, and typically only have mild, transient negative effects.

With the development of type 5 phosphodiesterase (PDE5) inhibitors over the past 15 years, the treatment of erectile dysfunction (ED) has undergone a revolution. As they were being examined to cure angina and hypertension, PDE5 inhibitors were inadvertently discovered to have a positive impact on erection in men.

The scientists who tested UK-92,480, sometimes known as Sildenafil or Viagra, first considered this to be of little consequence. However, as time went on, the emphasis of the trials shifted from the use of PDE5 inhibitors to treat erectile dysfunction to illnesses including angina and hypertension. In the United States and many other countries, tens of millions of men use PDE5 inhibitors like Sildenafil and other drugs.

1.1 Background of PDE5 inhibitor: ED medication

The relationship between NO and the PDE family led to an increase in drug development in the middle of the 1980s. Numerous physiological effects of NO had significant effects on various disorders. The PDE enzyme is present in all tissues of the body and has 11 different known isoenzymes that are expressed at varying levels. Although it is present everywhere, the PDE5 enzyme is more common in penile tissue. 

Before identifying the connection between NO and PDEs, non-selective PDE inhibitors (such as theophylline) were in use, but selective PDE inhibitors were yet to be created. Since then, several selective PDE inhibitors have been authorized to treat a range of conditions, including ED and pulmonary hypertension.

2. Mechanism of Inhibition: Physiology of Penile Erection

The typical physiology of penile erection, which is a medical condition for which the majority of PDE5 inhibitors are currently prescribed, must first be understood to comprehend the mechanism of PDE5 inhibitors. 

Following sexual stimulation, nerve impulses in the corpora cavernosa release neurotransmitters that cause endothelial cells to produce nitric oxide. This nitric oxide then diffuses into nearby smooth muscle cells and stimulates the formation of cGMP, which causes vasodilation and an increase in penile blood flow. 

ED pills inhibit the production of PDE-5 enzyme in the smooth muscles. 

This buildup of cGMP in the vascular smooth muscle results in dilating blood arteries through the phosphorylation of many downstream effector molecules. As well as improving endothelial function, PDE5 is also reduce the death of smooth muscle cells in the corpus cavernosum.

The most common phosphodiesterase in the corpus cavernosum is PDE5. However, mammalian PDE has been found in at least 11 families. 

There are more than 50 different species of PDE as a result of the association of some PDE types with multiple genes and the presence of two or more splice variants in some mRNAs. 

Some PDE subtypes degrade only cyclic adenosine monophosphate (cAMP) or only cyclic guanosine monophosphate (cGMP), whereas others do both. For instance, PDE11 breaks down both cAMP and cGMP, unlike PDE4 and PDE5, which only break down cAMP. PDE inhibitors’ cross-reactivity can be largely ascribed to similarities in their homologous catalytic domain. 

Human corpus cavernosum tissue contains messenger RNA for the PDE isoforms PDE1A, PDE1B, PDE1C, PDE2A, PDE3A, PDE4A, PDE4B, and PDE4C.

2.1 Physiological mediator of ED

Nitric oxide (NO) is released during sexual arousal by endothelial cells and nerve terminals in the corpus cavernosum. A cGMP-dependent chain of actions is started when NO stimulates guanylate cyclase to change guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). The buildup of cGMP causes the corpus cavernosum’s smooth muscles to relax and the blood flow to the penis to increase. 

PDE5 is an enzyme that specifically cleaves and degrades cGMP to 5′-GMP in the corpus cavernosum smooth muscle. PDE5 inhibitors have a structure that is comparable to that of cGMP; they bind to PDE5 competitively and prevent cGMP hydrolysis, which improves the effects of NO. Therefore, the lengthening of an erection is caused by an increase in cGMP in smooth muscle cells.

The relaxation of corpus cavernosum smooth muscles is not directly impacted by PDE5 inhibitors. Consequently, for an erection to occur after injection, sufficient sexual excitement is required.

