Latent autoimmune diabetes in Saudi adults aged 30-55 years old seen at a tertiary hospital in Riyadh, Saudi Arabia

ABSTRACT

Introduction:

Latent autoimmune diabetes in adults (LADA), also known as Type 1.5 diabetes, is often misdiagnosed because of a lack of both awareness and standardized diagnostic criteria. We investigated the disease characteristics of LADA and determined different biochemical parameters that may indicate long-term glycemic control and associations with chronic diseases.

Method:

This was a cross-sectional study of all LADA cases seen between January 2022 and July 2025 at our institution. We included all adult patients aged 30 years and above, collected and analyzed the demographics, clinical, and laboratory parameters.

Result:

One hundred and forty-eight patients were included in the study, 89 (60.1%) males and 59 (39.9%) females, mean age was 38.15 ± 6.3 years. Glycemic control was recorded in 34 (23.0%) patients. Thirty-seven patients (25.0%) had obesity, 41 (27.7%) were hypertensive and 35 (23.6%) had hypothyroidism. Female patients had significantly higher median level of urine albumin, and higher mean BMI. Hypothyroidism and obesity were significantly more prevalent among female patients than males. Patients with uncontrolled glycemia had higher prevalence of obesity and elevated LDL.

Conclusion:

In this Saudi population, the prevalence of glycemic control in LADA patients is low. Some patients may have normal FBS and HbA1c levels. Obesity may not always be present, and patients can be lean to obese. Hypothyroidism in LADA were more common in older and female patients. We cannot rule out the role of ethnicity and race because of the genetic, environmental, and lifestyle variables that were not considered.

Introduction

Latent autoimmune diabetes in adults (LADA), also known as Type 1.5 diabetes, is a gradually progressing form of diabetes that shares traits with both Type 1 and Type 2 diabetes.[1] Similar to Type 1 diabetes, this form of autoimmune diabetes usually affects individuals after the age of 30 and is characterized by the progressive autoimmune response that destroys the pancreatic cells that produce insulin.[2] In contrast to Type 1 diabetes, LADA develops more slowly, and people may not need insulin treatment initially after being diagnosed.[1,2] At a rate of 5–10%, LADA is frequently misdiagnosed as Type 2 diabetes.[3]

The exact diagnosis of LADA continues to be up for debate, and the presence of misdiagnosed autoimmune diabetes patients may contribute to our understanding of its genetic foundation in comparison to other traditional forms of diabetes.[3] LADA was often misdiagnosed because of a lack of both awareness and standardized diagnostic criteria.[4,5,6] LADA is characterized by a level of insulin resistance similar to Type 1 diabetes, a faster drop of C-peptide than Type 2 diabetes, and an intermediate amount of β-cell dysfunction between that in Type 1 and Type 2 diabetes.[7,8,9] To differentiate LADA from Type 1 or Type 2 diabetes, however, there are additional traits for this population that might lead to diagnostic screenings.[10]

Patients with Type 1 diabetes typically have higher titers for at least one autoantibody, are generally lean from unintended weight loss, have a poor response to lifestyle changes and oral medications, and typically develop the disease before the age of 35.[11] On the other hand, people with Type 2 diabetes usually have a starting age of over 35, respond well to lifestyle changes and oral medications, are frequently overweight or obese, and have negative autoantibody test results.[10] Patients with LADA respond initially to lifestyle changes and oral medications, but as β-cell activity deteriorates, their response decreases.[7] LADA has a median age of start that is more typical of Type 2.[7,8,9]

Despite having a prevalence that is nearly identical to that of Type 1 diabetes, the worldwide impact of LADA is yet unknown.[12] One study reported an overall pooled prevalence of 8.9% for LADA, with prevalences ranging from 2.3% to 18.9% in Bahrain and the United Arab Emirates, respectively. North America had the highest prevalence (13.5%), followed by the Middle East and North Africa (9.5%), Africa (9.4%), Southeast Asia (9.2%), Western Pacific (8.3%), and Europe (7.0%).[12] A greater frequency of 12% was recorded in Scandinavian nations.[13] Research conducted in Iran found that 14.2% of people had LADA.[14] A 2015 study conducted in the United Arab Emirates found that 2.6% of people have LADA.[15]

