Disability treatment – Philippine Cerebral Palsy

Ex-dentist apologizes for not spotting tooth decay and botching treatment

Antoine L. Cassell — Mon, 09 May 2022 04:03:03 +0000

A dentist has been found to have breached the health and disability code, after failing to properly diagnose a dental injury on a patient. Stock / 123rf

A young woman whose dentist botched a procedure and failed to properly spot the tooth decay says she almost lost one of her teeth – if she hadn’t seen another dentist in time.

The woman suffered from a serious tooth injury, which previous x-rays should have been obvious to her dentist, the Assistant Commissioner for Health and Disability found.

But the potentially harmful lesion was only discovered when the patient visited a dentist abroad, who alerted her to the decay of not one but seven of her teeth.

According to the findings of Deputy Commissioner Dr Vannessa Caldwell, the patient started seeing the New Zealand dentist in 2011 as a teenager.

On the first visit, an X-ray was taken, with the dentist, whose name is suppressed, commenting that the patient’s teeth were “very well cared for”.

But the patient claims that the doctor did not raise the issue of early mineral loss – clearly visible on the x-ray.

There was no reference to mineral loss on the patient’s clinical notes of the visit.

The patient continued to be seen for annual checkups for the next two years. During a visit in 2013, the dentist noticed a lesion on a tooth, but there was no evidence in clinical notes that this had been discussed with the patient.

A year later, the patient returned to the office, with the dentist performing “restorative treatment” on the tooth.

In January 2015, a year after the restoration work, the patient contacted her dentist concerned about a dark spot on the tooth.

A week later, restoration work was again undertaken on two teeth – one of which was the same tooth that had been operated on 12 months previously.

The dentist said in his clinical notes that he “didn’t trust” his original work.

The patient consulted again in August 2015 and again in June 2016. No problems were reported and no advice was provided to the patient in the clinical notes.

The patient then moved abroad for three years, returning to the practice for a check-up in February 2019.

Two other lesions were identified, but the dentist advised the patient to return in six to nine months to reassess any corrective action.

During the same appointment, the patient expressed concern about her sore wisdom teeth, but the dentist told her they were fine.

The patient returned to the practice that same month for restorative work on one tooth, as well as another restoration on the same tooth which had now received three restorative works.

But the patient was worried about the advice she had received. Four months later, she visited another dentist while she was abroad.

The new dentist discovered several lesions on seven teeth, including one described as being so large that the patient was warned she was at risk of losing the entire tooth.

It was also discovered that the same wisdom teeth that the patient had complained about earlier had lesions. They were removed shortly thereafter.

In June 2020, when the patient visited another dentist, he recommended that the repair work undertaken on a tooth by her previous dentist be redone – the fourth time the treatment had to be repaired.

In total, the patient says she has attended more than 20 dental appointments since her last appointment with her original dentist in 2019.

In her investigation, the deputy commissioner found that the problems with the most badly damaged tooth should have been detected by the New Zealand dentist in 2019.

The dentist also failed to provide the patient with adequate information about the issues affecting her wisdom teeth.

The failure of both counts was a violation of the Code of Rights of Consumers of Health and Disability Services.

The dentist at the center of the complaint no longer practices and has already issued a formal apology for the harm caused to the patient.

Caldwell ordered the dentist to consider the patient’s impact statement and ordered him to undergo a competency exam if he ever returned to practice.

Causes, symptoms, treatment of cerebral hyperperfusion syndrome

Antoine L. Cassell — Fri, 15 Apr 2022 16:53:46 +0000

Cerebral hyperperfusion syndrome (CHS) is a rare but life-threatening risk of carotid endarterectomies and carotid artery stenting. These are surgical procedures that are used to increase blood flow in the carotid arteries, the main vessels that supply blood to the neck, brain and face.

CHS can cause swelling and bleeding in your brain. The death rate is as high as 50 percentand many who survive have permanent disabilities.

The term “CHS” is often used interchangeably with “reperfusion brain injury” or “reperfusion syndrome.” Read on to learn more about the causes of CHS and how it is managed.

Meaning of “hyperperfusion”

“Hyperperfusion” is the medical term for increased blood flow to an organ. The prefix “hyper” means increased or excessive, and “perfusion” refers to the passage of blood through a blood vessel.

Cerebral hyperperfusion is defined as an increase greater than 100% in blood flow in the carotid artery compared to baseline. Some people develop symptoms with an increase in blood flow as low as 20-40%.

CHS is a potential risk of carotid artery revascularization surgeries. These surgeries aim to increase blood flow in the carotid artery to prevent strokes in people with carotid artery disease. Blockages in the carotid arteries account for 15% of all strokes.

CHS was first discovered as a risk of a type of surgery called carotid endarterectomy, but it can also occur after stenting the carotid artery. It can develop immediately after surgery or up to a month later.

The exact reason why some people develop CHS remains unclear. Several factors are thought to contribute to this.

Loss of self-regulation

Normally, your brain regulates itself to maintain constant pressure when blood flow changes. Researchers believe that in some people with chronically low blood flow in the carotid artery, the brain may lose its ability to self-regulate and the blood vessels may remain chronically relaxed.

