Cardio Diabetes_2017 book

628 An Overview of Legal Issues in Hypertensive and Diabetic Patients

GCDC 2017

Cardio Diabetes Medicine 2017 629

An Overview of Legal Issues
in Hypertensive and Diabetic Patients

Dr. T.N.Ravisankar

MBBS,FCGP,DFM,PGDMLE.
Medico legal consultant, Chennai

Abstract: in medico legal situation in the present day context.

Diabetic and Hypertensive patients need to be evalu- Though an initial assessment of the diabetic case
ated in total in outpatient and as inpatient. The equip- status with a digital glucometer is ideal,but to labela
ment used need to be calibrated regularly as per the patient to be a diabetic, one will have to definitely
protocols of the manufacturing company do venous blood glucose fasting, post- prandial and
HbA1c, which will be the most appropriate.Trying to
Diabetes and hypertension, the two major non com- treat a patient without doing all these above investi-
municable diseases in this country, has either con- gations and later found thepatient going for an hy-
tributed directly or indirectly for medico legal prob- poglycaemia with oral hypoglycaemic agents scan
lemsfor the practising physicians. result in medico legal litigation against the physician.
It will be aclear case of negligence, if you have not
The Diagnosis of a diabetes and hypertension in a properly assessed before starting any of the oral hy-
patient has not been of greatapprehension.For the perglycaemic agents or for the fact that insulin has
practitioner the first job as the patient enters is to- become the first line of treatment by some of the
takePulse and Blood Pressure of the patient. Quit aggressive physicians or diabetalogists.
often the job is also doneby paramedicalandtrained
personal in a busy practitioner office. It is very im- Both diabetes and hypertensionhas one major re-
perative that BP apparatus is well maintained. The sponsibility cast upon the physician is to communi-
concept of no mercury is getting percolated in the so- cate with the patient on the nature of the disease.
ciety byPollution control board. We have been talking Whatever you read in your text books which may
to our students, until 2010 the value of mercury,BP run in volumes and volumes, it is ideal to condense
apparatus. But today, the situation has changed and itin regional language which patient can understand
we have moved to the digital era andwe are now and communicate to him what the disease process
using more often adigital BP apparatus.When the is, why it happens in an individual running into the
physicians take the BP, the patients are happy and family history and also life style of the individual and
confident about it. Thevast majority of the busy phy- the mental status. Both Hypertension and Diabetes
sician and cardiologist do depend on the paramedical almost have similar social economic factors. Today,in
to take the BP.In thatsituations, we use the digital BP the fast world, every person is stressed upon and
apparatus. The most important aspect of digital BP this issue will have to be informedto the patient.Com-
apparatus, it has to be calibrated in a regular interval. municating on the life style, stress factors,causative
The number of times apparatus is used per day will factors of both diseasesare very much needed be-
have to be calculated, take an average, get aninfor- cause tomorrow the patient might find fault on the
mation from the company where you have bought treating physician that he has not explained to him
the BP apparatus and the calibration is to be done what is cause for the onset of disease process and
appropriately.The small change in the systolic BPor when the disease process has started and what has
diastolic BP between 140/100 or 101/110 can always trigger the whole issue.
make a difference if it is not been intervened at the
appropriate time. Who takes the BP and where the BP All medico-legal experts will always say communica-
is taken and what apparatus is a very important issue tion is one major factor that contributes orprevents

Cardio Diabetes Medicine

630 An Overview of Legal Issues in Hypertensive and Diabetic Patients

alitigation being cast upon practising physician and For a patient who is undergoing a surgical procedure
here again this two metabolic disorders really needs it is important that both hypertension and diabetes
the physician to spend time on the first occasion at will have to be evaluated totally before the patient-
least, when he is diagnosing. We need to explain to proceeds in for a surgical procedure.It is a young
the patient about the disease nature, the complica- age or a middle age and if you find Hypertension,
tion that is likely to happen ifit’s not treated properly. it is important that ECG, renal parameters, ECHO
In the present days quiet a number of patient always cardiogram will have to be performed before the pa-
enquire about the alternative system of medicine or tient under goes a surgical procedure. Be it a small
the other of various modality for treating their hyper- sterilisation, or a major Whipple’sprocedure, the total
tension and diabetes All the allopathic practitioner evaluation ofon cardiac status if he is going to hyper-
will have to inform is that it is ailment which is life tension is absolutely necessary. The patient may not
long and nothing can be done other than three mo- have complication or a normal ECG but we needed
dality of treatment which is almost education of the documentation of normal ECHO to prove the patient
disease, life style modification and medicines. If the was normal prior to surgery. If the patient develops
patient wants to have other modality of treatment ei- any complication intra operatively it is not the oper-
ther ayurveda, siddha and homeopathy the patient is ating surgeon and anaesthetist who are responsible
free to undergo to the treatment but please inform but also the physician or the cardiologist who gives
them that crosspathy by the patient is at their risk. the fitness for the patient for the procedure.

The treating physician will have to inform the patient, For a Diabetic patient to be subjected for a surgical
that if the patient undergoescrosspathy treatment on procedure both renal parameters and cardiac param-
his own, the treating physician is not responsible for eters will also have to be assessed with biochemi-
any of the adverse effects that can happen to the cal analysis of urea createnine as well as ECG and
patient. One of the most important factors, docu- ECHO cardiogram to prove that the patient is fit for
mentation in all this patient isan absolutely necessity. surgical procedure. All we need is documentation of
The poor patient compliance for drug and followup the physical status of the individual to undergo the
is the hall mark of a classical Indian citizen or the surgical procedure.
Indian patients, who reports to the doctor. In uncon-
trolled diabetic and uncontrolled hypertension, the
physician always, informs him to visit atleastonce a
month to have a proper follow up.Please documentin
the prescription that you have requested the patient
to come for regular followup and mention when he
is to come for follow up.If the patient reviews at a
later date or delays himself by three months or six
months and come back with uncontrolled Diabetes
and Hypertension,the prescription should carry the
information of poor patient compliance for drug and
followup. This is very important for the future in case
the patient develops complication and sues the Doc-
tor on medical negligence. This one document can
save the Physician at the appropriate time. Medical
council of India now advocates computerising your
records. A copy of such prescription will be of great
value in the legal issues.

In an inpatient set-up,Hypertension and Diabetes are
the two major co-morbid conditions for all the pa-
tients in the intensive care,orfor the patientswho are
going in for surgical procedure.It is easy in an inten-
sive care to inform the attenders, that the patient is
suffering from Hypertension and Diabetes based on
the investigations, advice that outcome depends on
the recovery of the patient on these two modalities.

GCDC 2017

Cardio Diabetes Medicine 2017 631

Susceptible and Prognostic Genetic Factors
Associated with Diabetic Peripheral Neuropathy:

A Literature Review

Dr. VHW Dissanayake, LBL Prabodha, ND Sirisena,

Human Genetics Unit, Faculty of Medicine,
University of Colombo,

Kynsey Road, Colombo 8, Sri Lanka.

