Saturday January 25, 2020

Joint Surgery May Spike up Blood Sugar Levels in Diabetics

Haemoglobin A1c above 6.59 for people with insulin-dependent diabetes and 6.6 without the condition was associated with an elevated risk for post-operative hyperglycemia

0
//
Knee Joint. Pixabay.

People with diabetes who undergo joint replacement surgery are at higher risk of experiencing elevated blood sugar levels after the operation, increasing their chances of developing infections and other complications, a new study suggested.

Patients with insulin-dependent diabetes were more than five times as likely as those without the condition to develop hyperglycemia, or high blood sugar, after surgery, said researchers, including Bradford Waddell from the Hospital for Special Surgery (HSS) in the US.

“If your patient comes in with diabetes and is dependent on insulin, you need to be more cognizant of controlling their blood sugar in the perioperative period because they’re at higher risk,” said Waddell.

For the study, presented at the 2019 annual meeting of the American Academy of Orthopaedic Surgeons, the team reviewed medical charts of 773 men and women who had undergone total hip or knee replacement surgeries between 2011 and 2016.

Of those, 437 had insulin-dependent diabetes, while 336 had not the condition. It included patients with a diagnosis of diabetes whose blood sugar was being controlled using the hormone insulin and compared them with diabetics who did not require insulin.

Diabetes
Representational image. Pixabay

Patients requiring insulin can be considered to have more severe diabetes and have a greater chance of experiencing elevated blood glucose in the perioperative period, Waddell said.

Patients with higher blood glucose over the previous three months — as measured by Hemoglobin A1c — were more likely to experience post-operative hyperglycemia regardless of which group they were in.

Also Read- Excessive Hygiene Can Cause Antibiotic Resistance, Says Study

Hemoglobin A1c above 6.59 for people with insulin-dependent diabetes and 6.6 without the condition was associated with an elevated risk for post-operative hyperglycemia.

However, despite the increased risk for elevation in blood sugar after surgery, the incidence of post-operative joint infections did not differ between the two groups of patients. The author also noted that a limitation of the study was that it was underpowered to detect the risk of infection. (IANS)

Next Story

Drugs That Treat Arthritis in Dogs Can Kill Cancer Cells: Study

Drug for arthritis in dogs can fight cancer in people

0
Cancer Cells
Drugs for diabetes, inflammation, alcoholism and even for treating arthritis in dogs can also kill cancer cells. Pixabay

Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.

The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.

The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.

Cancer Cells
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. (Representational Image). Pixabay

The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.

“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).

Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.

The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways.

“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.

Cancer Cells
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cells lines from the Broad’s Cancer Cell Line Encyclopedia. (Representational Image). Pixabay

Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.

For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

Also Read- Mothers Find Gaps in Accessibility of Breastfeeding Resources at Work: Research

Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.

For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)