When blood flow increases after surgery, the brain may not constrict blood vessels appropriately to protect the beds of tiny blood vessels called capillaries.

Chronic high blood pressure

People with severe narrowing of the carotid artery often have high blood pressure. It is thought that high blood pressure that is already present may contribute to the development of CHS. Chronic high blood pressure can damage small blood vessels and lead to a breakdown of the blood-brain barrier.

Researchers found evidence of leakage of the protein albumin after breakdown of the blood-brain barrier in animal studies. This leakage can potentially activate a pathway that causes brain swelling and seizures.

Damage caused by nitric oxide and free radicals

Nitric oxide is a vasodilator, which means it relaxes blood vessels and lets more blood flow through.

It’s thought nitric oxide may contribute to autoregulatory and blood-brain barrier dysfunction in CHS. The buildup of harmful molecules called free radicals can damage brain tissue to 48 hours.

Dysfunction of baroreceptors

Baroreceptors are specialized receptors that sense blood pressure and send signals to your brain to up-regulate or down-regulate blood flow. During surgery, the nerves that carry information from these receptors can be damaged. This damage can lead to increased blood pressure that is difficult to control, even with medication. Fluctuations in blood pressure due to baroreceptor damage can last up to 12 weeks.

Most people with CHS have mild symptoms, but they can progress to severe and life-threatening symptoms if left untreated. The most common symptoms are:

Less common symptoms include:

This condition can be fatal in some cases.

CHS is a rare risk of carotid surgery. A study of 4,689 people undergoing carotid endarterectomy and 4,446 people undergoing carotid artery stenting found an incidence of 1.9% and 1.16%, respectively.

What can increase the risk of getting CHS?

Extensive studies have revealed that the three most common conditions associated with the development of CHS are:

more than 90% blockage of the carotid artery
severe blockages (or plaques) of blood vessels in the brain
long-standing pre-existing high blood pressure

Studies have also identified the following as risk factors for developing CHS after carotid surgery:

to be assigned female at birth
chronic kidney disease
left carotid disease
progressive neurological disorders
recurrent hemorrhaging (bleeding)
brain damage (tumors or damaged areas)
microvascular disease (disease of small blood vessels)
reduced ability of blood vessels in the brain to respond to changes in blood flow

What risks does CHS pose to your health?

If left untreated, CHS can lead to severe brain swelling, bleeding, permanent disability, or death.

A 2018 review of studies noted that 47% of CHS cases resulted in stroke, and more than half of strokes were fatal or disabling.

Treatment for CHS often includes intravenous drugs to lower blood pressure, such as labetalol and clonidine.

Antiepileptic drugs may be given to prevent seizures or to treat seizures if they occur.

Mannitol and hypertonic saline solution can be used to treat brain swelling. However, if these treatments are effective in the long term is not clear.

Surgery may be needed if bleeding occurs.

Taking steps to keep your blood pressure within a healthy range can help prevent CHS, as high blood pressure is considered a risk factor for its development.

Prompt identification and treatment of CHS is essential to prevent life-threatening complications. It is recommended that blood pressure be monitored by medical professionals continuously at least every 15 minutes for 24 hours or more after surgery.

Management of CHS focuses on reducing swelling, seizures, and bleeding, which are major causes of brain damage.

In the early stages, the swelling is usually reversible, but if it progresses to hemorrhage, the outlook is not as good. Until 30 percent people remain at least partially disabled and the mortality rate reaches 50%.

CHS is a rare risk of surgeries used to increase blood flow in the carotid artery. It is defined as an increase of more than 100% in blood flow in the carotid artery compared to baseline.

CHS can lead to serious complications such as permanent disability or death. Early recognition of CHS is key to receiving prompt treatment. Common early symptoms include headache, facial pain, or eye pain on one side. Seek immediate medical attention if you experience any of these symptoms within a month of carotid surgery.

Dystrogen Therapeutics’ Investigational DT-DEC01 Chimeric Cell Therapy for the Treatment of Duchene Muscular Dystrophy Shows Improvements in Safety and Functionality | DNA RNA and Cells

Antoine L. Cassell — Fri, 08 Apr 2022 09:06:48 +0000

Dystrogen Therapeutics’ Investigational DT-DEC01 Chimeric Cell Therapy for the Treatment of Duchene Muscular Dystrophy Shows Improvements in Safety and Functionality

Details: Category: DNA RNA and Cells; Posted on Friday 08 April 2022 11:06; Hits: 388

Results continue to strengthen the safety and tolerability profile of DT-DEC01

The first review of functional outcomes in the low-dose cohort revealed improvements 3 months after administration of DT-DEC01

Therapy independent of the genetic mutation of the DMD patient, thus making DT-DEC01 a universal therapy for all DMD patients