ABSTRACT INTRODUCTION

Type 2 diabetes mellitus (T2D) is a disorder of glu- Diabetes mellitus is one of the foremost non-com-
cose metabolism. It is a complex process involving municable diseases of the current period affecting
the regulation of insulin secretion, insulin sensitivity, more than 387 million people worldwide [1]. Type 2
gluconeogenesis and glucose uptake at the cellular diabetes mellitus (T2D) is a disorder of glucose me-
level. Diabetic peripheral neuropathy (DPN) is one of tabolism. It is a complex process involving the reg-
the debilitating complications that presents in ap- ulation of insulin secretion, insulin sensitivity, gluco-
proximately 50% of diabetic patients. It is the prima- neogenesis and glucose uptake at the cellular level.
ry cause of diabetes-related hospital admissions and Dysregulation of one or more of these processes due
non-traumatic foot amputations. The pathogenesis to environmental or genetic factors can lead to al-
of diabetic neuropathy is a complex process that in- tered glucose metabolism causing diabetes mellitus
volves hyperglycaemia induced oxidative stress and [2,3]. More than 90% of cases of T2D show higher
altered polyol metabolism that changes the nerve incidence of insulin resistance. This phenomenon is
microvasculature, altered growth factor support acquired due to sedentary lifestyle in combination
and deregulated lipid metabolism. Recent literature with multifactorial genetic susceptibility. T2D is as-
has identified that there are several heterogeneous sociated with increased morbidity and mortality due
groups of susceptible genetic loci which clearly con- to its debilitating and progressive nature and asso-
tribute to the development of DPN. Several studies ciated complications. The condition usually leads to
reported that some patients with pre-diabetes de- multi-organ failure due to macrovascular and micro-
velop neuropathic complications, whereas others vascular involvement [2-5].
demonstrated little evidence of neuropathy even
after long-standing diabetes. There is emerging ev- Uncontrolled T2D can complicate pregnancy out-
idence that genetic factors may contribute to the comes. Different kinds of birth defects are more
development of DPN. This paper aims to provide an commonly seen in babies born to women with dia-
up to date review of the susceptible and prognostic betes [3].Twin studies can estimate the multifactorial
genetic factors associated with DPN. An extensive genetic involvement in T2D more precisely and have
search of scientific literature published in PubMed reported high degree of heritability of diabetes re-
using the search terms ‘Diabetic peripheral neurop- lated conditions such as disorders of first phase in-
athy/genetics’, ‘genome-wide association study’ was sulin response, basal and insulin stimulated glucose
carried out and most recent and relevant literature uptake [6]. There are different methods for mapping
was used for this review. the genetic susceptibility loci in the pathogenesis of
T2D. Candidate gene studies and genome-wide stud-
KEY WORDS ies are commonly used to identify the association of
susceptible genetic loci of T2D. The latter includes
Type 2 diabetes mellitus; Diabetic peripheral neu- both genome-wide linkage studies (GWL) and ge-
ropathy; Susceptible genetic loci, Prognostic genetic nome-wide association studies (GWAS) [6].With the
factors, Common genetic variants. advent of recent molecular genetic techniques and
rapid screening methods, the method of investi-

Cardio Diabetes Medicine

632 Susceptible and Prognostic Genetic Factors Associated
with Diabetic Peripheral Neuropathy: A Literature Review

gation has shifted to the use of molecular genetic derangements and cardiovascular risk factors [16].
markers for understanding the genetic aetiology of The mechanisms underlying the pathogenesis of
T2D [6,7]. The common susceptible genetic variants DPN are different between types 1 and type 2 diabe-
are known to have a prominent effect on the risk of tes mellitus [17]. Recent literature has reported that
T2D across the world in multiple ethnic groups [8,9]. there are different groups of susceptible genetic loci
Some variants appear to exert more pronounced ge- which are clearly involved in the development of DPN.
netic effects in specific ethnic groups. Most loci asso- Different studies reported that some patients with
ciated with T2D map to regulatory or intronic regions pre-diabetes develop neuropathic complications,
of the genome [9]. whereas others reported little evidence of neuropa-
thy even after long-standing diabetes. This observa-
Diabetic peripheral neuropathy (DPN) is one of the tion confirms the involvement of genetic aetiological
debilitating complications of diabetes that presents factors associated with the development of DPN [18].
in approximately 50% of patients. It is the primary These data from different studies suggest that T2D
cause of diabetes-related hospital admissions and and its complications may have shared genetic risk
non-traumatic foot amputations [4,5,10]. The molecu- factors [12,18].
lar mechanisms involved in the development of DPN
is a complex process that includes activation of the GENETIC AETIOLOGY AND PATHOGENESIS
polyol pathway, exaggerated oxidative stress, over OF DPN
activity of protein kinase C and increased formation
of advanced glycation end-products in the presence The pathogenesis of DPN is a complex process and
of hyperglycemia. In addition, there is increasing is involved with hyperglycaemia induced oxidative
evidence that genetic factors could also contribute stress and altered polyol metabolism that changes
to the development of DPN [10,11]. The consequenc- the nerve microvasculature, growth factor support
es of diabetic neuropathy include neurogenic pain, and lipid metabolism [19]. It is important to identi-
numbness, lack of coordination of voluntary move- fy these factors alone or in combination to arrange
ments and a susceptible to foot ulceration that lead effective DPN treatment, as better understanding of
to infection and toe or foot amputations. The rate of the mechanisms underlying the onset and progres-
toe or foot amputations is 15 times greater in dia- sion of DPN is of prime importance in the process
betic patients compared with individuals without di- of management [20]. Different groups of cell types
abetes. To date, approximately 80 T2D susceptibility in diabetic complication prone tissues are targets of
genetic loci have been reported in different ethnic damage due to uncontrolled hyperglycemia. Schwann
groups worldwide [12-14]. The majority of studies on cells are the prime target of hyperglycaemia which re-
the prevalence and associated aetiological factors of sults in cell damage leading to altered axon integrity
DPN have been conducted in Western countries. Few and defective growth factor signaling [21,22]. Defec-
data are available for Asian populations [15]. tive inflammatory pathways including advanced gly-
cation end products/receptor (AGE/RAGE) signaling
The objective of this paper is to provide an up-to- in axons and Schwann cells have been reported in
date review of the susceptible and prognostic genet- experimental animals with diabetic neuropathy which
ic factors associated with DPN. The genetic variants contributed to nerve damage [23].
associated with DPN were identified by an exten-
sive search of scientific literature using the criteria Lu et al., 2017, in China, studied single nucleotide
described below. The most recent and relevant pa- variants (SNVs) from previously identified ten ge-
pers published in the15 years from January 2002 to netic loci and analyzed the association of these loci
December 2016 were searched in PubMed using the with peripheral nerve function in patients with T2D.
search terms ‘Diabetic peripheral neuropathy/genet- They found that rs5219 of KCNJ11 gene polymorphism
ics’, ‘genome-wide association study’. Only the full (E23K, G>A) was associated with peripheral nerve
text articles published in English were included for function. The results obtained from nerve conduc-
this review. tion studies (NCS), showed that the allele ‘A’ had a
protective effect on peripheral nerve function. They
DIABETIC PERIPHERAL NEUROPATHY also found that SNVs rs7756992 of CDKAL1 and
rs7903146 of TCF7L2 were associated with DPN in
According to the Toronto Consensus Panel on Dia- this Chinese T2D population [24].
betic Neuropathy, diabetic peripheral neuropathy is
defined as a symmetrical, length dependent sen- Yigit et al., 2013, identified 230 unrelated patients with
sorimotor polyneuropathy that develops on a back DPN at the outpatient clinics of the Physical Thera-
ground of longstanding hyperglycemia, associated py and Rehabilitation Department of Gaziosmanpa-