The characteristics of LADA are influenced by varying patterns of antibody positivity, which in turn affects the time required for insulin.[16] Patients with LADA were more likely to be taking noninsulin antidiabetic medications, and the median interval between their diabetes and LADA diagnoses was 60 months.[17] In addition to having a lower BMI than people with Type 2 diabetes, people with LADA also had autoimmunity against one or more of the following antibodies: insulin autoantibodies (IAA), tyrosine phosphatase–related islet antigen 2 (IA-2), autoantibodies to glutamic acid decarboxylase (GAD), and islet cell autoantibodies (ICA).[7,18]

Because many patients with LADA may be mistakenly diagnosed with Type 2 diabetes, and its prevalence may be higher than that of traditional type 1 diabetes, there is a need to increase the knowledge of the disease spectrum and biochemical features of LADA. Understanding the characteristics of LADA and distinguish this condition from type 2 diabetes greatly benefit clinicians for early management and precise diagnosis, as well as benefits patients to seek early care and mitigate long-term complications. Unfortunately, LADA remains a poorly defined disease in this region. We therefore carried out this study to gain a thorough understanding of the disease spectrum LADA and pertinent clinical concerns that could aid in improving the diagnosis and treatment of patients with LADA. Furthermore, we aimed to determine different biochemical parameters that may indicate long-term glycemic control and associations with chronic diseases.

Methods

We conducted a cross-sectional study of all LADA cases seen between January 2022 and July 2025 at our institution. We included all adult patients aged 30 years old and above. Patients diagnosed with Type 1 diabetes and those aged less than 30 years old were excluded from the study. Sample size was calculated using the formula Z1-α/22 P (1-p)/d2, where Z1-α/22 is the standard normal variation at 5% Type 1 error, P is the average expected proportion in the population, and d is the absolute error or precision. Assuming a 10% population proportion based on previous studies, a 5% precision at 80% at 95% standard normal variate, the estimated sample size was 139 patients.[12,13,14,15]

We identified the eligible patients from the electronic medical database of our institution and collected the data on demographics, anthropometric, medical history, concomitant diseases, and laboratory results. Collected data were encoded in a Microsoft Excel worksheet prior to analysis. Data cleaning was performed to ensure completeness and accuracy of the information. Missing information was reviewed from the database.

Statistical analysis was performed using the Statistical Program for Social Sciences (SPSS) version 26.0 (Armonk, New York, USA). Normality testing was performed using the Kolmogorov-Smirnov test to ensure normality of distribution of continuous variables. Descriptive analysis was performed, and results are expressed as numbers and percentages for categorical variables and as mean and standard deviation or median and interquartile range for continuous variables. Differences in the distribution of patients’ characteristics were done using the Chi-square test (for proportions ≥5) or Fisher’s Exact test (for proportions with expected frequency of <5). Student’s t-test (unpaired) for means and the Wilcoxon test for medians were used to compare between groups. Pearson correlation or Kolmogorov-Smirnov test was performed to determine the association of variables with their corresponding P and rho values. A P value of < 0.05 was considered statistically significant.

To ensure privacy and confidentiality of collected information, identifying details of patients were coded as serial numbers and not disclosed in this report. Informed consent was not applicable for this medical chart review, and the investigators have obtained appropriate permissions from the institution to access the hospital database.

Results

One hundred and forty-eight patients were included in the study, 89 (60.1%) males and 59 (39.9%) females. The mean age was 38.15 ± 6.3 years (30-55 years old). The mean body mass index (BMI) was 26.46 ± 5.4 kg/m². Table 1 shows the detailed demographic and clinical characteristics of all patients. Table 2 shows the laboratory results for all patients. There were 95 patients (64.2%) with elevated fasting blood sugar (FBS), while 114 patients (77.0%) had elevated HbA1c. Glycemic control was recorded in 34 (23.0%) patients. Thirty-seven patients (25.0%) had obesity, 41 (27.7%) were hypertensive and 35 (23.6%) had hypothyroidism.

Table 1.

Demographic and clinical characteristics of 148 patients with LADA

Parameters	Results
Gender, n (%)
Males	89 (60.1%)
Females	59 (39.9%)
Age in years, mean±SD	38.15±6.3
Systolic blood pressure in mmHg, mean±SD	121.67±14.5
Diastolic blood pressure in mmHg, mean±SD	72.60±10.8
Weight in kg, mean±SD	75.46±18.9
Height in cm, mean±SD	166.03±15.9
Body mass index in kg/m2, mean±SD	26.46±5.4

BMI – body mass index, SD – standard deviation, mmHg – millimeters mercury, kg- kilogram, m² – square meter

Table 2.