3. Different types of PDE5 inhibitors

There are several PDE5 inhibitors available. Lodenafil, Udenafil, and Mirodenafil are other non-FDA marketed drugs.

3.1 Sildenafil Citrate

Sildenafil was the first PDE5 inhibitor and the first medication of its sort to be sold to the general population. The key advantages of Sildenafil are its availability, low cost, and extensive history. 

It has been used for many years and has been the focus of numerous clinical investigations. 

Sildenafil communicates with the catalytic domain via the L region, Q pocket, and H pocket. It does not interface with the M subsite directly. Sildenafil does not interact with the Zn2+ and Mg2+ metal ions of the M-subsite directly; instead, its pyrazole N2 atom forms a hydrogen bond with a water molecule, which then forms two hydrogen bonds: one with Tyr612 in the Q-pocket and the other with a water molecule that coordinates to the Zn2+ ion. 

Through a bidentate hydrogen connection, the side chain amide group of the conserved Gln817 interacts with the amide group of the pyrazolopyrimidinone moiety of Sildenafil. The connection between Gln817 and the purine ring of cGMP forms a bidentate hydrogen bond, which is like this interaction.

3.2 Vardenafil

Apart from the piperazine ring substitution (methyl in sildenafil vs. ethyl in vardenafil) and the piperazine ring’s position in the active site, vardenafil and sildenafil are structurally quite similar. The heterocyclic ring structure that mimics the purine ring of cGMP is another area where they diverge. 

Similar binding interactions were found to exist between the two inhibitors. 

Despite having identical structural and binding properties to sildenafil, vardenafil is a more effective and focused PDE5 inhibitor. Compared to sildenafil, it has an enzyme affinity that is at least 20 times higher.

3.3 Tadalafil

Tadalafil is more selective than sildenafil or vardenafil because it has 200–600 times greater affinity for PDE5 than PDE6. Tadalafil was said to bind PDE5 differently than sildenafil because it interacts with the L area but forms alternative binding modes with the Q pocket. 

In contrast to a bidentate hydrogen bond, the -amide group of Gln817 forms a solitary hydrogen link with the NH of the indole ring in tadalafil.

4. Clinical Efficacy and Indications in ED treatment

PDE5 inhibitors have been tested for their effectiveness and safety using both objective and patient-reported subjective efficacy measures. Optimal prescribing practices, improved patient-provider communication, and higher pharmacological knowledge are all factors that contribute to improved long-term treatment success.

In men over 50, ED and lower urinary tract symptoms (LUTSs) brought on by benign prostatic hyperplasia (BPH) are prevalent medical conditions. Epidemiological research indicates a significant link between the two. 

It has been demonstrated that lower urinary tract tissue from rats contains PDE5 mRNA. In animal investigations, the dose-dependent effects of sildenafil, tadalafil, and vardenafil on the contraction of isolated urethral and prostatic strips and LUTSs were seen. 

The only medication approved for the treatment of LUTSs secondary to BPH with or without ED is tadalafil 5 mg once daily.