GCDC 2017

Cardio Diabetes Medicine 2017 633

sa University Tokat, in Turkey. They investigated the VARIANTS ASSOCIATED WITH DEFENSE
distributions of the genotype and allele frequencies RESPONSE AND INFLAMMATORY
of the MTHFR gene C677T variant among patients RESPONSE IN THE PATHOGENESIS OF
with DPN and matched control group. They identified DPN
a statistically significant difference of MTHFR gene
C677T polymorphism between the patients with DPN Hur et al., 2011, reported that the molecules which are
and the control group [25]. involved with the process of inflammation such as
chemotactic agents and cytokines are involved with
Decreased levels of peroxisome proliferator activated the development and progression of DPN as well as
receptor alpha (PPARA) in chromosome 22 and lipid diabetic nephropathy [28,].
metabolism-related gene apolipoprotein E (APOE) in
chromosome 19 have been identified confirming the Kakoki et al., 2010, identified that the bradykinin re-
findings that altered lipid metabolism may play a role ceptor B2 (BDKRB2) is of particular interest in disease
in the progression of DPN [26]. Monastiriotis et al., progression of DPN. BDKRB2 gene was found to be
2013, reviewed literature to identify the association involved in progressive glomerulosclerosis and also
between APOE polymorphism and DPN and found susceptibility to DPN .
that the 4 allele of the apolipoprotein E gene is sig-
nificantly associated with pathogenesis of DPN [26]. Membrane associated adenosine A3 receptor (ADO-
RA3), is also involved in the pathogenesis of DPN .
The Alpha2B adrenergic receptor encoded by ADR- Variants of DBKRB2 and ADORA3 were found to be
A2B gene located on chromosome 2 is associated involved in enhanced inflammation and dysregulated
with an array of functions. A polymorphism (12Glu9) defense responses, thus contributing to more sub-
resulting in the insertion/deletion of three glutamic stantial nerve damage in patients with progressive
acid residues in the third intracellular loop has been DPN [28,31].
described frequently in the literature [27]. In the ner-
vous system, this polymorphism has been identified VARIANTS ASSOCIATED WITH
to be linked with autonomic nervous dysfunction. This GLUCOSE METABOLIC PROCESSES
is particularly increased with sympathetic nervous AND PPAR SIGNALING PATHWAY IN THE
system activity and Papanas et al., 2007, found a PATHOGENESIS OF DPN
significant association in this indel allele distribution
of alpha2B adrenoceptor gene amongT2D patients According to Hur et al., 2011, PPARG, which encodes
with DPN in comparison with matched T2D patients a nuclear receptor for glitazone, plays a key role in
without neuropathy [27]. regulating glucose and lipid metabolism [28,]. Ag-
onists of PPARG are effective in treatment of DPN
NETWORK OF GENES ASSOCIATED WITH and nephropathy in experimental animal models
COMMON VARIANTS OF DPN [28,]. Another key gene is APOE, encoding an apoli-
poprotein, which regulates the normal catabolism of
Hur et al., 2011, examined two groups of DPN patients. triglycerides and cholesterol. A polymorphism of this
A network of transcription factor jun (JUN), leptin gene is linked to the progression of DPN .
(LEP), serpin peptidase inhibitor E Type 1(SERPINE1),
apolipoprotein E (APOE) and peroxisome proliferator GENETIC VARIANTS INVOLVED IN
activated receptor gamma (PPARG) were examined DIFFERENT PHENOTYPES OF DPN
to identify their potential relationship. Further subset
of genes related to defense response, inflammato- According to Cheng et al., 2015, in an experiment
ry response, regulation of lipid metabolic processes involving both human and animal models, sensory
and PPAR signaling pathways were then analyzed neurodegeneration in the chronic stage of diabetes
to identify the association of gene expression and was found to be associated with early damage to the
development of DPN [28].They demonstrated that in- distal axons of both upper and lower limbs neurons
creased glucose metabolism due to hyperglycaemia showing a pattern that accounts for the distribution
resulted in increased oxidative stress, mitochondrial of ‘‘glove -and-stocking’’ loss of sensation charac-
dysfunction and cell death in both in vitro and in vivo teristically seen in DPN. These changes accompany
models of diabetic neuropathy [28]. widespread abnormalities involving electrophysiolo-
gy and alterations in gene expression that indicate
a degenerative phenotype. However, existing knowl-
edge on the development of DPN which includes
oxidative and nitrergic stress, polyol accumulation,

Cardio Diabetes Medicine

634 Susceptible and Prognostic Genetic Factors Associated
with Diabetic Peripheral Neuropathy: A Literature Review

microangiopathy, inappropriate AGE-RAGE signaling, with DPN progression in diabetic rat models . Thiore-
and/or mitochondrial dysfunction account for diverse doxin, which regulates cellular oxidative stress with
mRNA changes that alter miRNA expression patterns its antioxidant activity, also plays an important role in
resulting in diverse DPN phenotypes. associated diabetes. Thioredoxin’s antioxidant activ-
ity is significantly inhibited by hyperglycaemic states
GENETIC VARIANTS INVOLVED IN in the blood and it complicates diabetes by playing
GENDER DIMORPHISM OF DPN an important role by deregulating vascular oxidative
stress and inflammation in diabetic patients .
Significant gender dimorphisms in the responsive-
ness of patients to anti diabetic drugs have been A study in North Catalonia, Spain by Jurado et al.,
reported in the literature . These observations high- 2012, identified the protective effect of a single angio-
lighted the importance of understanding the gender tensin-converting enzyme (ACE) gene polymorphism
specific differences in manifestation of diabetes mel- on the development of DPN in T2D patients. Despite
litus and its complications such as DPN. ACE gene variants which are associated with dia-
betic renal disease and/or diabetic retinopathy, the
O’Brien et al., 2016, reported the first instance of a heterozygous genotype stands as a protective fac-
female T2D mouse model presenting with a neuro- tor against the development of DPN . Heterozygous
pathic phenotype including decreased intra-epider- (D/I) ACE gene polymorphism reported a statistically
mal nerve fiber density, impaired motor and sensory significantly reduced risk of developing DPN whereas
nerve conduction velocities and thermal hypoalgesia homozygous (D/D) ACE gene polymorphism report-
. A GWAS involving 961 diabetic neuropathic pain ed an increased risk of developing DPN .
cases and 3260 diabetic controls in the Genetics of
Diabetes Audit and Research Tayside by Meng et al., Mitochondrial transcription factor A (TFAM) is locat-
2015, found a cluster in the 1p35.1 region, the zinc fin- ed in mitochondria, and its level regulates mtDNA
ger and SCAN domain containing 20 (ZSCAN20) with copy number. Chandrasekaran et al., 2015, showed
a lowest P value of a variant at rs71647933 in females that TFAM over expression prevented a decrease in
and a cluster in the 8p23.1 region next to HMGB1P46 mtDNA copy number in diabetic dorsal root ganglia
with a lowest P value of a variant at rs6986153 in (DRG) neurons, helped prevent DPN, and protected
males were significantly associated with DPN. This DRG neurons from oxidative stress in experimental
GWAS on diabetic neuropathic pain provides evi- mouse models .
dence for the sex-specific involvement of 1p35.1 re-
gion (ZSCAN20) and 8p23.1 region (HMGB1P46) . Aldo-keto reductase family 1 member B (AKR1B1) in
chromosome 7 encodes a member of the aldo-keto
OTHER GENE LOCI INVOLVED IN THE reductase superfamily, which consists of more than
PATHOGENESIS AND PROGNOSIS OF DPN 40 known enzymes and proteins. This catalyzes the
reduction of a number of aldehydes and is thereby
A fibrinolysis regulating gene, SERPINE1 encodes implicated in the development of diabetic complica-
for plasminogen activator inhibitor 1 (PAI-1) and has tions by catalyzing the reduction of glucose to sorbi-
been identified in association with higher incidences tol. Saraswathi et al., 2015, identified significant asso-
of diabetes and its complications, diabetic neuropa- ciation of AKR1B1 gene mutations in painful diabetic
thy and nephropathy in knock out PAI-1mice. The cell neuropathy .
cycle controlling JUN is also involved in progression
of DPN and is associated with inflammation and in- There is increasing evidence that microRNAs act as
sulin resistance which is activated in multiple tissues regulators of gene expression in multiple biological
including the peripheral sensory nerves of patients processes and associated complications [. Ciccacci et
with type 1 and 2 diabetes . al., 2014, looked for an association between variants
in miRNA genes and DPN. The results of this study
Three other subsets of important gene variants were identified a role for MIR146a and MIR128a SNVs in the
documented in literature associated with ‘cell projec- susceptibility to DPN and were shown to have a sig-
tion and axonogenesis’ involving nerve growth fac- nificant association . The rs2910164 (G>C) in MIR146a
tor receptor (NGFR) and ‘cellular homeostasis and is associated with lower risk and rs11888095(C>T) in
inflammatory response’ involving thioredoxin, and MIR128a is associated with higher risk of suscepti-
‘cytoskeletal protein binding’ with stathmin 1 (STMN1) bility to DPN .
genes. NGFR exhibits protection against nerve cell
and axonal damage and the expression of nerve Nitric Oxide (NO) production and local release in the
growth factor receptor protein in plasma correlates tissues significantly contributed to endothelial dys-
function. The process takes place by the modulation

