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\def\citeauthor{~Gautham~Chakra~R,
              ~Rajeswari~G,
              ~Alekya~B,
              ~Mahaboob~Ali~Sk,
              ~Noorul~Kareem~M,
              ~Prekshasri~S}
\def\citetitle{A Tertiary Care Hospital's Prescription Pattern for Diabetes Mellitus}
\def\copyrightstmt{This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial- ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.}
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\def\RunningAuthor{Gautham Chakra R et al.}
\firstPage{62}
\articleType{Original Article}
\receivedDate{25 Apr 2023}
\acceptedDate{17 May 2023}
\revisedDate{16 May 2023}
\journalVolume{2}
\journalIssue{2}
\journalDoi{ijebr.v2i2.514}
\copyrightYear{2023}
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\title{A Tertiary Care Hospital's Prescription Pattern for Diabetes Mellitus}
\author{Gautham~Chakra~R\textsuperscript{*}\textsuperscript{1}\textsuperscript{\href{https://orcid.org/0009-0008-6415-1840}{\XeTeXLinkBox{\includegraphics[height=7pt]{orcid-logo-pharmascope.pdf}}}},  
            Rajeswari~G\textsuperscript{2},  
            Alekya~B\textsuperscript{2},  
            Mahaboob~Ali~Sk\textsuperscript{2},  
            Noorul~Kareem~M, 
            Prekshasri~S\textsuperscript{2}~\\[5pt]{\textsuperscript{1}Department of Pharmacy Practice, Saastra College of Pharmaceutical Education \& Research, Jwalamukhi temple, Varigonda, Nellore, Andhra Pradesh 524311}~\\{\textsuperscript{2}Saastra College of Pharmaceutical Education \& Research, Jwalamukhi temple, Varigonda, Nellore, Andhra Pradesh 524311}}

\begin{abstract}
Hyperglycemia produced on by type-1 or type-2 diabetes mellitus characterises the complex group of metabolic disorders known as diabetes mellitus. Because concomitant conditions can aggravate DM as well as increase the risk of complications, it is important to evaluate the prescription patterns in these individuals. The unique and general characteristics of diabetes patients, such as the available dose forms, the unexpected administration of medications to patients, and reported drug interactions, including common co-morbidities encountered in diabetic patients, all add to the challenges that the practitioner treating individuals. Due to the aforementioned factors, the study was created to help reduce prescription errors, provide safe dosage regimens, educate patients by closely monitoring the patients' glycaemic control and other responses to therapy, as well as promote the responsible and sensible use of medications. This study used questionnaires as a tool and was a prospective observational study that lasted six months. The study is being done at Global Hospital Lb. Nagar's medical ward. Those who visited OP and were admitted to the hospital's Medicine ward between October 2016 and March 2017 are included in the study. The following requirements must be met for a patient to enlist. Males (62.30\%) and females (32.90\%) made up the study's gender distribution. The age distribution was determined to be as follows: 30{\textendash}35 years (8\%), 35{\textendash}45 years (14\%), 45{\textendash}55 years (56\%), 55{\textendash}65 years (38\%), 65{\textendash}75 years (19\%), and 75{\textendash}85 years (10\%). The comorbid diseases identified in the 94 patients overall were hypertension, hyperthyroidism, chronic renal disease, infections of the urinary tract, as well as coronary artery disease (CAD).
\end{abstract}\def\keywordstitle{Keywords}

\begin{keywords}Tertiary Care,\newline Prescription,\newline Diabetes Mellitus,\newline Hyperglycemia
\end{keywords}
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\makeatletter{\raggedright{\Large$^\ast$}Corresponding Author\par Name:\ Gautham~Chakra~R~\\ Phone:\ +91 7674016126~\\  Email:\ gauthamrowdhra05@gmail.com
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\section{INTRODUCTION}
Hyperglycemia brought on by type-1 or type-2 diabetes mellitus characterises the complex group of metabolic illnesses known as diabetes mellitus.