5. The future direction of ED treatment: Pharmacotherapy

  • A more recent PDE5 inhibitor called udenafil has the same affinity for PDE5 that sildenafil does. Udenafil was proven to be a safe and effective treatment for ED in a parallel-group Phase three trial conducted in Korea. This trial was multi-center, double-blind, and placebo-controlled, and the volunteers received a fixed dose. Currently, udenafil is offered in various nations under the brand name Zydena, including Korea and Russia (Dong-A PharmTech Co, Seoul, South Korea). One hundred sixty-seven individuals with ED of various origins and severity were randomly selected. They received a placebo or udenafil at fixed doses of 100 or 200 mg as needed for 12 weeks in this parallel-group phase III trial.
  • PDE5 inhibitor mirodenafil has been marketed as M-Vix (Korea, 2007). (S. K. Chemicals, Seoul). In Korea, a multi-center, randomized, double-blind, placebo-controlled, parallel-group, fixed-dose research revealed that the medication is efficient and well-tolerated in treating ED caused by a variety of etiologies.
  • Since not all patients react favorably to the available PDE5 inhibitors, as was already mentioned, different ED medications are necessary. Phase III clinical studies for Avanafil, one of these novel medications, are now being conducted.
  • Avanafil is an oral ED drug that has been developed to be a highly effective and quick-acting PDE5 inhibitor. It is a pyrimidine derivative that has a molecular weight of 483.95 Da.
  • For the purpose of treating ED, tissue engineering is being researched. A sural autologous nerve graft was developed as a successful technique for preserving the continuity of the cavernous nerves after radical prostatectomy.

Furthermore, it is shown that endothelial and smooth muscle cells from the human body can create well-vascularized corporal tissue in vivo when they are placed in a mesh of acellular collagen matrix.

To create pure, smooth muscle, we have outlined cell isolation techniques and evaluated their culture compositions, omitting primarily fibroblasts.

6. Conclusion

The PDE5 inhibitors that are now on the market, such as the more recently approved avanafil, offer ED sufferers a secure, practical, and efficient way to enhance erectile function. These medications have replaced other ED treatments as the first-line therapy because of their comfort, quick start-up, and tolerability. However, it is challenging to decide whether an agent is superior to another due to the need for sufficient head-to-head trials.

More research comparing these drugs is needed to determine the potential benefits of each, especially in specific patient subsets. According to each patient’s response and need, prescribing options are available with all PDE5 inhibitors.

Reference

  1. Huang SA, Lie JD. Phosphodiesterase-5 (PDE5) Inhibitors In the Management of Erectile Dysfunction. P T. 2013 Jul;38(7):407-19. PMID: 24049429; PMCID: PMC3776492.
  2. Wharton, J., Strange, J. W., Møller, G. M., Growcott, E. J., Ren, X., Franklyn, A. P., … & Wilkins, M. R. (2005). Antiproliferative effects of phosphodiesterase type 5 inhibition in human pulmonary artery cells. American journal of respiratory and critical care medicine, 172(1), 105-113.
  3. Paick J-S, Kim SW, Yang DY, et al. The efficacy and safety of udenafil, a new selective phosphodiesterase type 5 inhibitor, in patients with erectile dysfunction. J Sex Med. 2008;5(4):946–95.
  4. Alwaal, A., Al-Mannie, R., & Carrier, S. (2011). Future prospects in the treatment of erectile dysfunction: focus on avanafil. Drug Design, Development, and Therapy, 5, 435-443.
  5. Paick JS, Ahn TY, Choi HK, et al. Efficacy and safety of mirodenafil, a new oral phosphodiesterase type 5 inhibitor, for treatment of erectile dysfunction. J Sex Med. 2008;5(11):2672–2680
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CategoriesCompany Updates

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

by admin

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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CategoriesInspiration

Interactions of PDE5 inhibitors – Diseases

by admin

Introduction:

Men worldwide are affected by the prevalent multifaceted condition known as erectile dysfunction (ED). Clinical outcomes are influenced by physical sickness, coping mechanisms for life’s pressures, or an unpleasant relationship. The first-line treatment for ED is phosphodiesterase type 5 (PDE5) inhibitors, which are known to be effective and well-tolerated.

The most popular and extensively researched PDE5 inhibitors include sildenafil, tadalafil, and vardenafil. When deciding which PDE5 inhibitor is the most effective for a given patient, developing an individualized treatment plan, and moving beyond “experience-based” subjective opinions, unfounded ideas, and prejudice regarding currently available drugs, make sure to consider the data gathered during a routine diagnostic workup for ED.