Laboratory results of 148 patients with LADA

Laboratory tests	Results
Fasting blood glucose, mean±SD	9.24±4.0 (3-23)
Fasting blood sugar categories, n (%)
Normal	53 (35.8%)
Elevated	95 (64.2%)
HbA1c, mean±SD	8.56±1.8 (5-13)
HbA1c categories, n (%)
Normal	34 (23.0%)
Elevated	114 (77.0%)
Glycemic control	34 (23.0%)
Thyroid stimulating hormone, median (IQR)	2.52 (1.63, 4.22)
Hypothyroidism, n (%)
Positive	35 (23.6%)
Negative	113 (76.4%)
Urine albumin, median (IQR)	0.61 (0.34, 1.82)
Albuminuria, n (%)
Yes	3 (2.0%)
No	145 (98.0%)
Glutamic acid decarboxylase, median (IQR)	389.56 (81.4, 2000)
Glutamic acid decarboxylase positive, n (%)	148 (100.0%)
Tissue transaminase 2, median (IQR)	1.20 (0.61, 1.68)
Tissue transglutaminase positive, n (%)	5 (3.4%)
LDL, mean±SD	2.91±0.9
Elevated LDL. n (%)	31 (20.9%)
Obesity, n (%)	37 (25.0%)
Hypertension, n (%)	41 (27.7%)

SD – standard deviation, mmHg – millimeters mercury, kg- kilogram, m² – square meter, IQR – interquartile range, LDL – low density lipoprotein, HbA1c – glycosylated hemoglobin, n – number

As to gender, female patients tend to have significantly higher median levels of microalbuminuria (P = 0.031), and higher mean BMI (P = 0.025) compared to males. Hypothyroidism and obesity were significantly more prevalent among female patients than males (P < 0.001 and P = 0.042, respectively) [Figure 1]. On the other hand, male patients had significantly higher mean diastolic blood pressure than females (P = 0.024). Furthermore, a significantly greater proportion of male patients had hypertension than females (P = 0.041). Age, TSH, glutamic acid decarboxylase, tissue transaminase, LDL, albuminuria and systolic blood pressure were not significantly different across gender (P > 0.05) [Table 3].

Figure 1.

Significant differences in the prevalence of hypothyroidism, obesity, and hypertension according to gender

Table 3.

Comparison of parameters according to gender

Parameters	Male n=89	Female n=59	P
Age in years, mean±SD	37.55±5.3	39.05±7.4	0.154
TSH, median (IQR)	2.97 (1.76, 4.36)	2.39 (1.52, 4.2)	0.630
Hypothyroidism, n (%)	8 (9.0%)	27 (45.8%)	<0.001
Urine albumin, median (IQR)	0.85 (0.38, 2.82)	1.11 (0.49, 2.64)	0.031
Glutamic acid decarboxylase, median (IQR)	460.98 (91.62, 1596.64)	809.81 (83.80, 2000)	0.134
Tissue transaminase, median (IQR)	1.27 (0.80, 2.03)	1.08 (0.49, 1.75)	0.561
LDL, median (IQR)	2.76 (2.18, 3.33)	2.86 (2.22, 3.54)	0.677
Systolic blood pressure in mmHg, mean±SD	123.52±15.3	118.90±12.8	0.058
Diastolic blood pressure in mmHg, mean±SD	74.24±11.3	70.15±9.7	0.024
BMI in kg/m2, mean±SD	25.62±5.4	27.66±6.0	0.025
Obesity, n (%)	17 (19.1%)	20 (33.9%)	0.042
Hypertension, n (%)	30 (34.1%)	11 (18.6%)	0.041
Glycemic control, n (%)	22 (24.7%)	12 (20.3%)	0.535
Albuminuria, n (%)	2 (2.2%)	1 (1.7%)	0.815
Tissue transglutaminase positive, n (%)	3 (3.4%)	2 (3.4%)	0.317
Elevated LDL, n (%)	19 (24.1%)	12 (22.2%)	0.807