GCDC 2017

Cardio Diabetes Medicine 2017 635

of the nitric oxide synthase (NOS) enzymes responsi- and the risk of DPN .
ble for NO synthesis. Endothelium derived NO plays
a key role in the regulation of vascular tone and has GENETIC VARIANTS OF DPN IN DIFFERENT
vaso-protective effects by removing superoxide radi- ETHNIC POPULATIONS
cals and suppressing platelet aggregation, leukocyte
adhesion, and smooth muscle cell proliferation. How- Up-to-date there were only few ethnic groups have
ever, dysfunctional endothelial nitric-oxide synthase described population specific genetic variants as-
(eNOS) might play a critical role in the pathogenic sociated with DPN. In a study conducted by Lu et
pathway leading to diabetic vascular complications al., 2017, ten SNVs associated with pathogenesis of
including DNP. Therefore, eNOS is considered as a T2DM were studied and they identified rs5219 on
candidate for the progression of DPN. KCNJ11 (E23K) gene is significantly associated with
peripheral nerve function in a Chinese population
In the early stages of DPN, abnormalities in the vasa with T2D [24]. Jia Y, Tong and Min L., 2015, studied
nervorum and loss of nerve fibers can be seen in as- the significance of functional GRP78 gene variants
sociation with hyperglycemia. Damage to the nervous in predicting the onset of type 2 diabetic peripher-
tissue results in an increase intravascular endothelial al neuropathy in the Chinese population. This study
growth factor (VEGF) plasma levels in diabetic animal suggested that the GRP78 rs391957 promoter poly-
models . The ischemia and hypoxia in the nerves of morphism is a potential risk factor for type 2 diabetic
patients with T2D due to microangiopathy of vasa peripheral neuropathy in this population . Prasad et
nervorum has always been observed and may be a al., 2015, studied forty-two patients with T2D from
key pathogenic mechanism of DPN . An association the Institute of Diabetology, Madras Medical College
study by Ghisleni et al., 2015, showed a clear associa- and Rajiv Gandhi Government General Hospital in
tion between diabetic polyneuropathy and the C936T Chennai, Tamil Nadu, India. In this study, the extent
polymorphism of the VEGF gene and the C242T poly- of DNA damage in patients suffering from T2D, both
morphism of the p22phox allele of CYBA gene. with and without neuropathy was analyzed. No ge-
netic variants were evaluated in this study. The data
Functional GRP78 variants in heat shock protein demonstrated that the frequency of DNA damage
family A (Hsp70) member 5 (HSPA5) genes are like- was significantly higher in the T2D patients with DPN
ly to have some influence on the gene expression, than in the controls [60]. Stoian et al., 2015, conduct-
which results in the dysfunction of peripheral nerves ed a study in the University Center of TırguMures,
and neuropathy. According to Jia Y, Tong Y and Min Romania. In their case control study, which included
L, 2015, functional GRP78 rs391957 variants, which a total of 182 participants, including 84 unrelated pa-
are located in the promoter region 57168556T>C are tients with T2D and an age-matched control group
known to cause abnormal promoter activities signifi- consisting of 98 unrelated individuals without T2D,
cantly associated with DPN . they evaluated the influence of GSTM1, GSTT1, and
GSTP1 variants on T2D and DPN risk. Their data sug-
Adiponectin gene (ADPN) serves as a protective fac- gested that GSTM1, GSTT1 and GSTP1 gene variants
tor in preventing diabetes progression by suppress- were not associated with individual susceptibility to
ing inflammatory responses and increasing insulin developing DPN in patients with T2D in Romanian
sensitivity . SNVs of ADPN may influence T2DM, population .
but ADPN variants SNV45 (45T/G, rs2241766) and
SNV276 (276G/T, rs1501299) are the two most prom- An association study of C936T polymorphism of
inent variants influencing the disease progression, the VEGF gene and the C242T polymorphism of the
specially pathogenesis of DPN . A case control study p22phox gene with T2D and DPN in a population of
conducted by Ji et al., 2015, to evaluate the associa- Caucasian ethnicity was studied by Ghisleni et al., in
tion between ADPN gene variants and pathogenesis 2015. According to their results, the C936T polymor-
of DPN in T2D patients indicated an increased risk phism of the VEGF gene and C242T polymorphism
of DPN in T2D patients, by down-regulating ADPN of the p22phox gene did not correlate with the risk
expression which resulted in significantly reduced of developing diabetes mellitus or neuropathic signs
circulating ADPN plasma levels. Furthermore, they and symptoms. When considering the results of oth-
reported that the polymorphism frequencies of GG er studies, a substantial heterogeneity in the findings
and GT haplotypes in the DPN group were signifi- is observed, which demonstrates a complex link be-
cantly lower than the matched control group, while tween the risk factors of DM, and genetic predispo-
the frequency of the TG haplotype in the DPN group sition to DPN .
was markedly higher than the control group, showing
the clear association between ADPN gene variants

Cardio Diabetes Medicine

636 Susceptible and Prognostic Genetic Factors Associated
with Diabetic Peripheral Neuropathy: A Literature Review

CONCLUSION

Although targeted gene sequencing is still a method of choice to identify rare functional mutations in mono-
genic disorders, exome sequencing becomes an attractive and cost-effective alternative when other disease
mapping strategies provide few or ambiguous results. This review has attempted to identify the common
susceptibility and prognostic genetic factors associated with DPN in T2D (Table 1). Knowledge about these
factors is vital as DPN is one of the debilitating complications associated with T2D and identification of the
common genetic variants would be valuable for the future development of gene panels targeted for the early
detection and prognosis of DPN. Together with these gene panels, further gene expression studies will need
to be conducted to modulate effective targeted therapies for DPN in these patients.