More than 346 million individuals globally, according to the WHO, develop DM (1). Without any help, this number is more likely to quadruple by 2030 \unskip~\cite{2106768:29287985}.

Diabetes is a difficult condition to adequately treat. Because diabetic nephropathy is a significant contributor to early morbidity, this study aims to evaluate the function of clinical chemists in addressing it. 40\% of all patients in the United Kingdom who require dialysis have kidney failure as a result of diabetic nephropathy, which is a significant source of early morbidity and mortality in individuals with diabetes mellitus (I). Hyperglycemia brought on by type-1 or type-2 diabetes mellitus characterises the complex group of metabolic illnesses known as diabetes mellitus.

More than 346 million individuals globally, according to the WHO, develop DM (1). Without any help, this number is more likely to quadruple by 2030 \unskip~\cite{2106768:29288006}.

Diabetes is a difficult condition to adequately treat. Because diabetic nephropathy is a significant contributor to early morbidity, this study aims to evaluate the function of clinical chemists in addressing it. 40\% of all patients in the United Kingdom who require dialysis have kidney failure as a result of diabetic nephropathy, which is a significant source of early morbidity and mortality in individuals with diabetes mellitus (I).  Approximately 10\% as well as 30\%, respectively, of people with type 1 (insulin-dependent) diabetes mellitus (IDDM) develop nephropathy within 10 and 20 years, respectively. Nearly 20\% of diabetics under the age of 50 die from nephropathy, which is also strongly linked to an elevated risk of cardiovascular disease. Additionally, it takes less time to develop in people with type I1 (non-insulin-dependent) diabetes mellitus (NIDDM). Antihypertensive medication has long been recognised for its advantages in reducing the rate of deterioration in renal function, which has made the need for effective therapeutic intervention to postpone or prevent renal failure development a priority. Angiotensin converting enzyme (ACE) inhibitors, however, have recently produced some quite impressive results. Whether ACE inhibitors can stop the progression of early disease with micro-albuminuria to advanced nephropathy is still unknown \unskip~\cite{2106768:29287999}.

\textbf{Classification of Diabetes }

The majority of diabetic patients split into one of two broad categories: type 1 diabetes, which is brought on by a complete lack of insulin, or type 2 diabetes, which is characterised by the presence of insulin resistance and an insufficient increase in insulin secretion as a form of compensatory insulin resistance \unskip~\cite{2106768:29287997,2106768:29287984}. 

\textbf{Type 1 diabetes:}

The pancreatic cells are destroyed autoimmunely in this type of diabetes. 90\% of people have antibodies against insulin, glutamic acid decarboxylase, and islet cells at the time of diagnosis, which are markers of immunological destruction of the cell. Although this type of diabetes typically affects kids and teenagers, it can affect people of any age. While adults often experience LADA for many years, younger people often have a high rate of -cell breakdown as well as manifest with ketoacidosis.

\textbf{Type 2 diabetes:}

This form of diabetes is characterized by insulin resistance and a relative lack of insulin secretion, with progressively lower insulin secretion over time. Most individuals with type 2 diabetes exhibit abdominal obesity, which causes insulin resistance. In addition, hypertension, dyslipidaemia (high triglyceride levels and low HDL-cholesterol levels), and elevated plasminogen activator inhibitor type 1 (PAI-1) levels are often present in these individuals. Type 2 diabetes has a strong genetic predisposition and is more common in all ethnic groups other than those of European ancestry.

\textbf{Epidemiology:}

In 2011, 366 million people were expected to have DM; by 2030, this number will have increased to 552 million. Every country is seeing an increase in the prevalence of type 2 diabetes, with 80\% of those affected residing in low- and middle-income nations. In 2011, 4.6 million people perished from DM. By 2030, 439 million individuals are predicted to develop type 2 diabetes. Due to environmental as well as behavioural risk factors, there are significant regional differences in the incidence of type 2 diabetes. In the next 20 years, it is expected that the prevalence of diabetes in adults in which type 2 DM is becoming more prevalent{\textemdash}will rise. A large portion of this rise will take place in emerging nations, where the majority of patients are between the ages of 45 as well as 64 \unskip~\cite{2106768:29288002}.