Background of the study:

A researcher must understand the normal physiology of penile erection for a better understanding of the mechanism of action of PDE5 inhibitors. Penile erection is an area of medicine that currently involves the usage of PDE5 inhibitors. After sexual stimulation, nerve impulses release neurotransmitters in the corpora cavernosa, which causes endothelial cells to produce nitric oxide. The endothelial cells further diffuse into the adjacent smooth muscle cells that stimulate the formation of cGMP, leading to vasodilation and increased circulation of penile blood.

A healthy and active love life can significantly improve one’s quality of life. Sexual health is crucial to one’s entire health and well-being. Heart disease patients frequently experience sexual dysfunction, particularly erectile dysfunction (ED) in men (CVD). Risk factors and pathophysiological connections between CVD and ED include endothelial dysfunction, inflammation, and low plasma testosterone levels.

ED has been demonstrated to be a distinct and early predictor of future CVD events, offering a crucial window for starting preventative interventions. As a result, ED screening and diagnosis are vital for the primary and secondary prevention of CVD since they provide an accessible and affordable alternative to other investigative cardiovascular diagnostics.

After discussing the various pharmacological properties and the patient’s unique sexual habits, preferences, and expectations, the doctor and patient should jointly decide on the optimal PDE5 inhibitor for each patient in the clinical context. Unfortunately, it is still debatable whether information related to the patient or any aspect of his illness should affect the decision of one treatment over another, and if so, how. In addition, matching a given patient’s profile to a specific PDE5 inhibitor frequently depends more on subjective opinions than objective data.

PDE5 inhibitors and their interaction with other diseases:

  • Diabetes:
    The doctor and patient should mutually choose the best PDE5 inhibitor for each patient in the therapeutic setting after discussing the numerous pharmacological features and the patient’s particular sexual habits, preferences, and expectations. Sadly, it is still debatable whether information related to the patient or any aspect of his illness should affect the decision of one treatment over another, and if so, how.

    In addition, matching a given patient’s profile to a particular PDE5 inhibitor frequently depends more on subjective judgment than objective data.

  • CV Diseases:
    The Second Princeton Consensus Panel’s guidelines state that people with cardiovascular disease are divided into three risk clusters: low, middle, and high.

    ED is a crucial precursor for CV events that occurred two to five years ago. Given that they share the same pathogenetic mechanism, i.e., endothelial dysfunction—these two disorders are inextricably linked.

    It is crucial to optimize the therapy of cardiac heart failure (CHF) before treating ED in individuals with CHF. As CHF symptoms subside and exercise capacity rises, sexual function improves. PDE5 inhibitors are the first-line therapy if this strategy is unsuccessful. PDE5 inhibitors are safe and effective in treating erectile dysfunction (ED) in patients with CHF who are NYHA Classes II and III.

    In addition, there is a link between an increase in EF by PDE5 inhibitors and improving depressive symptoms and quality of life. Sexual activity is still not advised for NYHA IV patients because it is just as risky for them as doing simple housekeeping or ascending a flight of stairs.

  • MetS and obesity
    Although preliminary cross-sectional data did not reveal any correlation between ED and obesity, longitudinal investigations have unequivocally shown a causal link between baseline obesity and the development of ED, how body weight affects the effectiveness of PDE5 inhibitors when taking sildenafil daily and tadalafil in single and repeated doses has been examined. The effectiveness of the medication was, in every instance, unrelated to baseline BMI. However, there are no data on vardenafil.

    A significant component of MetS, a collection of metabolic abnormalities linked to insulin resistance and an elevated risk of developing cardiovascular and metabolic illnesses, is central obesity. In addition, numerous epidemiological studies have indicated that MetS may be a risk factor for ED.

  • Dyslipidemia:
    Several clinical studies have identified an association between ED and hyperlipidemia (dyslipidemia). There is a connection between low-density high lipoprotein cholesterol (LDL-C) levels and ED.

    Hypercholesterolemia at baseline was also demonstrated as a predictor of ED 25 years later.