Gene Chromosomal location Variants Associated risk/Remarks Ref.
Advanced Glycation End Receptor 6p21.32 rs1800624 Higher risk/ Defective inflammatory [23]
(AGER) 3p25.2 pathways [28]
Peroxisome proliferator activated 14q32.2 rs1801282 Higher risk/ Defective inflammatory [30]
receptor alpha (PPARA) 11p15.1 pathways [24]
Bradykinin receptor B2 (BDKRB2) 6p22.3 rs1799722 Higher risk/ Defective inflammatory [24]
10q25.2-q25.3 pathways/African-Americans [24]
Potassium voltage-gated channel 1p36.22 E23K, G>A rs5219 Higher risk/Chinese population/ [25]
subfamily J member 11 (KCNJ11) 19q13.32 Altered signaling pathways [26]
CDK5 regulatory subunit associat- 2q11.2 rs7756992 Higher risk/Chinese population [27]
ed protein 1 like 1 (CDKAL1)
Transcription factor 7 like 2 Chromosomal location rs7903146 Higher risk/Chinese population [50]
(TCF7L2) 5q33.3 [50]
Methylenetetrahydro folate reduc- 2q21.3 C677T r Higher risk/ Altered folate metab- [40]
tase (MTHFR) 8q23.1 s1801133 olism [40]
Apolipoprotein E (APOE) 1p35.1 4 allele - rs429358 - rs7412 Higher risk/ Altered lipid metabolism [41]
Adrenoceptor alpha 2B ( 7q22.1 12Glu9 rs879255577 Higher risk/Defects in regulation [44]
ADRA2B) 17q21.33 of neurotransmitter release from [46]
17q23.3 Variants sympathetic nerves
Gene rs2910164 (G>C) Associated risk/Remarks [48]
microRNA 146a (MIR146a) 7q33 rs11888095 (C>T) Lower risk
microRNA128a (MIR128a) rs6986153 Higher risk
High mobility group box 1 Males/Higher risk
pseudogene 46 (HMGB1P46) rs71647933
Zinc finger and SCAN domain Females/Higher risk
containing 20 (ZSCAN20) rs1799768
Serpin family E member 1 (SER- Progressive type of DPN
PINE1) rs734194
Nerve growth factor receptor Progressive type of DPN
(NGFR) rs1799752
Angiotensin-converting enzyme diallelic polymorphism: Japanese population
(ACE) Presence/absence of 287bp Lower risk
in intron 16 Higher risk
Aldo-keto reductase family 1 mem- Heterozygous D/I
ber B (AKR1B1) Homozygous D/D Higher risk /
rs5053 Altered glucose metabolism
rs759853

GCDC 2017

Cardio Diabetes Medicine 2017 637

Vascular endothelial growth factor 6p21.1 C936T / rs3025039 Higher risk [54]
(VEGF) rs2010963 [54]
16q24.2 rs699947 Higher risk [55]
Cytochrome b-245 alpha chain 9q33.3 C242T Higher risk
(CYBA) rs4673 [57,58]
Heat shock protein Promoter region
family A (Hsp70) 57168556T>C
member 5 (HSPA5) rs391957
Adiponectin (ADIPOQ)
3q27.3 45T / G, rs2241766 Higher risk
276G/T rs1501299 Higher risk

Table 1: Genetic factors and its variants associated with DPN

References peripheral diabetic neuropathy in type 2 diabetes mellitus in a tertiary
care setting.J Diabetes Invest. 2014, 5(6):714-721.
1. International Diabetes Federation (2013). IDF Diabetes Atlas (6th ed.).
Brussels, Belgium: International Diabetes Federation. 16. Tesfaye S, Boulton A.J.M, Dyck P.J, Freeman R, Horowitz M, Kempler P,
Lauria G, Malik R.A, Spallone V, Vinik A, Bernardi L, ValensiP.Diabetic neu-
2. M.G.M.Wolfs, M.H. Hofker, C. Wijmenga, T.W. van Haeften. Type 2 dia- ropathies: update on definitions, diagnostic criteria, estimation of severity,
betes mellitus: New genetic insights will lead to new therapeutics. Current and treatments. Diabetes Care.2010; 33, 2285–2293.
genomics, 2009, 10: 110–118
17. Callaghan B.C, Cheng H.T, Stables C.L, Smith A.L, Feldman E. L. Diabetic
3. Sunita Singh. The genetics of type 2 diabetes mellitus: A review. Journal neuropathy: one disease or two? Curr.Opin. Neurol. 2012, 25, 536–541.
of Scientific Research.Banaras Hindu University, Varanasi.2011, 55: 35-48.
18. Papanas N, Vinik AI, Ziegler D. Neuropathy in prediabetes: does the clock
4. Edwards, J. L., Vincent, A. M., Cheng, H. T., & Feldman, E. L. Diabetic start ticking early? Nat Rev Endocrinol 2011, 7: 682–690.
neuropathy: Mechanisms to management. Pharmacology & Therapeutics,
2008, 120(1), 1–34. 19. Edwards JL, Vincent AM, Cheng HT, Feldman EL. Diabetic neuropathy:-
mechanisms to management. PharmacolTher 2008, 120: 1–34.
5. Centers for Disease Control and Prevention (2014). National Diabetes
Statistics Report: Estimates of diabetes and its burden in the United 20. Figueroa-Romero C, Sadidi M, Feldman EL. Mechanisms of disease: the
States, 2014. Atlanta, GA: US Department of Health and Human Services. oxidative stress theory of diabetic neuropathy. Rev EndocrMetabDisord
2008, 9: 301–14.
6. Cristian Guja, Paul Gagniuc and Constantin Ionescu-tîrgovişte. Genetic
factors involved in the pathogenesis of type 2 diabetes. Proc. Rom. Acad., 21. Yu C, Rouen S, Dobrowsky RT. Hyperglycemia and downregulation of cave-
Series B, 2012, 1, 44–61. olin-1 enhance neuregulin-induced demyelination. Glia 2008, 56:877–87.

7. Uma JyothiKommoju&Battini Mohan Reddy. Genetic etiology of type 2 22. McGuire JF, Rouen S, Siegfreid E, Wright DE, Dobrowsky RT. Caveolin-1and
diabetes mellitus: a review. Int J Diabetes Dev Ctries (April–June 2011) altered neuregulin signaling contribute to the pathophysiological progres-
31(2):51–64. sion of diabetic peripheral neuropathy. Diabetes 2009, 58:2677–86.

8. Sunil K. Kota, Lalit K. Meher, SrutiJammula, Siva K. Kota, Kirtikumar D. 23. Lukic IK, Humpert PM, Nawroth PP, Bierhaus A. The RAGE pathway:
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abetes; its role in treatment modalities. Diabetes & Metabolic Syndrome: Ann NY AcadSci 2008, 1126: 76–80.
Clinical Research & Reviews 6, 2012, 54–58.
24. Lu J, Luo Y, Wang J, Hu C, Zhang R, Wang C, Jia W. Association of type
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of Diabetes Investigation. 2013 May.4 (3) 233-244. population with diabetes. J Diabetes Investig.2016 Jun.

10. Vincent AM, Russell JW, Low P, et al. Oxidative stress in the pathogenesis 25. Yigit S, Karakus N, Inanir A. Association of MTHFR gene C677T muta-
of diabetic neuropathy. Endocr Rev, 2004, 25: 612–628. tion with diabetic peripheral neuropathy and diabetic retinopathy. Mol Vis
2013, 19: 1626–1630.
11. Yagihashi S, Mizukami H, Sugimoto K. Mechanism of diabetic neuropathy:
where are we now and where to go? J Diabetes Investig, 2011, 2, 18–32. 26. Monastiriotis C, Papanas N, Trypsianis. The epsilon 4 allele of the APOE
gene is associated with more severe peripheral neuropathy in type 2 di-
12. Imamura M, Maeda S. Genetics of type 2 diabetes: the GWAS era and abetic patients. Angiology 2013, 64: 451–455.
future perspectives [Review]. Endocr J 2011, 58: 723–739.
27. Papanas N, Papatheodorou K, Papazoglou D, et al. An insertion/deletion
13. Zeggini E, Scott LJ, Saxena R, et al. Meta-analysis of genome-wide asso- polymorphism in the alpha2B adrenoceptor gene is associated with pe-
ciation data and large-scale replication identifies additional susceptibility ripheral neuropathy in patients with type 2 diabetes mellitus. ExpClinEn-
loci for type 2 diabetes. Nat Genet 2008, 40: 638–645. docrinol Diabetes 2007, 115: 327–330.

