Gardner Syndrome Case Study

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Gardner Syndrome Case Study



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Cushing's Syndrome - Case Study - Neurology Medicine Video - V-Learning

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I get Ivermectin from my vet to to prevent heart-worm disease in my dog. I am all for natural health in myself and my pets, but it seems a little weird to me that this would be used for covid. Vets also use this for cows etc. You can find it in some feed stores. I feel like the FDA needs to back off any natural treatment, let us make our own decisions. Genet at [email protected].

It can be purchased online or at your local farm supply store, no Rx required. Excellent for Covid as well as killing many other parasitic infections, perhaps ones you get from your family pet. How do we get Ivermectin if our doctor is opposed and how long and in what dosage do we take it! Bad side effects. Here is a way to get ivermectin. Hi Natalie, I believe my incorrect response to your question may have gotten away before I could correct it. I am also wearing a mask and being careful to avoid crowds. Very few visitors to my flat.

I also took the capsules a few years ago for a gut infestation. No side effects then either. Good luck! Please review the studies, many of which are peer reviewed, of Ivermectin use for Covid This a proven drug that has over 40 years of proven use. Stop censorship of valuable information and effective proven treatments. Government over-reach has no place in our Constitution, Health or Life. Can you tell me the names of the trials for Ivermectin and Covid and how this paste was administered? This is my first post.

Someone needs to start giving a sh! There must be some good politicians in there somewhere? Ivermectin is a safe, low-cost, effective medication. It has no side effects. We must have something such as this that is easily acquired and easily used! I have taken Ivermectin for Covid and I highly believe in its effectiveness. I know of farmers who have taken it before it was ever mentioned and they had full recoveries when millions were dying. Please do not take this away from the masses It will save lives. Good morning Pamela! Can you tell me more about your dosage? I am writing you about Ivermectin. It is unfathomable to me that there is no major study in the works for Ivermectin after so much consistent good results.

I heard Dr Fauci for the first time postering for early treatment antivirals like Monoclonal therapies. I hope to see a BIG change soon. My notes.. A double-blind Israeli study has concluded that Ivermectin, an inexpensive anti-parasitic widely used since , reduces both the duration and infectiousness of Covid, according to the Jerusalem Post 2. In Mexico.. Iveremctin on his patients. Here in Siam our Med. They did this with HCQ as well. No suprise! Show me the rational behind ivermectin actually working? It is a paraticide, a wormer. How does it work with a mRNA virus? I have puzzled this since the information first came out. It will answer your questions. Everything is explained, and trial proofs are exhibited, on that website.

I know Ivermectin is used as a parasitic drug in cows and horses and has been around for many years. Drug companies need to be halted from making a quick buck via new unfounded and questionable alternatives, and should be penalized if they do not work for the greater good of society in times like this! Ivermectin has been proven to treat Covid with good results. I want Drs. Ivermectin is a safer, better alternative and Drs. The FDA wants to discredit cheap drugs because there is no kickback for them. All the wrong reasons. The so called Covid vaccines are they really helping anyone? Why are there so many people dying after taking the Covid shots? Ivermectin as a prophylaxis for Covid like hydroxychloroquine has been totally politized as an effective drug to be used by the medical profession by the main stream media in America especially CNN MSNBC ABC NBC CBS first by their collective hatred for Donald trump who advocated for use of these drugs against Covid and secondly because they derive so much of their ad revenue from the Pharmaceutical industry they are basically told to deprive the public of the value of these two drugs, in other words big Pharma tells media to debunk these two drugs because they cannot make billions of these drugs.

Your email address will not be published. Presence of endocrine disrupting chemicals in most brands is a major hazard. A new report highlighted by Environmental Health News demonstrates that most diapers and menstrual pads contain volatile organic compounds VOCs and phthalates, endangering millions of babies and seniors w Tell them this is ridiculous with our new Action Alert!