\textbf{Etiology:}

When the pancreas stops producing enough insulin or when the body becomes resistant to insulin, type 2 diabetes can occur. Although the exact cause of this is uncertain, environmental as well genetic variables, including obesity as well as inactivity, appear to play a role \unskip~\cite{2106768:29288001}.

\textbf{Signs and Symptoms:}

Type 2 diabetes can be present for years without symptoms. Keep an eye out for: increased hunger, increased thirst, as well as frequent urination. losing weight, Fatigue, vision fuzziness, slow-healing wounds or recurrent infections, darker skin patches \unskip~\cite{2106768:29287986}.

\textbf{Risk Factors: }

Some factors include{\textemdash}such as body weight, distribution of fat, increased appetite, excessive thirst, weight loss, more frequent urination, blurred eyesight, excessive exhaustion, sores that don't heal, inactivity, ancestry, race, age, as well as Pregnancy-related diabetes, polycystic ovaries, as well as prediabetes \unskip~\cite{2106768:29287992}. 

\textbf{Diabetic Emergencies:}

People with type 1 as well as type 2 DM frequently have low blood sugar. The majority of instances are minor and are not emergencies. Effects might range from uneasy sensations, shaking, sweating, and increased appetite in mild cases to more serious problems like confusion, behavioural abnormalities, seizures, unconsciousness, and (rarely) fatal brain damage or death in serious instances. Self-medication for mild instances involves consuming sugar-rich foods as well as beverages. Serious cases, which can cause coma, need to be treated with intravenous glucose or glucagon infusions \unskip~\cite{2106768:29287982}.

\textbf{Treatment}

\textbf{Pharmacological therapy for type 2 DM:}

Improved glucose control as well as fewer long-term problems are linked to early pharmacologic therapy beginning in type 2 diabetes. The following drug classes are utilised in the management of type 2 diabetes \unskip~\cite{2106768:29287994}:


  
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  \item \relax Biguanides
  \item \relax Alpha-glucosidase inhibitors
  \end{enumerate}
  Thiazolidinediones (TZDs) Insulin treatment was only given to type 2 diabetic patients whose blood sugar levels could not be controlled by oral medications and dietary adjustments. However, there is mounting evidence that early use of insulin may enhance overall diabetes management as well as the maintenance of the pancreas' capacity to produce insulin.

Some diabetic individuals only received insulin treatment if their type 2 diabetes could not be managed with oral medications as well as dietary adjustments. In contrast, there is mounting evidence that early use of insulin may enhance overall diabetes control as well as the maintenance of the pancreas's capacity to produce insulin.

\textbf{Insulin therapy }

]Some persons with type 2 diabetes also require insulin therapy. Because of its advantages, insulin therapy is now frequently administered earlier than it ever was. Insulin needs to be administered since it is hampered by regular digestion. Your doctor may advise using a variety of insulin kinds both during the day and at night, depending on your needs. People with type 2 diabetes frequently begin using insulin with one long-acting injection at night. A fine needle as well as syringe or an insulin pen injector, which resembles an ink pen but has an insulin cartridge instead of ink, are used to provide injections of insulin \unskip~\cite{2106768:29287983}.

There are numerous varieties of insulin, as well as each one functions differently. Options consist of:

Insulin glulisine (Apidra)

Insulin lispro (Humalog)

Insulin aspart (Novolog)

Insulin glargine (Lantus)(38)

Insulin detemir (Levemir)

Insulin isophane (Humulin N, Novolin N)

Describe to your doctor the benefits and drawbacks of certain medications. After carefully weighing several considerations, such as expenses and other aspects of your health, you can select which drug is ideal for you. Your doctor may also recommend blood pressure and cholesterol-lowering drugs in addition to diabetes meds that will prevent heart and also the blood vessel disease, as well as low-dose aspirin therapy.