    As a result, various investigations have shown that lipid-lowering medication can improve EF in both clinical and experimental tests. Statin therapy may also enhance the effects of PDE5 inhibitors and EF. In addition, the effectiveness and safety of all three PDE5 inhibitors have been established in patients with dyslipidemia. Vardenafil was successful in males with dyslipidemia regardless of LDL-C levels or the total to high-density lipoprotein cholesterol ratio, according to specific drug data.

  • Prostatic Disorders
    Numerous epidemiological studies have suggested that there may be a cause-and-effect relationship between lower urinary tract symptoms (LUTS) and ED beyond simple age-related coincidence. Studies on each of the three PDE5 inhibitors now on the market have demonstrated improvements in LUTS and ED in men with severe issues in both areas without appreciable adverse effect augmentation. Radical prostatectomy (RP) is still the go-to treatment for men with clinically localized prostate cancer, but postoperative ED is a frequent consequence. It is mainly explained by transient neuropraxia of the cavernous nerve, which causes penile hypoxia, smooth muscle apoptosis, fibrosis, and veno-occlusive dysfunction. The idea of early penile rehabilitation- preventing ED after RP by combating post-RP pathophysiological changes during neural repair- is one of the most promising new therapies. In addition, PDE5 inhibitors can help penile erections when needed. While there are inconsistent findings from daily usage of short-acting PDE5 inhibitors, evidence with tadalafil 5 mg daily dosing is still lacking.
  • Endocrine disorders:
    Hormonal imbalance may be a secondary cause of ED. Hypogonadism is common in ED patients, and hyperprolactinemia and thyroid problems are often uncommon.

    More research is required to fully understand the impact of thyroid hormones on male sexual response, as hyperprolactinemia primarily affects sexua
    l desire.

    Overall, the net effect of testosterone (T) on erection is moderate since it positively regulates both the enzymatic pathways required for its start (positive influence on nitric oxide synthase [NOS] and adverse effect on RhoA/ROCK) and termination (positive impact on PDE5). T’s primary physiological activity is to time modify the erectile process in response to sexual desire, concluding erections with sex. Therefore, it is generally agreed that the parts of male sexual behavior that are most T-dependent are sexual ideas and drives.

    For all the reasons mentioned above, treating hypogonadism improves penile erection dysfunction in clinical and experimental animal models. T administration, on the other hand, is mainly ineffectual in normally eugonadal people. According to this data, a meta-analysis of placebo-controlled clinical trials demonstrated that investigations of middle-aged and older men with low T (T concentration 12 nmol/L, 346 ng/dL) resulted in a substantial but moderate improvement of all areas of sexual performance compared to placebo. It’s interesting to note that the meta-regression study showed an inverse relationship between the baseline T concentration and the effect of T on EF.

    Numerous studies have suggested that hypogonadal ED patients may respond less favorably to PDE5 inhibitors because androgens influence the production of both NOS and PDE5 [35]. However, according to several uncontrolled and four randomized placebo-controlled investigations, hypogonadism interferes with the effects of PDE5 inhibitors on EF (Table 3). Therefore, based on the findings of these trials, it is possible to increase total efficacy from 33% to 100% by using T and PDE5 inhibitors.

    All of these findings highlight the idea that hypogonadism must be excluded and, if present, thoroughly treated before any PDE5 inhibitors are prescribed.

  • Stroke:
    Suppose PDE5 inhibitors are given 24 hours after a stroke. In that case, recent animal studies have shown significantly enhanced cGMP levels and angiogenesis, significantly reducing infarct size, and increasing protection against ischemia-reperfusion injury. PDE5 inhibitors may counteract the effects of declining cGMP levels in aging by increasing neuronal development and short-term memory.