14. Allan H. Ropper, Kenneth C. Gorson, Clifton L. Gooch, David H. Weinberg, 28. Hur J, Sullivan K, Pande M, Hong Y, Sima A. A. F, Jagadish H.V, Kretzler
Ann Pieczek, James H. Ware, Joshua Kershen, Adam Rogers, DraskoSimov- M and Feldman E.L. The identification of gene expression profiles asso-
ic, Peter Schratzberger, Rudolf Kirchmair and Douglas Losordo. Vascular ciated with progression of human diabetic neuropathy.Brain. 2011 Nov,
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Randomized, Double-Blinded Trial. Ann Neurol 2009, 65:386–393.

15. Dipika Bansal, KapilGudala, HariniMuthyala, Hari Prasad Esam, RamyaN-
ayakallu, Anil Bhansali. Prevalence and risk factors of development of

Cardio Diabetes Medicine

638 Cardio Diabetes Medicine 2017

Can The Projected World Center of Chronic Disease
Be Converted to The Worlds Control Centre of
Chronic Disease?

Dr.Alexander Thomas, President,AHPI
Dr.V.C.Shanmuganandan, Joint Director,AHPI

Dr.John Tharakan, Consultant,AHPI

Introduction: heart disease (IHD) and stroke constitute the major-
ity of CVD mortality in India (83%), with IHD being
The epidemiological transition in India in the past two predominant.11 The ratio of IHD to stroke mortality in
decades has been dramatic; in a short timeframe, the India is significantly higher than the global average,
predominant epidemiological characteristics have and is comparable to that of Western industrialized
transitioned from infectious diseases, diseases of countries. Together, IHD and stroke are responsible
under nutrition, and maternal and childhood diseases for more than one-fifth (21.1%) of all deaths and
to non-communicable diseases (NCDs).8 The disease one-tenth of the years of life lost in India (years
burden attributable to maternal disorders, measles, of life lost is a measure that quantifies premature
protein-energy malnutrition, and diarrheal diseases mortality by weighting younger deaths more than
decreased >50% in the past 2 decades, whereas older deaths).8 The years of life lost attributable to
life expectancy at birth increased from 58.3 to 65.2 CVD in India increased by 59% from 1990 to 2010
years, resulting in the ageing of the population during (23.2 million to 37 million).8
the same period.8 Consequently, the NCD burden
increased rapidly in India, with a proportional rise in In the urban areas of India, the prevalence of dia-
burden attributable to CVD.8 Nearly two-thirds of the betes mellitus has almost doubled in the past 20
burden of NCD mortality in India is currently years, from 9% to 17%, and in rural areas it has
nearly quadrupled, from 2% to 9%.47In 2013, the In-
contributed by CVD-related conditions.9Despite wide ternational Diabetes Federation estimated that
heterogeneity in the prevalence of risk factors across 65.1 million people in India had diabetes mellitus,
different regions (explained below), CVD is the a high proportion of whom were adults of working
leading cause of death in all parts of India, includ- age.71 It is estimated that the number of individuals
ing the poorer states and rural areas.10 The disease with diabetes mellitus will increase to an alarming
transition in India in the past 2 decades resembles 101 million by 2030.71 An estimate based on the
the accelerated epidemiological transition model with ICMR-INDIAB study indicates that the number of
a rapid shift to the age of delayed chronic diseases. individuals in India with prediabetes (impaired fast-
ing glucose or impaired glucose tolerance) is 77
According to the Global Burden of Disease study million.69 In addition, based on epidemiological
age-standardized estimates (2010), nearly a quar- data and conversion rates among control groups in
ter (24.8%) of all deaths in India is attributable to intervention studies, the conversion rate from pre-
CVD11 The age-standardized CVD death rate of 272 diabetes to diabetes mellitus is high.72–74 Diabetes
per 100 000 population in India is higher than the awareness and control are poor in rural regions in
global average of 235 per 100 000 population . comparison with urban regions.69,70 Diabetes mellitus
continues to have a positive social gradient (with a
It is interesting to note that the public health strategy higher burden among the rich and well educated), with
in India is still in the process of making this transi- the exception of certain settings such as industrial
tion of addressing NCDs. The health infrastructure worksites.66,75,76 However, a recently concluded study
in the country which has focussed on communica- on risk factors of CVD in urban and rural Delhi
ble diseases has not been recalibrated to address suggests that there is no difference in the prevalence
the increasing NCD burden in the country. Ischemic

GCDC 2017

Can The Projected World Center of Chronic Disease Be Converted to 639
The Worlds Control Centre of Chronic Disease?

of diabetes mellitus across various SES groups (D. scope that the newer technologies being developed
Prabhakaran, unpublished data, 2014). have to offer if appropriately leveraged.

However, in order to slow down the progression of While it is easy to get carried away by the potential
this epidemic, it is important to detect and manage that technology has to offer, it is imperative that what-
Cardiometabolic disease (CMD) at the earliest India ever technology we propose to use is customised in
today possesses as never before, a sophisticated ar- a manner that ensures its efficient use in the Indian
senal of interventions, technologies and knowledge context. Furthermore, the current policies that are in
required for providing health care to its people. Tech- place are not very conducive to the rapid deployment
nologies presently available can play a major role of innovative technologies to enhance the health and
in facilitating such interventions at a very low cost wellbeing of patients. It thus becomes essential that
especially in the area of Cardiometabolic diseases a mechanism is developed to incorporate expertise
(CMD). Technology has proven to be a major boon in available in the areas of information technology, ba-
the provision of healthcare in different parts of the sic sciences, engineering, CMD and public health to
world. Pilot studies done in many developing coun- develop possible technology platforms to address
tries have shown the benefits of leveraging technol- issues related to CMD in the Indian population and
ogy to address health care needs on a large scale at provide a cost effective way in which quality health
reasonable costs. Some of these technologies have care can be provided at the grass root levels. The
played an important role in surveillance, prevention, key deliverables of this group of esteemed experts
diagnosis and treatment thereby reducing the CMD would be to:
burden to a certain extent over the last few years.
Identify the technologies available and come up with
Since the burden of CMD in India is large, technol- the specifications for a suitable information technol-
ogy can be leveraged in multiple ways to overcome ogy platform that would facilitate remote diagnosis
this burden. This includes as a platform between the and treatment of CMD based on scientifically sound
physician and the patient, between physicians in the clinical protocols.
same speciality, physicians from varying specialities
and among patients themselves. Technology is also a Develop health delivery systems that candove-tail
highly effective tool for collating and analysing data into existing health systems at different levels to ad-
thereby determining the best treatment management dress the health care needs related to CMD all over
plan possible. There is significant evidence to show the country.
that the optimal combination of health care and tech-
nology can play a key and diverse role in healthcare Provide an active platform for networking between
delivery, reducing costs and increasing quality of the government, private health care providers and the
care being provided. community on how information technology can be
effectively used with respect to CMD in the health
Technology can be broadly classified into sector.
four areas:
Advocate for policy reforms at the national and state
Medical devices levels as and where required with a focus on facil-
itating the prevention, care and treatment of CMD
Big Data/ Artificial Intelligence through the use of newer technologies.

Information Technology The Organising Committee of this Global Cardio Dia-
betes Conclave 2017 has done a wonderful job of get-
Health Management Information systems ting together experts in various aspects of CMD from
all over the globe. The contributions of this conclave
Some of the technologies that have made an impact can be significantly enhanced if detailed and serious
in the delivery of CMD care include advances in im- thought is given to the establishment of a group of
aging and mobile phone technology, surgical tech- experts as described above. Formation of this group
niques, electronic health records, Nano medicine, along with timely follow up of the decisions they take
telemedicine, decision support systems, availability will sound the death knell to CMD in India. It is only
of newer bio-friendly devices, sophisticated software through the implementation of such innovative and
that is capable of analysing millions of clinical data out of the box approaches that the projected world
points per second and providing diagnostic and ther- centre of Chronic Disease will be converted to the
apeutic guidance. While going into the details of the Worlds Control Centre of Chronic Diseases.
technologies available is beyond the scope of this
article, the idea is to give an overview of the huge

Cardio Diabetes Medicine

640 Cardio Diabetes Medicine 2017

Health Insurance
A Comprehensive Study

Dr. S. Prakash, MS,FRCS(Glasg), FAIS

Chief Operating Officer,
Star health and allied insurance Co.Ltd.