\textbf{Bariatric surgery }

If you have type 2 diabetes and a body mass index (BMI) above 35, you might be a candidate for bariatric surgery, which involves weight loss. Depending on the method used, blood sugar levels return to normal in 55 to 95 percent of diabetic patients. Other weight-loss procedures have less of an impact on blood sugar levels than surgeries that bypass a part of the small intestine [Figures~\ref{f-735d3b8826a3}, \ref{f-41c79280a5ac} and~\ref{f-a6bb21e6ddd6}] \unskip~\cite{2106768:29288000}.

Pre-mixed insulin, which is a combination of intermediate-acting and short- or rapid-acting insulin in a single bottle or insulin pen, may be an alternative in some circumstances [Figures~\ref{f-4da683148997}, \ref{f-957578877e6e} and~\ref{f-a327341e554b}].
    
\section{METHODOLOGY}

    
\section{MATERIALS AND METHODS}
\textbf{Source of data}

Case report forms of type II Diabetes Mellitus patients.

\textbf{Rationality of the Study}


\begin{table*}[!htbp]
\caption{\boldmath {Oral Agents for the Treatment of Type 2 DM} }
\label{tw-0013a2adc047}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.1869\linewidth-2\tabcolsep}p{\dimexpr.36629999999999995\linewidth-2\tabcolsep}p{\dimexpr.2234\linewidth-2\tabcolsep}p{\dimexpr.2234\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Class & Primary Mechanism of Action & Agent(s) & Available as\\
\tblmidrule 
Sulfonylureas &
  The beta cells' initial impact is to secrete more insulin; they may also slow the rate at which the liver produces glucose as well as improve the sensitivity of the insulin receptor. &
  Acetohexamide \mbox{}\protect\newline Chlorpropamide \mbox{}\protect\newline Tolazamide \mbox{}\protect\newline Tolbutamide \mbox{}\protect\newline Glipizide \mbox{}\protect\newline Glyburide \mbox{}\protect\newline Glimepiride &
  Dymelor \mbox{}\protect\newline Diabinese \mbox{}\protect\newline Tolinase \mbox{}\protect\newline Orinase \mbox{}\protect\newline Glucotrol \mbox{}\protect\newline DiaBetaMicronase \mbox{}\protect\newline Amaryl\\
Short-acting insulin secretagogues \mbox{}\protect\newline  &
  Interacting with K+ channels on beta islet cells increases insulin production. lowers post-meal hyperglycemia. Existing glucose levels determine how much insulin is released. &
  Nateglinide \mbox{}\protect\newline Repaglinide &
  Starlix \mbox{}\protect\newline Prandin\\
Thiazolidinediones \mbox{}\protect\newline  &
  Elevates target-cell responses to insulin; lowers hepatic gluconeogenesis; action dependent on insulin. &
  Pioglitazone \mbox{}\protect\newline Rosiglitazone &
  Actos \mbox{}\protect\newline Avandia\\
Sodium-glucose cotransport-2 (SGLT-2) inhibitor \mbox{}\protect\newline  &
  Sodium-glucose transporter-2 (SGLT2) inhibitor with high selectivity. &
  Dapagliflozin &
  Farxiga\\
Amylin analogue \mbox{}\protect\newline  &
  Reduce the production of glucagon \mbox{}\protect\newline Gastric emptying gradually \mbox{}\protect\newline Enhance appetites &
  Pramlintide \mbox{}\protect\newline  &
  Symlin \mbox{}\protect\newline \\
a-Glucosidase inhibitors &
  Delayed intestinal carbohydrate absorption &
  Acarbose \mbox{}\protect\newline Miglitol \mbox{}\protect\newline  &
  Precose or generic Glyset\\
Glucagon-like peptide-1 (GLP-1) receptor agonists (Injectable drugs) \mbox{}\protect\newline  &
  A glucagon-like peptide-1 (GLP-1) that suppresses glucagon, slows stomach emptying, and acts as an incretin mimic. &