    PDE5 inhibitors were used in a study to measure cerebral blood flow, but the results showed no change in blood velocity. In individuals with erectile dysfunction, pulmonary hypertension, and other conditions with a compromised endothelial dilatory

  • Hypertension
    Between 15% and 25% of patients receiving treatment for hypertension have ED. Men with systolic blood pressure (SBP) > 140 mm Hg report ED more than twice as frequently as those with SBP 140 mm Hg. Additionally, it has recently been shown that pulse pressure, the arithmetic difference between SBP and diastolic blood pressure, can predict significant CV incidents in patients with ED.

    Compared to more recent medications such as calcium antagonists, angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, and nebivolol, older antihypertensive drugs like diuretics, beta-blockers, and centrally acting drugs have been more frequently linked to detrimental effects on sexual function.

    However, the few placeboes- or active comparator-controlled studies that have been published thus far did not note an adverse effect of beta-blockers and thiazide diuretics. Therefore, this point has not yet been fully clarified. In contrast, spironolactone therapy causes undeniable sexual complaints because of its antiandrogen effects.

    Possible interactions between PDE5 inhibitors and antihypertensive medications are a common clinical problem. PDE5 inhibitors are typically well tolerated when provided to patients taking antihypertensive drugs. However, patients taking PDE5 inhibitors should take caution when taking alpha-blockers or beta-blockers interacting with alpha-adrenergic receptors. Alpha-blockers should be started at the lowest dose, especially in individuals already taking a PDE5 inhibitor at the recommended dosage.

    In contrast, alpha-blockers patients should start PDE5 inhibitors at the lowest suggested amount. Therefore, it is crucial to monitor the Blood pressure and adjust the antihypertensive dose. It is because no particular studies have been done on individuals receiving any antihypertensive medication starting daily treatment with tadalafil 5 mg.

Conclusion:

The PDE5 inhibitors now on the market, such as the more recently approved avanafil, offer ED sufferers a secure, practical, and efficient way to enhance erectile function. Due to their convenience, quick start of the action, and tolerability, these medications have taken the place of other ED treatments as the first-line therapy. 

Therefore, deciding whether an agent is superior to another is challenging due to insufficient head-to-head trials. However, more research comparing these drugs is required to discern the potential advantages of each, particularly in particular patient subsets. In addition, according to each patient’s response and need, prescribing options are available with all PDE5 inhibitors. Therefore, consider each agent’s cost, simplicity of use, and side effects while determining the best course of action.

The factors that a healthcare professional should note during the visit of the ED patient and their importance for selecting a PDE5 inhibitor are outlined. Unless there are apparent contraindications, all PDE5 inhibitors currently on the market may be effective in treating any patient with ED. Sildenafil, tadalafil, and vardenafil are the three commonly used PDE5 inhibitors; nevertheless, there are distinctions between them that may impact the therapeutic outcome, patient satisfaction with the prescribed medication, and long-term adherence to treatment.

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CategoriesLifestyle

How to consume the Krrista Range of ED Pills?

by admin

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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Sexual Dysfunctions in men – Consequences that Nobody Talks About

by admin

Male arousal is a complex process of brain, hormones, emotions, nerves, muscles, and blood vessels. Therefore, a medical problem in any of these processes can result in erectile dysfunction. And while people suffering from the disorder mostly focus on the reasons, hardly anybody discusses the impace of ED that is much more than just biological.

To understand the consequences of erectile dysfunction on men, we shall first understand the problem in depth.

Some of the most common erectile disorders men face are as follow-

  • Trouble getting or maintaining an erection
  • Premature ejaculation
  • Delayed ejaculation
  • Decreased libido or reduced sex drive.

If you or someone close to you is suffering from any of the above mentioned problems, keep reading.

Most of the times, ED can be the result of an underlying disease such as hypertension, ischemic heart disease, and diabetes mellitus. Prevalence of ED also rises with age. However, ED can also affect younger men aged 18 to 25. Men with radical prostatectomy for prostate cancer are also frequently diagnosed with ED.