We adopted our present name in Over recent years, we have worked more and more closely with The Alliance for Natural Health, a UK based organization founded by the distinguished food scientist Dr Robert Ver Certainly Americans spend more than any other industrialized country on healthcare. But America falls short in how long we live—or how well. Pesticides in your Froot Loops is only one of the problems.

Last week we discussed the difficulty of knowing what is and is not in the nearly 2, page House Healthcare bill. Here is a really bizarre example. Some commentators noted that the House bill provided for jail time of up to five years for anyone who failed to buy mandated insurance and als August 12, Mild cases may display cough and tachypnea but can progress to acute respiratory distress syndrome ARDS with dyspnea, hypoxemia, and bilateral opacities on chest X-ray. ARDS may sometimes require mechanical ventilation. Of note, in patients with CRS the need for mechanical ventilation is oftentimes not due to respiratory distress but instead a consequence of the inability to protect the airway secondary to neurotoxicity [ 26 ].

Patients with severe CRS can also develop renal failure or signs of cardiac dysfunction with reduced ejection fraction on ultrasound. In addition, patients with severe CRS frequently display vascular leakage with peripheral and pulmonary edema. In severe cases CRS can be accompanied by clinical signs and laboratory abnormalities that resemble hemophagocytic lymphohistiocytosis HLH or macrophage activation syndrome MAS.

Some patients develop neurotoxicity after administration of T cell-engaging therapies. Neurologic symptoms might span from mild confusion with word-finding difficulty, headaches and hallucinations to aphasia, hemiparesis, cranial nerve palsies, seizures and somnolence. The pathophysiology of the neurologic symptoms is poorly understood, but the lack of a strict temporal association with CRS indicates that it might, at least in part, be independent from CRS. In addition, experience from clinical trials suggests that treatment of the neurologic symptoms is different from that of CRS. The incidence of CRS in patients receiving cancer immunotherapy varies widely depending on the type of immunotherapeutic agent.

With most conventional monoclonal antibodies the incidence of CRS is relatively low, whereas T cell-engaging cancer immunotherapies carry a particularly high risk of CRS. Although most responding patients experience at least some degree of CRS there seems to be no direct association between the severity of CRS and clinical response. CRS does not seem to be a prerequisite for response to T cell-engaging therapies. Some patients show complete remission without obvious signs of CRS, while other patients display severe symptoms and laboratory abnormalities but no clinical response. Clinical studies identified a number of predictors of CRS severity.

The risk of CRS is influenced by factors related to the type of therapy, the underlying disease, and characteristics of the patients. Disease burden is among the most important predictors of severe CRS after CAR T cell therapy or bispecific T cell-engager administration [ 5 , 31 , 32 , 33 , 34 , 35 ]. Similar observations have been made in a murine lymphoma model, were injection of CAR T cells into mice with high tumor burden resulted in lethal CRS, whereas mice with low tumor burden did not show signs of CRS [ 37 , 38 ]. The administered dose of the active agent is another factor that affects the risk of CRS [ 33 , 35 , 39 ].

Furthermore, the strength of T cell activation and the degree of T cell expansion seem to correlate with the severity of CRS [ 40 ]. Children seem to be at a higher risk of developing CRS than adults. The causes of the higher incidence of CRS in pediatric patients are unknown but may be related to higher cell dose used or the more immature immune system of children. The type of T cell-engaging agent affects the overall risk as well as the onset of CRS.

Even though the activation of T cells is the common underlying trigger in all types of T cell-engaging therapies, there are also important differences between the different therapeutic agents that affect the incidence, time course, and clinical management of CRS. Since CAR T cells can persist in the circulation for more than 1 year, the risk for CRS extends for a longer period of time but generally is highest up to 2 weeks after infusion. However, due to differences in the patient populations and differences in the definition of CRS, no definitive conclusions can be drawn with regard to CAR design and the associated risk of CRS. A higher incidence of CRS was observed after lymphodepletion with cyclophosphamide or fludarabine [ 26 ].