MIAMI, FL, USA and WARSAW, Poland I April 7, 2022 I Dystrogen Therapeutics, Corp., the leader in chimeric cell therapies, today announced positive results from an ongoing study conducted in Poland under a hospital waiver protocol of DT-DEC01 (chimeric cells expressing the dystrophin (DEC)), the company’s experimental cell therapy for Duchenne muscular dystrophy (DMD). The results include functional and safety data over 1 to 3 months from three clinical trial participants in the low-dose cohort. During this period, no adverse events (AEs and SAEs) associated with DEC treatment were observed. DT-DEC01 is being developed for the treatment of DMD, a devastating neuromuscular disease associated with a lack of the protein dystrophin. DT-DEC01 is a modified chimeric cell that engrafts into skeletal and cardiac muscle, delivering a full-length dystrophin gene and related components of a healthy muscle cell, the absence of which is strongly associated with progressive degeneration and a shortened lifespan characteristic of the disease.

“There is currently no approved treatment for people with DMD that results in cure or significant reduction of the disease – a disease that causes significant disability in boys and young men and usually results in early mortality. It is very encouraging that we continue to see consistent results, positive data from our investigational cell therapy DT-DEC01 on multiple metrics, as we know the community needs more options,” said Maria Siemionow, MD Ph.D. ., Scientific Director of Dystrogen Therapeutics. “Improvements in functional measures at 1 and 3 months in participants of the low-dose cohorts who received DT-DEC01 are markedly different from what a matched natural history group according to age would predict with DMD. When combined with the strong and sustained expression of dystrophin results in preclinical studies and an encouraging safety profile seen to date, today’s results reinforce our confidence in DT-DEC01 and provide additional evidence supporting this approach as we move to the higher dose cohort in the next stage of clinical testing.

The Data and Safety Monitoring Board (DSMB) reviewed the data from the low dose clinical cohort (2 million DEC cells per kg) and issued a positive opinion on the safety of DT-DEC01 therapy. The DSMB recommends launching the 4M/kg cohort.

Cohort 1 (low dose):

Patient 02B. (7 year outpatient with Exon 3-12 deletion) 3 months post treatment showing improvement on a number of subjective and objective tests. Improvement in EMG (objective test) compared to baseline before treatment. Improved 6MWD, improved 10-meter walk/run time, grip strength and others. Increased number of steps via activity tracking.

Patient 03B. (Non-ambulatory age 15 with Exon 48-50 deletion) 2 months after treatment increased activity level from baseline. Improved grip strength, improved spirometry, improved upper limb strength.

Patient 04B. (outpatient 6-year-old child with nonsense mutation), 1 month after treatment, increase in number of steps via activity monitoring compared to baseline.

About DT-DEC01

DT-DEC01 is a chimeric cell therapy. The Advanced Therapeutic Drug (ATMP) is made using Dystrogen’s proprietary cell engineering technology that creates a DEC cell. Clinically, DEC cells have been shown to express CD56 at significantly higher levels than Duchenne patient myoblasts. DEC cells express favorable HLA characteristics that have multiple advantages. In preclinical studies, DEC cells have also been shown to express clinically significant levels of dystrophin compared to controls. DEC cell therapy has demonstrated significant functional improvement in cardiac, diaphragm, and other skeletal muscle strength and related function in preclinical trials. Because DEC therapy is designed to prevent an immune system response from being triggered, a major advantage of DEC therapy is that it does not require immunosuppression. The therapy is not associated with any genetic manipulation and therefore does not involve any risk of off-target mutation, does not use viral vectors and its use does not depend on the genetic mutation of the DMD patient, thus making DEC a therapy Universal for all DMD patients.

About Dystrogen Therapeutics Corp.

Dystrogen Therapeutics is a clinical-stage life sciences company engaged in the development of therapies for rare genetic diseases. The company was founded on the pioneering work of Professor Maria Siemionow, a world-renowned scientist and surgeon who led the team that performed the first near-total face transplant in the United States. Professor Siemionow’s research initially focused on creating chimeric cells that play a role in modulating the immune system’s response to a transplant. This led to the development of dystrophin-expressing chimeric cell therapy (DEC) which is designed to prevent the immune system from attacking chimeric cells. DECs are engineered cells and belong to a family of therapeutic technologies called Advanced Therapy Medicinal Products (ATMP). Using Dystrogen’s patented cell engineering technology, DECs are made by combining a defective cell from the Duchenne patient with a normal, functioning cell from a healthy donor. This new chimeric cell is composed of both donor and recipient cell structures, but resembles the patient’s immune system as its own cell and therefore does not trigger an immune response while it is functioning (i.e. that it produces dystrophin) like the patient’s normal cell. This offers a unique advantage and allows the patient’s body and immune system to accept the chimeric cell without rejection. In this way, Dystrogen has created dystrophin-producing cells that can be delivered intraosseously and then distributed systemically to be transplanted into the patient’s muscles (such as heart, diaphragm, skeletal muscles) and, as our research and related peer-reviewed publications demonstrate, increase their dystrophin levels. Increased dystrophin levels have been shown to correlate with improved functional outcomes, which has been confirmed in preclinical studies on DEC.

THE SOURCE: Therapeutic Dystrogen