Brief overview of male arousal

The relationship between the individual’s mind and body during regular sexual activity is complex. For example, an erection results from interactions between the neurological, circulatory, and endocrine (hormonal) systems. The interaction of these systems controls the male sexual response

Following are the major elements of male arousal-

Desire:- The desire to participate in sexual activities is sometimes referred to as sex drive or libido. Words might set it off, images, smells, sounds, or physical contact. Excitement is the initial stage of the sexual response cycle, triggered by desire.

Excitement:- The next step is excitement or sexual arousal. Nerve impulses from the brain are transmitted to the penis during excitation via the spinal cord. A larger opening of the corpora cavernosa and corpus spongiosum arteries, which provide blood to the erectile tissues, results in a response (relaxing and dilating). These areas see a considerable increase in blood flow due to the enlarged arteries, which causes them to swell up. This growth strains the veins that typically drain blood from the penis, compressing them and delaying the blood flow, which raises blood pressure inside the penis.

Erection and rigidity are the results of this increased penile pressure.

All around the body, muscle tension rises as well. As a result, excitation and tension in the muscles increase throughout the plateau stage.

Orgasm:-The height of arousal during a sexual encounter is called an orgasm. When an orgasm occurs, the body’s muscles become even tenser, the pelvic muscles clench, and ejaculation follows.

Ejaculation:-Male reproductive organs such as the ducts of the epididymis, the seminal vesicles, the prostate, and the vas deferens all have muscles that are stimulated by nerves to contract during ejaculation. Semen is forced into the urethra by these contractions—the muscles surrounding the urethra contract, pushing the semen out of the penis even further. Additionally, the bladder’s neck tightens, obstructing the flow of semen backward into the bladder.

Causes of Sexual dysfunction

There are several causes of sexual dysfunction. There may be physical causes or psychological causes. Some of these causes are mentioned below:-

Decreased Libido

Decreased libido is one of the most common causes of sexual dysfunction. Some of the key factors contributing to a reduced sex drive or libido are:

  • Unhealthy or desultory lifestyle
  • Unhealthy eating habits
  • Relationship difficulties
  • Stress, worry, or depression
  • Hormone levels decline as you age
  • Alcohol or drug abuse
  • Low testosterone

Post-Traumatic Stress Disorder

Witnessing or suffering a traumatic event, such as a major accident, physical or sexual assault, or war and conflict can lead to post-traumatic stress disorder (PTSD), a mental health condition.

Some of the Symptoms of PTSD include:

  • Persistent, unsettling thoughts, flashbacks, or dreams about the traumatic incident.
  • Isolation from anybody or anything that might bring back bad memories of the traumatic experience.
  • Extremely strong reactions to stimuli, both emotionally and physically, as well as a shift to a negative frame of mind.

Medication Side-effects

Medications such as those for high blood pressure and depression, as well as alcohol and recreational drugs, can all interfere with proper sexual functioning. Some medical interventions may also impact sexual ability. Nerve injury, which can occur during some surgical procedures, is one potential reason for diminished sexual function.

Psychological effects of Sexual Dysfunction

Sexual dysfunction can be upsetting. One qualitative investigation indicated that the most common immediate reaction was emasculation. Many young men have described this experience as ‘absolute humiliation’ and a ‘deep feeling of being less than everybody else’.

This might intensify insecurities and affect love relationships.

Some individual’s incapacity to please their spouses was another key problem; some felt they were ‘letting their partners down’ or feared their partners would leave them because of it.

Men with sexual dysfunction oten feel isolated. A young man wrote that he felt embarrassed and unsupported if he told his friends. Based on this narrative, many discuss or laugh about their sex lives as if nothing was amiss. There is a cultural expectation that ‘men are meant to always want sex’. When you don’t live up to that norm, you are bound to feel humiliated. Such situations sometimes intensify the impact of the problem.