TSH – thyroid stimulating hormone, SD – standard deviation, mmHg – millimeters mercury, kg- kilogram, m² – square meter, IQR – interquartile range, LDL – low density lipoprotein, HbA1c – glycosylated hemoglobin, n – number

According to age groups, there were no significant differences in the results between patients age 40 and above. Although there were no significant differences, younger patients who have LADA (age < 40 years old) tend to have higher TSH levels, higher glutamic acid decarboxylase and transaminase levels, LDL, BMI, obesity, and albuminuria, as well as positive tissue transaminase. A higher prevalence of glycemic control was observed among patients < 40 and years old (P = 0.662). On the other hand, older patients (age 40 and above) had more cases of hypothyroidism (P = 0.273), hypertension (P = 0.754), and elevated LDL levels (P = 0.380) [Table 4].

Table 4.

Comparison of parameters according to age groups

Parameters	Age <40 n=96	Age 40 and above n=52	P
Gender, n (%)
Male	60 (62.5%)	29 (55.8%)	0.425
Female	36 (37.5%)	23 (44.2%)
TSH, median (IQR)	2.97 (1.76, 4.36)	2.39 (1.52, 4.2)	0.215
Hypothyroidism, n (%)	20 (20.8%)	15 (28.8%)	0.273
Urine albumin, median (IQR)	0.50 (0.30, 1.85)	0.57 (0.34, 1.01)	0.797
Glutamic acid decarboxylase, median (IQR)	623.26 (78.38, 2000)	398.04 (97.63, 2000)	0.895
Tissue transaminase, median (IQR)	1.39 (0.79, 2.09)	1.07 (0.25, 1.32)	0.229
LDL, median (IQR)	2.91 (2.30, 3.37)	2.60 (2.06, 3.81)	0.251
Systolic blood pressure in mmHg, mean±SD	120.89±14.6	123.14±14.3	0.372
Diastolic blood pressure in mmHg, mean±SD	72.59±10.5	72.61±11.5	0.994
BMI in kg/m2, mean±SD	26.55±5.7	26.27±4.7	0.763
Obesity, n (%)	26 (27.1%)	11 (21.2%)	0.426
Hypertension, n (%)	26 (27.1%)	15 (29.4%)	0.754
Glycemic control, n (%)	82 (85.4%)	43 (82.7%)	0.662
Albuminuria, n (%)	3 (3.1%)	0	0.552
Tissue transglutaminase positive, n (%)	4 (4.2%)	1 (1.9%)	0.261
Elevated LDL, n (%)	18 (20.9%)	13 (27.7%)	0.380

TSH – thyroid stimulating hormone, SD – standard deviation, mmHg – millimeters mercury, kg- kilogram, m² – square meter, IQR – interquartile range, LDL – low density lipoprotein, HbA1c – glycosylated hemoglobin, n – number

Although there were no significant differences in the results of all parameters investigated between patients who had controlled glycemia versus patients who had uncontrolled glycemia, patients who had uncontrolled glycemia had lower median TSH, urine albumin, glutamic acid decarboxylase and tissue transaminase levels than those with controlled glycemia. There was a higher prevalence of obesity as well as a higher prevalence of elevated LDL among patients with uncontrolled glycemia [Table 5].

Table 5.

Comparison of parameters according to glycemic control in 148 patients with LADA

Parameters	Controlled glycemia n=34	Uncontrolled glycemia n=125	P
Age in years, mean±SD	38.15±6.6	38.15±6.2	0.999
Gender, n (%)
Male	22 (64.7%)	67 (58.8%)	0.535
Female	12 (35.3%)	47 (41.2%)
TSH, median (IQR)	3.43 (2.52, 4.47)	2.35 (1.78, 4.00)	0.371
Hypothyroidism, n (%)	6 (26.1%)	29 (23.2%)	0.765
Urine albumin, median (IQR)	0.94 (0.45, 4.09)	0.48 (0.30, 1.30)	0.332
Glutamic acid decarboxylase, median (IQR)	594.75 (41.40, 1614.91)	518.12 (90.78, 2000)	0.159
Tissue transaminase, median (IQR)	1.21 (1.00, 2.39)	1.11 (0.53, 1.66)	0.301
LDL, median (IQR)	2.30 (2.07, 3.66)	2.81 (2.47, 3.38)	0.132
Systolic blood pressure in mmHg, mean±SD	120.64±14.1	121.96±14.7	0.645
Diastolic blood pressure in mmHg, mean±SD	73.03±10.5	72.47±10.9	0.796
BMI in kg/m2, mean±SD	25.74±4.9	26.65±5.5	0.403
Obesity, n (%)	5 (21.7%)	32 (25.6%)	0.798
Hypertension, n (%)	8 (36.4%)	33 (26.4%)	0.439
Albuminuria, n (%)	1 (2.9%)	2 (1.8%)	0.666
Tissue transglutaminase positive, n (%)	1 (2.9%)	4 (3.5%)	0.987
Elevated LDL, n (%)	5 (15.8%)	26 (25.7%)	0.238