Health Insurance Industry in India – The Scheme is an earmarked fund set up by government
Advent with explicit benefits in return for payment. The social
health insurance includes the Central Government
The Government of India, post-independence, laid Health Scheme (CGHS) and Employees State Insur-
stress on primary health care and put in continu- ance Scheme (ESIS) [6]. Community health insurance
ing efforts to uplift the health care system across scheme is any non-profit insurance scheme aiming
the country[1]. India’s tryst with health insurance primarily at the informal sector and formed on the ba-
programme goes back to the late 1940’s and early sis of a collective pooling of health risks and payment
50’s when the civil servants were provided the Cen- therefore. Community Health Insurance schemes in-
tral Government Health Scheme and formal sector volve pre-payment and the pooling of resources to
workers were provided the Employees State Insur- cover the costs of health-related mishaps [7].
ance Scheme. These schemes were contributory but
heavily subsidized health insurance programmes[2]. Private Health Insurance is voluntary. The insurer
As a consequence of liberalization of the economy generally collects the premium from individuals who
since the early 1990s, the government opened up the can afford to pay and then invests this to supplement
private sector including health insurance in 1999. This the insurance fund[8].Insurance is a pooled fund.
development threw open the possibility for higher
income groups to access quality care from private Government Health Insurance Schemes (GHIS’s) are
tertiary care facilities[3]. However, since 2007, India usually for the poorest and vulnerable sections of the
has witnessed a deluge of new initiatives, both by the community. Under these schemes, the premium is
central government and a host of state governments totally subsidized by the government from tax-based
also entering the revenues and is paid directly to the insurer. The major
GHIS’s schemes are the Universal Health Insurance
bandwagon of health insurance [4]. One of the rea- Scheme (UHIS), Rajiv Arogyashri Scheme (RAS),
sons for initiating such programs may be traced to Rashtriya Swasthya Bima Yojana (RSBY), Vajpayee
the commitment of the governments in India to scale Arogyasri Scheme, Karnataka and Chief Minister Ka-
up public spending in health care[2]. India spends laignar Health Insurance Scheme, Tamil Nadu.
about 6% of GDP on health care, out of which 22 %
of overall spending occurs in the Government sector Given that government has liberalized the insurance
while 78% of overall spending in private sector[4]. industry, health insurance is now known to be a
Sunrise Industry. It had been noted that Health In-
In India, the advent of Health Insurance occurred with surance, if left only to the Private Market would only
the launch of the Mediclaim policy in November 1986 be available to those with a considerable capability
by the General Insurance Corporation. Thereafter to pay. There is a need for alternative finances, in-
several kinds of policies have been floated contin- cluding provision for medical insurance at a much
uously in this field by both public and private health wider level. Health insurance is emerging to be an im-
insurers[5]. The types of health insurance are as: So- portant financing tool in meeting health care needs
cial health insurance (SHI) schemes are statutory of the poor[9].It was found that the market trend and
programmes financed mainly through wage-based penetration level of health insurance business and
contributions and related to level of income. An SHI the premium level and index of growth of health in-

GCDC 2017

Health Insurance - A Comprehensive Study 641

surance business is continuously rising up in India Being Inclusive
[5].It has been noted that a large majority of Indian
population depends on the private sector, mostly in There are some common and permanent exclusions
the form of out of pocket spending that accounts for about which a policyholder must be aware of. It must
more than 70% of all health spending in India. also be understood that the exclusions are not stan-
dard for all policies but there are some which the in-
Growth of Public Sector Vs Private Sector sured needs to know about before purchasing health
insurance.
In 2003-04, there was 36.78 percent growth in total
premium out of which private sector growth rate was Specific Ailments[10]
157.02 percent and that of public sector was 28.89
percent.Initially the idea of running health insurance The expenses on the treatment of diseases such as
as a stand-alone product - as a one-line business was Cataract, Benign Prostatic Hypertrophy, Hysterecto-
disliked by people. The fact remains that any scheme my for Menorrhagia or Fibromyoma, Hernia, Hydro-
of health insurance to be introduced on large-scale in cele, Congenital Internal Disease, Fistula in anus,
India requires a tremendous attention to be given to Piles, Sinusitis and related disorders, Gall Bladder
the organisational capacity on the part of the insur- Stone removal, Gout and Rheumatism, Calculus dis-
ers and the regulators to bring together the different eases, Joint replacement due to Degenerative Condi-
elements that constitute Health Marketing. tion and age related Osteoarthritis and Osteoporosis
are generally not payable until a specific period of
The various providers of services fall under this clas- time, which differs from company to company. The
sification; behind all this the lusting fear that the per- specific diseases may also differ with the company
sons who are likely to be covered by this scheme
would be a moral hazard - the choice of selection, the Pre-existing diseases[11]
choice of ‘adverse selection’ to put it, which is going
to impinge on the ‘rating structure’ which insurance If the policy holder is already suffering from a disease
companies would like to adopt. The basic thing that then it is considered as a pre-existing disease which
keeps people away from getting into this business are not covered as Insurance is done for uncertain
is the fact that today in this country as distinct from things. Usually there is a waiting period of 2-4 years
any other advanced country in the world, we do not or more depending upon the type of disease & its risk
have a basic social structure affording State aid to if the insurer agrees to cover it. Pre-existing diseas-
people, on a regular basis. Other developed coun- es like cataract, kidney stones, arthritis, few chronic
tries have a National Policy on Health. Where they diseases, joints treatment and more are some which
have a system by which people are taken care of, for could be excluded.
their basic requirements on health, where provision
of health facilities is considered to be a fundamental Waiting Period clause[11]
duty on the part of the State, and expecting that to
be provided is considered to be a fundamental right. Except for accidents and deaths, most policies do not
provide cover immediately, even for those diseases
Star Health and Allied Insurance Co Ltd commenced which are not excluded. There usually is a waiting
its operations in 2006 with the business interests in period of 1-2 months post which the insured can reap
Health Insurance, Overseas Mediclaim Policy and the benefits of the policy.
Personal Accident. With no other insurance category
to focus and divide our attention, we use our resourc- Pregnancy[11]
es to focus on service excellence, design products
and use core competency of innovation to deliver the Costs like pregnancy, child birth, vaccination and
best to our customers. Today we have emerged as likewise would generally not be covered under a
India’s First Stand-Alone Health Insurance Company. health insurance policy. Pregnancy could have a
At Star Health Insurance, the Company offers a wide waiting period of 1-2 years. Therefore the insured can
range of Health Insurance products at affordable receive decent benefits for pregnancy if they plan for
prices to make health insurance every human being’s the child accordingly.
right. As a Company, single-mindedly dedicated to
Health insurance, Star Health have built a promising Surgeries[11]
path for the future of Indian population.
Surgeries such as joint replacement, cosmetic sur-
gery, dental surgery, are usually not covered in a
health insurance policy.

Cardio Diabetes Medicine

642 Cardio Diabetes Medicine 2017

Permanent exclusions[11] Further the look-back period was enhanced from 4
years to 7 years. With these changes the ambit of the
There could be some permanent exclusions like persons becoming eligible got broadened. Out-pa-
injuries in war, HIV, intentional injuries, congenial tient coverage was also introduced to take care
diseases, etc. of the consultation, diagnostics and expenses on
medicines and drugs. This would encourage routine
Having spoken about the exclusions, it can be check-up for health maintenance. There is an em-
noted how these exclusions can limit the benefit bedded Personal Accident cover against Accidental
of health insurance to various segments of the Death – this offers protection for the family of the
population. policyholder in case of any accidental mishap.