Sexual dysfunction can damage relationships outside of them. Those who are single may be hesitant to create new relationships or find sexual partners. Even when starting a new relationship, a person with sexual dysfunction may be afraid of rejection and hesitant to share it.

BIOLOGICAL IMPACTS OF ERECTILE DYSFUNCTION:

Erection dysfunction can cause relationship problems, affect your confidence, and may cause stress. But more than anything, it can lead to diseases and disorders.

Common health conditions associated with erectile dysfunction:

  • ED and cardiovascular disease: ED patients tend to have cardiovascular disease by 1.5 times in the future more than any other man. The risk of having this disease is the same for a person with a family history of heart attack, dyslipidemia, or smoking.
  • ED and diabetes: Erectile dysfunction can often be the first symptom in the men who have diabetes. However, in some men, these conditions occur simultaneously.
  • Hypertension and ED: Erectile dysfunction and high blood pressure can also occur simultaneously in most men. 35% of the men who have hypertension may suffer from ED, and 40% of the men who have ED may suffer from hypertension.
  • Lower urinary tract disorders: Men with ED are likely to suffer from lower urinary tract infections 2-9 times more. Some studies also show that with the severity of lower urinary tract infections, the risk of erectile dysfunction increases.

Diagnosis for all sexual dysfunction

A physical exam by a healthcare professional is often the first step of diagnosing ED. These exams can consist of the following:

  • Blood tests
  • Checking blood pressure.
  • Prostate examination with a rectal exam.
  • Testicles and penis examination.
  • If you have issues with blood flow to the penis, another test can reveal this.

Your symptoms, medical history, and sexual history must be discussed with your doctor. Do not feel uncomfortable, even though some questions could sound private. Therefore, it is crucial to respond honestly to prescribe the best course of treatment.

Treatment options for ED

  • Mechanical devices
    A constriction ring can help men who get an erection but can’t keep it up. As soon as an erection happens, an elastic ring is put around the base of the penis to stop blood from retreating and keep the penis tight. If the man cannot get an erection, he can place a hand-held vacuum erection gadget over his penis. The ring is then placed on the penis’s base to maintain the erection after this gadget gently vacuums blood into the penis. This method has some downsides, including penis bruising, coldness at the tip, and lack of spontaneity. A constriction ring and vacuum device may occasionally be used with medication.
  • ED pills
    Oral phosphodiesterase inhibitors are the main treatments for ED. Due to their ease of use and ability to promote spontaneity in sexual activity, oral phosphodiesterase inhibitors are used far more frequently than other medications. For example, some men prefer tadalafil because its effects can last up to 36 hours longer than other medications. When taken before meal and at least an hour before sexual activity, most phosphodiesterase inhibitors perform optimally.
  • Counseling or sex therapy
    For men whose ED is psychological, couselling by a certified expert can help. If there is trouble in paradise or you haven’t been doing fine mentally, a therapy might be your solution to cure erectile disorders.
  • Occasional testosterone treatment
    If low testosterone is the cause of ED, more testosterone may be administered as an injection, a patch, or a gel applied to the skin. Previous research suggested that these treatments may marginally raise the risk of a heart attack or stroke. The bulk of investigations, nonetheless, have not supported these conclusions. For example, unless a guy has low testosterone levels in his blood, more testosterone is not advised. A doctor can think about treating the man with a different medication if a pill seems to be the source of low testosterone levels.

Conclusion

Sexual dysfunction certainly has psychosocial risk factors. Therefore, in addition to medical examination and therapy, women and men with sexual dysfunction should receive psychosocial evaluation and treatment if available. More research is needed on how social and cultural influences affect sexual function. For instance, researchers should conduct a clinical assessment for occult cardiovascular disease in men who do not already have known cardiovascular disease but develop organic erectile dysfunction, especially in men under 70. This recommendation is based on solid evidence that erectile dysfunction is a sign of other types of cardiovascular disease.

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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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