This was most likely a consequence of the higher expansion rates secondary to the more pronounced lymphodepletion achieved by combination therapy. Clinically, CRS patients present with unspecific syndromes making the diagnosis challenging. It is important to distinguish CRS from other inflammatory disorders that present with similar clinical signs and symptoms but require different treatment. Tumor lysis syndrome TLS can mimic CRS and presents with symptoms such as fever, acute renal failure, cardiac arrhythmia, and seizures.

Although tumor lysis syndrome usually can be readily discriminated from CRS on the basis of characteristic laboratory abnormalities such as hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, it can sometimes be difficult to determine if CRS and tumor lysis syndrome occur concurrently [ 46 ]. It is important to distinguish patients with CRS from those with sepsis since the treatment for CRS could be detrimental if used in patients with sepsis.

Unfortunately, it is extremely difficult to distinguish sepsis from CRS. In fact, according to the most recent definition a large percentage of patients with severe CRS will fulfill the clinical criteria of sepsis, i. Furthermore, a significant proportion of these patients will also fulfill the criteria for septic shock since they have an elevated lactate and require vasopressors. Patients with CRS are at a high risk of infection and the immunosuppressive treatment that is administered for the treatment of CRS can mask some of the signs of infection thereby delaying diagnosis and treatment of infection. The infections typically began after the onset of CRS. Infections that occur in patients with CRS are predominantly of bacterial origin, followed by viral infections that primarily involve the respiratory tract.

Fungal infections are rare and were primarily observed in patients that had previously undergone autologous or allogeneic stem cell transplantation and were suffering from severe CRS [ 48 ]. It therefore is crucial to maintain a high degree of vigilance for infection and appropriate empiric antimicrobial therapy should be rapidly initiated if infection is suspected. All patients with CRS should receive an extensive diagnostic work-up to exclude infections, including a chest X-ray and blood cultures. Furthermore, before start of immunotherapy patients should be carefully checked for any signs of infection [ 49 ].

The mechanism that is responsible for the increased incidence of infection in patients with CRS is unknown. A plausible explanation could be that the massive release of cytokines in CRS induces a form of immune paralysis, which predisposes the patients to an increased risk of infection. This hypothesis is consistent with the observation that the incidence of infections is higher in patients with more severe CRS [ 48 ].

Table 2 summarizes some of the factors that help to distinguish CRS-related HLH from other conditions that present similarly. Patients with severe neurotoxicity require a thorough neurologic work-up which should include a careful neurologic exam and, if appropriate, brain imaging, a spinal tab and an electroencephalogram. Since most T cell-engaging agents contain non-human protein sequences there is a risk of allergic drug reactions. Hypersensitivity reactions can also present with rash and urticaria, fever, dyspnea, hypotension and gastrointestinal symptoms culminating in cardiorespiratory failure. Unlike in CRS symptoms of true type I reactions occur after repeated exposure to the causative agent [ 50 , 51 ]. However, so far only few cases of severe allergic reactions or anaphylactic shock related to immunotherapeutics have been described in the literature [ 52 ].

If anaphylactic shock is suspected epinephrine and antihistamines should be administered immediately [ 53 ]. Given that all these differential diagnoses have a clinical presentation that is very similar to CRS, making a definitive diagnosis of CRS is very challenging. Since some of the therapies given for conditions other than CRS can mitigate the effectiveness of immunotherapy, the development of reliable diagnostic test that help to make the diagnosis of CRS are a high priority for future research.

Such tests could greatly improve the effectiveness and safety of CAR T cell therapy. The pathophysiology of CRS is only incompletely understood. CRS is usually due to on-target effects induced by binding of the bispecific antibody or CAR T cell receptor to its antigen and subsequent activation of bystander immune cells and non-immune cells, such as endothelial cells. Activation of the bystander cells results in the massive release of a range of cytokines.