It is very important to make health insurance inclusive We have moved in the direction of providing holistic
to all segments of society. Product innovation is a key coverage. Thus Star protects the insured against any
strategy to any Health insurance company as it is to health contingency and also protects the insured’s
Star Health and Allied Insurance Co. Ltd. Star Health family against an accident contingency. The entire
has always been at the forefront of innovating on the revision was configured in the base operating sys-
processes and products continually to remain rele- tem with a special process flow created for medical
vant to the changing customer aspirations. Some of underwriting.
the most innovative products from Star Health are:
The retail business focus has given the Company
Star Cardiac Care Insurance policy a new thrust and direction to forge ahead with new
vigour and new innovative products in the health in-
Diabetes Safe Insurance Policy surance space. Our bouquet of specialised products
have made a splash in the Market giving the citizens
Senior Citizen Red Carpet Policy of our country a wider choice range in terms of af-
fordability and accessibility to various healthcare ser-
Sankalp vices. This has also helped in increasing the penetra-
tion of Health insurance and the spread of our reach.
Star Net Plus
This policy is for persons who have undergone for
Star Super Surplus Policy the first time the named surgery / intervention / cor-
rection for the existing Cardiac diseases. This policy
Star Wedding Gift Insurance has two Plan options – Gold Plan and Silver Plan and
each Plan has two distinct sections – One for Regular
Innovative Aspects of Star Cardiac Care: Hospitalization and another for hospitalization spe-
cifically for cardiac ailments.
Star Health Cardiac Care Insurance Policy is an exclu-
sive product to cover customers who have undergone The Silver Plan pays for expenses incurred as an in-
PTCA and CABG. Covers in-patient cardiac ailment patient for treatment in respect of all cardiac related
treatment expenses which require hospitalization of complications that necessitate surgery/intervention
at least 24 hours. Pre-existing cardiac ailments are while the Gold Plan pays for expenses incurred as
covered from the 91st day of policy commencement. an inpatient for treatment in respect of all cardiac
Pre-hospitalization medical expenses upto 30 days related complications that necessitate medical man-
prior to hospitalization Post hospitalisation medical agement, surgery/intervention.
expenses – Upto 7% of hospitalisation expenses
(excluding room rent) subject to a maximum of Rs. Under both the Plans regular hospitalization and all
5,000. The product is for persons who have under- Cardiac related ailments are covered. There is no
gone Bypass or PTCA. As the experimentation with Pre-acceptance medical screening. 405 day-care pro-
the affected persons is being done for the first time cedures and Out Patient Benefits are also available
we were moving cautiously limiting the eligibility to under this policy.
persons who have undergone Bypass Grafting, PTCA
within 4 year look back from the date of proposal. Insurance For Diabetes A Bitter - Sweet Pill

Our experience indicated that there are a few other India is home to 65 million diabetics & 50 million pre
areas that can be opened up without compromising -diabetes, and 56 per cent people remain unaware of
much on the safety. Hence the revised version was the fact that they have diabetes until it is too late. Type
launched with inclusion of more persons who have II diabetes is a lifestyle disease and obesity is at the
undergone Atrial Septal Defect (ASD) / Ventricular root of it. Diabetes also makes the patient prone to
Septal Defect (VSD) closure , Patent Ductus Arterio-
sus (PDA) and persons on who Angiogram was done
but no intervention was medically found necessary.

GCDC 2017

Health Insurance - A Comprehensive Study 643

additional complications like heart disease, strokes, becoming conscious about their health and the eco-
kidney failure, eye disease and foot problems. Death nomic consequences of falling sick. They are gradu-
from heart ailments is the leading cause of death ally realizing the significance of health insurance in
among people suffering from Type II diabetes. today’s precarious world.

Diabetes is a silent killer. What was the disease of References
the old has now become a disease that has begun
to affect people in their twenties and thirties. Being 1. 1.K Ranson, and M. Jowett, Developing Health Insurance in India: Back-
diagnosed with diabetes in one’s youth severely im- ground Paper to the Government of India., Workshop on Health Insurance.
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ty. The burden of treatment, rising medical costs and
the fear of losing one’s hard earned income due to 2. 2.PHFI, “A Critical Assessment of Existing Health Insurance Models in
health complications can leave one medically and India”, a report submitted to the Planning Commission, Government of
financially vulnerable. India, New Delhi, 2011.

According to industry estimates, In India, an approxi- 3. 3.A. Mahal, Assessing private health insurance in India: Potential impacts
and regulatory issues, Economic and Political Weekly, Vol.37 (6), 2000,
mate of 85-95% of all health care costs are borne by pp. 559–71.

individuals and their families from household income 4. 4.D. Singh, A Study on the Development of Health Insurance – its History,
Current Scenario and Future Prospects in India, D. Subrahmaniam Award
as most people are not insured. With insur- with report presented, 2011.

ance, the average claim size of a diabetes policy is 5. 5.V. Bishnoi and R. Saharan, Health Insurance in India: Introspects and
Prospects, The Icfai Journal of Risk & Insurance, Vol.4 (3), 2007, pp.
Rs 50,000. Diabetes costs for treatment for 5 years 58-68.

is Rs. 1,50,000 and for 10 years is Rs 4,00,000. The 6. 6.N. Devadasan and S. Nandraj, Planning & Implementing Health Insur-
ance Programmes in India, Institute of public Health, 2006.
average monthly expense for a diabetic comes to
7. 7.Devadasan et al., Community Insurance in India: An overview, Economic
around Rs 5,000 – Rs 9,000, this excludes the ac- and Political Weekly, 2004, pp. 3179-83.

tual treatment (doctor’s consultations, medical tests 8. 8.Institute of Public Health, Training Manual on Health Insurance, Ban-
galore, 2006.
and treatment costs). In the scenario that additional
9. 9.I. Gupta and M. Trivedi, “Beyond a Piecemeal Approach”, Economic &
complications like heart disease, strokes or kidney Political Weekly, June 24, 2006, pp. 2525- 28.

failure happens, the additional cost of treatment is 10. 10.Exclusions in a Health Insurance policy | Medimanage.com [Inter-
net]. Medimanage.com. 2017 [cited 13 September 2017]. Available from:
hiked by about Rs 20,000 a month. http://www.medimanage.com/my-health-insurance/articles/your-medi-
claim-policy-excludes-these-expenses.aspx
A standard medical policy sometimes does not offer
adequate cover for the advanced treatments. One of 11. 11.Exclusions of Health Insurance Policy [Internet]. Policybazaar.com. 2017
the main reasons why most people face complica- [cited 13 September 2017]. Available from: https://www.policybazaar.com/
tions while dealing with the disease is that it is di- health-insurance/general-info/exclusions-of-health-insurance-policy
agnosed very late. Buying a health insurance well in
time, when you are young and healthy, means paying
a lesser premium as compared to when diabetes is
knocking at your door. A healthy person can buy a
health insurance cover of Rs 7,000 – Rs 9,000 per
year as compared to Rs 18,000 – Rs. 20,000 per year
for a diabetic patient.

There are policies that also cover non- diabetic health
issues that crop up while being treated for diabetes.
While some insurance providers don’t let you take
a diabetes cover if you have already contracted dia-
betes, there are a few policies that provide cover to
such patients as well. It is important that all these fac-
tors are taken into consideration when one decides
to invest money into a policy that covers diabetes.

Conclusion

Health Insurance is a growing segment of India’s
economy. The rising trend of the share of health port-
folio indicates the increase in the level of awareness
of customers. This signifies that the general public is

Cardio Diabetes Medicine