TSH – thyroid stimulating hormone, SD – standard deviation, mmHg – millimeters mercury, kg- kilogram, m² – square meter, IQR – interquartile range, LDL – low density lipoprotein, HbA1c – glycosylated hemoglobin, n – number

A significant positive correlation was noted with elevation of fasting blood glucose and increased urine albumin (r = 0.199, P = 0.030), Also, an elevated HbA1c was significantly correlated with microalbuminuria (r = 0.254, P = 0.002) and increased serum LDL (r = 0.271, P = 0.002). Obesity was significantly correlated with elevated SBP (r = 0.230, P = 0.005) and hypertension (r = 0.199, P = 0.016). Logistic regression analysis for predictors of glycemic control did not reveal any significant results for age groups (OR = 1.009, 95%CI = 0.453 – 2.250, P = 0.982), female gender (OR = 0.778, 95%CI = 0.351 – 1.724, P = 0.536), microalbuminuria (OR = 1.697, 95%CI = 0.149 – 19.307, P = 0.670), elevated LDL (OR = 1.872, 95%CI = 0.653 – 5.367, P = 0.243), obesity (OR = 1.378, 95%CI = 0.544 – 3.491, P = 0.500), hypertension (OR = 1.041, 95%CI = 0.437 – 2.479, P = 0.928) and hypothyroidism (OR = 0.674, 95%CI = 0.285 – 1.594, P = 0.369).

Discussion

In this study, we investigated different associated factors for glycemic control among patients diagnosed with LADA in a Saudi population aged 30 years old and above. Determining the associated factors for glycemic control in patients with LADA is crucial for optimal and personalized treatment, delaying the progression to insulin dependence, and preventing severe microvascular and macrovascular complications.[1] Importance of identifying these associated factors including BMI and lifestyle allows clinicians to select therapies that preserve beta-cell function and prevent long-term serious complications like retinopathy, nephropathy, neuropathy and cardiovascular disease.[19]

Elevation of fasting glucose in patients with LADA is primarily caused by autoimmune-mediated destruction of pancreatic beta cells, leading to insufficient insulin production to maintain normal glucose homeostasis.[19] This study showed that not all patients with LADA show elevations of FBS and HbA1c. LADA patients have elevations of FBS and HbA1c above the normal range, although the levels can vary.[20] Elevations of fasting glucose in patients with latent autoimmune diabetes (LADA) vary due to the heterogeneous nature of the disease, specifically the variable rates of autoimmune beta-cell destruction and differing degrees of underlying insulin resistance.[21]

Obesity was observed in 25% of our patients with LADA, as shown in Table 2 and Figure 1. Obesity significantly increases the risk of developing LADA, a link that is stronger when combined with other risk factors like high-risk genes or a family history of diabetes. Obesity can promote the onset of LADA by increasing insulin resistance, even though LADA is an autoimmune disease. In LADA patients, obesity is also linked to lower levels of specific autoantibodies and better initial insulin sensitivity, though it can lead to the need for more intensive treatment over time.[22] However, one article suggested that not all patients with LADA are obese. While a nonobese, lean body mass index (BMI) was once considered a key feature of LADA (to differentiate it from Type 2 diabetes), research has shown that LADA patients can span the spectrum from lean to obese.[23] LADA is a heterogeneous condition. Some studies report an average BMI in the normal range, while many large-scale European and North American studies find the mean BMI of LADA patients falls into the overweight or even obese categories, and more importantly, the autoimmune component is a key factor, and symptoms can be similar to those of Type 2 diabetes.[24]