We know little about how the initial activation of CAR T cells results in the distortion of the cytokine network that drives the inflammatory process in CRS. Depending on a number of characteristics of the host, the tumor, and the therapeutic agent the administration of T cell-engaging therapies can set off an inflammatory circuit that overwhelms counter-regulatory homeostatic mechanisms and results in a cytokine storm that can have detrimental effects on the patient. Figure 2 summarizes our current understanding of the pathophysiology of CRS. Reported inducers of CRS. These cytokines trigger a chain reaction due to the activation of innate immune cells like macrophages and endothelial cells with further cytokine release. Interleukin 6 IL-6 seems to hold a key role in CRS pathophysiology since highly elevated IL-6 levels are seen in patients with CRS [ 5 , 55 , 56 , 57 ] and in murine models of the disease [ 58 ].

IL-6 can signal via two different modes. Of note, the IL-6 receptor does not possess intracellular signaling domains. In trans-signaling, IL-6 binds to the soluble form of the IL-6 receptor, which has been cleaved from the cell surface by metalloproteinases. IL-6 contributes to many of the key symptoms of CRS. In addition, IL-6 likely contributes to cardiomyopathy that is often observed in patients with CRS by promoting myocardial dysfunction [ 61 ]. Recently, Teachey et al. They subsequently validated these findings in 12 pediatric patients [ 62 ]. While limited due to the relatively small number of patients experiencing sCRS and limited availability of on-site cytokine measurement these tools might help in identifying patients that need a more intense monitoring and treatment.

A hallmark of severe CRS seems to be the activation of endothelial cells. Typical marker of endothelial activation such as Ang-2 and von Willebrand factor are often elevated in the serum of patients with CRS [ 26 ]. This indicates that the endothelium plays an important role in the pathophysiology of CRS both by amplifying the inflammatory response and as a target organ. The crucial contribution of endothelial dysfunction in the pathogenesis of CRS provides an explanation for some of the hallmarks of severe CRS, i. Importantly, endothelial activation and the ensuing vascular dysfunction might be the mechanistic factor linking CRS with neurotoxicity.

A recent study found that neurotoxicity after immunotherapy with CDtargeted CAR T cells was accompanied by findings consistent with endothelial activation [ 64 ]. The management of the toxicities of cancer immunotherapy is challenging clinical problem. Since T cell-engaging therapies are a relatively recent development there are still many unanswered questions regarding the optimal clinical management of CRS. The recommendations for the management of CRS are thus still evolving constantly.

Current treatment algorithms for CRS are based on expert opinion and represent the experience of the pioneers in the field of T cell-engaging immunotherapies [ 28 , 29 ]. Proposed pathomechanism of CRS. This leads to the activation of macrophages, dendritic cells, other immune cells and endothelial cells. These cells further release proinflammatory cytokines. Importantly, macrophages and endothelial cells produce large amounts of interleukin 6 IL-6 which in a positive feedback loop manner activates T cells and other immune cells leading to a cytokine storm. The current approaches to prevention and treatment of CRS in patients receiving these two types of T cell-engaging therapies therefore differ substantially.

ICU referral should be considered in all patients with CRS and early involvement of the critical care team is paramount [ 66 ]. Since even severe CRS has a relatively good prognosis when appropriately treated, patients with CRS should be offered the full spectrum of modern critical care including mechanical ventilation if necessary [ 67 ]. The management of CRS follows a grade- and risk-adapted strategy for monitoring and therapy [ 28 , 29 ].

Fever is an important clinical sign that should raise the suspicion of impending CRS in patients receiving T cell-engaging therapies. Therefore, patients who develop fever should be frequently reassessed for signs of CRS and outpatients should be admitted to hospital for closer observation [ 26 ]. Until better predictive biomarkers have been discovered, clinicians should therefore maintain a high alertness for the development of CRS in any patient following treatment with T cell-engaging therapies.

Low grade CRS is treated symptomatically with antihistamines, antipyretics and fluids. Additional diagnostic testing should be performed to rule out differential diagnoses. If an infection cannot be ruled out with certainty start of an empiric antibiotic therapy should be considered. Furthermore, all patients with early signs of CRS should be regularly evaluated for signs of further deterioration. Severe CRS represents a life-threatening situation that requires prompt and aggressive treatment. Based on the insight gained from the first clinical trials of blinatumomab a prophylactic protocol consisting of cytoreduction, dose adjustment, and premedication with corticosteroids has been devised, that resulted in a reduced incidence of severe CRS [ 68 ].

Unlike BiTEs, which can be given repeatedly, and can be interrupted if necessary, CAR T cell therapies are often administered only once and their final effective dose after in vivo expansion is unpredictable. Therefore, the primary aim in the setting of CAR T cell therapies so far has been to efficiently treat severe CRS once it develops while trying to avoid mitigation of the antitumoral immune response. IL-6 represents a particularly suitable target since IL-6 is of relatively little importance for T cell function [ 69 , 70 ] but, as already mentioned, is a central driver of many symptoms of CRS. By binding to membrane-bound as well as soluble IL-6 receptor tocilizumab interferes with both classical and trans-signaling pathways. Subsequent studies confirmed that administration of monoclonal antibodies against IL-6 siltuximab and its receptor tocilizumab led to rapid resolution of CRS symptoms [ 29 , 31 , 33 , 71 ].

As a consequence, tocilizumab has quickly become the gold standard for the initial treatment of severe CRS in patients receiving CAR T cells. In August , concurrently with tisagenlecleucel the FDA approved tocilizumab for the treatment of CRS in patients 2 years of age or older. The recommended dose for i. Patients that develop grade 3 or 4 CRS toxicity should immediately receive treatment with tocilizumab. Usually significant resolution of CRS related symptoms e. If no such effect is evident within 24 to 72 h a second administration is feasible. Of note, it should be taken into consideration that after administration of tocilizumab CRP can no longer be used as an indicator of CRS severity as blockade of IL-6 signaling results in a rapid decrease of CRP.

Currently, there are several other ILtargeting monoclonal antibodies in late stage clinical development, which could also potentially be used to treat CRS. Clazakizumab is another monoclonal antibody targeting IL Corticosteroids should generally be avoided as first line treatment of CRS in patients receiving CAR T cells and should be reserved for cases refractory to IL-6 blockade or patients with severe neurotoxicity. Since tocilizumab does not cross the blood-brain-barrier it does not seem to be very effective against CRES and corticosteroids are thought to be more effective than IL-6 targeting in this setting [ 29 ]. The current recommendations therefore prefer the use of corticosteroids for the treatment of the neurologic adverse effects of T cell-engaging therapies.

Monoclonal antibodies that target IL-6 directly, thereby eliminating it from the circulation, might be advantageous in patients with severe CRS and concurrent neurotoxicity, since tocilizumab does not cross the blood brain barrier and therefore fails to inhibit IL-6 signaling in the CNS. If corticosteroids are used in patients receiving T cell-engaging immunotherapy, the duration of treatment should be kept as short as possible to minimize the detrimental effects on the effectiveness of immunotherapy.

However, a case of sCRS that was unresponsive to tocilizumab, etanercept, and glucocorticoids has been published [ 35 ]. In those cases other immunosuppressants, such as the IL-6 monoclonal antibody siltuximab [ 73 ], T cell-depleting antibody therapies such as alemtuzumab and ATG, IL-1R-based inhibitors anakinra or cyclophosphamide might be of benefit. Other experimental therapies for CRS include ibrutinib [ 74 ]. Moreover, there are several reports of successful use of cytokine adsorption in the setting of severe HLH unresponsive to standard treatment [ 75 , 76 ] that might also be effective in sCRS.

The administration of tocilizumab does not appear not to negatively affect response rates to T cell-engaging therapies [ 39 , 77 , 78 , 79 , 80 ]. Interestingly, in some studies even glucocorticoids did not seem to impact response rates [ 39 , 78 , 80 ]. In addition, smaller studies implicated a negative effect of glucocorticoid administration on patient outcome: In a case report of 3 patients suffering from chronic lymphocytic leukemia the only patient not completely responding to CDCAR T cell therapy received glucocorticoids for CRS treatment [ 40 ]. There are a variety of preventative measures that have the potential to reduce the incidence of CRS after immunotherapy [ 81 ].