Studies have shown a significant association between hypothyroidism and LADA. They are both autoimmune conditions, and patients with LADA have a higher risk of developing autoimmune thyroid diseases like hypothyroidism, often due to a shared autoimmune pathway.[25] In this study, 23.6% of our patients had hypothyroidism, which was more prevalent among female patients and older patients above 40 years old consistent with previous studies. Female patients with LADA have a significantly higher risk and prevalence of hypothyroidism due to a shared genetic susceptibility particularly within the HLA region, the common underlying immune system pathways that predispose an individual to multiple autoimmune conditions.[25,26]

On the other hand, we observed a higher rate of glycemic control among patients <40 years old. Although this did not reach statistical significance compared to patients 40 years old and above, most studies suggested that glycemic control tends to be worse among younger patients with LADA compared to older patients, as shown in Figure 2 and Table 4.[27] Younger patients with LADA typically experience a faster progression of the autoimmune destruction of their pancreatic beta-cells, leading to more severe insulin deficiency and a more rapid decline in C-peptide levels. This makes it harder to achieve and maintain good long-term glycemic control.[27,28] For this reason, many other unexplored factors for glycemic control among younger patients with LADA has not been uncovered in this study since younger patients with LADA are particularly susceptible to these complications over their lifespan.[29,30] Another probable reason is the significant race and ethnic differences in the prevalence and characteristics of LADA.[31] The differences in the characteristics of LADA across populations is largely due to a mix of genetic, environmental, and lifestyle factors.[31,32]

Figure 2.

Prevalence of albuminuria, elevated LDL, hypertension, obesity, hypothyroidism, and glycemic control according to age groups

Family medicine and primary care physicians (PCPs) gain crucial knowledge from LADA research such as this study that can directly improve patient outcomes by enabling more accurate diagnosis, personalized treatment and prevention of complications. LADA as mentioned earlier is frequently misdiagnosed as Type 2 diabetes due to its adult onset and initial noninsulin dependence. Studies provide PCPs with a better understanding of the clinical indicators that should prompt autoantibody testing, thus ensuring timely and correct diagnosis. Conversely, early, correct diagnosis and appropriate treatment lead to better glycemic control, which is essential for decreasing the risk of long-term microvascular and macrovascular complications associated with poor diabetes management.

This study has strengths and limitations. One of the limitations to the study is the very limited reports coming from Saudi Arabia to deduce a concrete conclusion on the description of the disease. In fact, only one study reported a hospital-based study which reported an 8.1% prevalence of LADA autoantibodies which was similar to those reported for diabetic patients in other ethnic groups.[33] Other limitations include the small sample size as well as the study was done at a single institution that may have underreported or overreported the general prevalence and characteristics of LADA, which may variate from different institutions. Despite this, we were able to characterize the LADA disease spectrum and attempted to find associations with glycemic control and comorbid conditions. Larger sample sized multicenter studies are warranted to substantiate the findings and find significant associations of the characteristic features of LADA with regards to glycemic control, comorbid conditions and other laboratory features.

Conclusion

Glycemic control in patients with latent autoimmune diabetes (LADA) was low at <25% and varied with some patients showing normal levels of FBS and HbA1c. Obesity, a key feature of LADA may not always be present to differentiate it with other types of diabetes, but the spectrum of LADA can span from lean to obese patients. Hypothyroidism is another feature of LADA more prevalent among female and older patients. Contrary to previous reports, older patients may also experience faster progression of the disease depending on the autoimmune destruction of the pancreatic cells. It is recommended that a careful consideration of a mix of genetic, environmental and lifestyle factors when diagnosing patients with LADA beyond the age of 30 years old.

Patients’ consent form

No separate consent form was required because all data were obtained from TrackCare, where patients have already given general consent for the use of their anonymized information in research. All data were fully deidentified, and confidentiality and institutional ethical guidelines were strictly followed.

Ethical approval (IRB)

The Institutional Review Board (IRB) of Security Forces Hospital granted the approval of the study (25-816-36/H-01-R-069 dated 19 August 2025).

Authors contributions

YAA – designed and supervised the study, primary author and review; BSA – writing of the manuscript; BA – data collection and writing; MA- data collection, analysis and writing; AA – data collection, analysis and writing; AI – data collection and writing; NTA – writing and review; FA – data collection and writing; MA – data collection and writing; RAA – data collection and review; AAA – data collection and review.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.