One approach for mitigation of CRS risk is dose-reduction. Dose adaption of CAR T cells to tumor burden and the type of malignancy was shown to be effective in preventing severe CRS [ 35 ] and dose-reduced readministration of blinatumumab after a grade IV CRS was shown to be safe [ 82 ]. It can be expected that the treatment algorithms for CRS will change in the future as we gain more and more experience with managing the side effects of T cell-engaging immunotherapeutics. The effective treatment of CRS with greatly benefit from the ongoing efforts for harmonization of the grading system and treatment protocols for CRS. The CRS is among the most frequent serious adverse events and a represents a major cause of morbidity following T cell-engaging immunotherapy.

Insights gained from studying the biological mechanisms of CRS and the clinical use of corticosteroids and IL-6 blockade have already improved the management of patients with CRS. However, there remain many unanswered questions and there still is amble room for improvement of the clinical management of CRS. With the growing use of T cell-engaging therapies there is an urgent need for clinical trials that improve the evidence base for the treatment of CRS. Our current management strategies for CRS are predominantly based on biologic reasoning, expert opinion, and retrospective analyses. In order to further improve the safety and effectiveness of the clinical management of CRS, randomized controlled trials that evaluate different treatment strategies for CRS are necessary.

Furthermore, a primary challenge in the future management of CRS will be to identify additional targets for specific therapeutic intervention in CRS. Given the apparent central role of the endothelium in the pathophysiology of CRS and neurotoxicity following T cell-engaging therapies further studies on the role of endothelial dysregulation in CRS appear particularly promising and should provide valuable insight that could lead to novel therapeutic approaches.

The clinical management of CRS could further be improved by the identification of biomarkers that reliably predict the development of CRS [ 83 ]. We will need to develop tools that guide treating physicians in fine-tuning the use of pharmacologic agents that interfere with these targets in order to ameliorate the adverse effects of CRS while maintaining the therapeutic activity of T cell-engaging therapy. Another promising line of research that will certainly help to improve the safety of T cell-engaging immunotherapy focuses on the optimization of the design of the compounds themselves [ 84 ]. Several research groups are focusing on the design of improved CAR constructs with high antitumor activity but a lower risk of CRS.

Such improvements in the construction of immunotherapies will likely result in a further reduction of serious adverse effects in the future. In the wake of the remarkable success of recently developed immunotherapies the field of immuno-oncology is poised to continue its rapid growth. As a consequence of the more widespread application of immunotherapeutic anticancer agents an increasing incidence of CRS cases can be expected in the upcoming years. A thorough understanding of the clinical presentation, underlying pathophysiology, and available therapeutic options as well as the most important differential diagnoses is crucial for the effective management of this clinical syndrome.

Basic research findings and investigations of patients with CRS will provide valuable insight into the underlying mechanisms of CRS and could aid in the development of molecularly-targeted treatment strategies to prevent and treat CRS. The case of IL-6 blockade in CRS illustrates the potential of targeted immunological interventions for the management of toxicities of cancer immunotherapy. With improved understanding of the pathophysiology and increasing clinical experience in toxicity management more specific mitigation of the CRS will hopefully make cancer immunotherapy safer and more effective.

Systemic reaction to the anti-T-cell monoclonal antibody OKT3 in relation to serum levels of tumor necrosis factor and interferon-gamma [corrected]. N Engl J Med. In vivo cell activation following OKT3 administration. Systemic cytokine release and modulation by corticosteroids. The impact of antithymocyte globulin on short-term toxicity after allogeneic stem cell transplantation. Bone Marrow Transplant. Cytokine-release syndrome in patients with B-cell chronic lymphocytic leukemia and high lymphocyte counts after treatment with an anti-CD20 monoclonal antibody rituximab, IDEC-C2B8. Cytokine release in patients with CLL treated with obinutuzumab and possible relationship with infusion-related reactions.

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