  Exenatide \mbox{}\protect\newline Liraglutide &
  Byetta \mbox{}\protect\newline Victoza\\
Biguanides &
  Reduce HGP \mbox{}\protect\newline Increase in muscle glucose absorption &
  Metformin \mbox{}\protect\newline  &
  Glucophage or generic \mbox{}\protect\newline \\
Bile acid sequestrant \mbox{}\protect\newline  &
  Reduce HGP \mbox{}\protect\newline Elevating incretin levels &
  Colesevelam \mbox{}\protect\newline  &
  WelChol \mbox{}\protect\newline \\
DPP-4 inhibitors \mbox{}\protect\newline  &
  Boost the release of glucose-dependent insulin \mbox{}\protect\newline Reduce the production of glucagon &
  Alogliptin \mbox{}\protect\newline Linagliptin \mbox{}\protect\newline Saxagliptin \mbox{}\protect\newline Sitagliptin \mbox{}\protect\newline  &
  Nesina \mbox{}\protect\newline Tradjenta \mbox{}\protect\newline Onglyza \mbox{}\protect\newline Januvia\\
Dopamine-2 agonist &
  Makes dopaminergic receptors active &
  Bromocriptine &
  Cycloset,  \mbox{}\protect\newline Parlodel\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Insulin Therapy for Type 2 DM} }
\label{tw-54717dae9f17}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.18669999999999998\linewidth-2\tabcolsep}p{\dimexpr.25310000000000002\linewidth-2\tabcolsep}p{\dimexpr.1602\linewidth-2\tabcolsep}p{\dimexpr.20\linewidth-2\tabcolsep}p{\dimexpr.20\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Insulin type & Generic and brand names & Onset & Peak & Duration\\
\tblmidrule 
Rapid-acting &
  Insulin aspart (NovoLog) \mbox{}\protect\newline Insulin glulisine (Apidra) \mbox{}\protect\newline Insulin lispro (Humalog) &
  15 min &
  30 to 90 min &
  3 to 5 hours\\
Short-acting &
  Insulin regular (HumulinR, Novolin R) &
  30 to 60  min &
  2 to 4 hours &
  5 to 8 hours\\
Intermediate-acting &
  Insulin NPH human  (HumulinR,Novolin N) &
  1 to 3 hours &
  8 hours &
  12 to 16  hours\\
Long-acting &
  Insulin glargine  (Lantus) \mbox{}\protect\newline Insulin detemir  &
  1 hour &
  No clear peak &
  20 to 26  hours\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Various drugs prescribed for diabetic patients with hypertension, ischemic heart disease, and dyslipidaemia } }
\label{tw-58e4fe9da37f}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.1681\linewidth-2\tabcolsep}p{\dimexpr.216\linewidth-2\tabcolsep}p{\dimexpr.192\linewidth-2\tabcolsep}p{\dimexpr.216\linewidth-2\tabcolsep}p{\dimexpr.2079\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Comorbidity & Drugs prescribed & Total drug usage (\%) & Controlled diabetic patients (\%) & Uncontrolled diabetic \mbox{}\protect\newline patients (\%)\\
\tblmidrule 
Hypertension &
  CCBs &
  21.44 &
  29.0 &
  16\\
 &
  \ensuremath{\beta }-Blockers &
  14.30 &
  14.37 &
  14.24\\
 &
  AT1-antagonists &
  19.40 &
  14.3 &
  22.72\\
 &
  ACE inhibitors &
  2.05 &
  4.12 &
  2.6\\
 &
  \ensuremath{\alpha }-Antagonist &
  2.05 &
  4.12 &
  2.6\\
 &
  Combinations &
  8.17 &
  9.25 &
  7.4\\
IHD &
  Clopidogrel &
  12.2 &
  9.4 &
  12.55\\
 &
  Aspirin &
  3.0 &
  6.6 &
  2.6\\
 &
  Combinations &
  4.0 &
  4.12 &
  4.084\\
Dyslipidaemia &
  Statins &
  19.3 &
  22.07 &
  17.63\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Drug Prescribing Pattern} }
\label{tw-2a0c6505418b}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.2868\linewidth-2\tabcolsep}p{\dimexpr.3731999999999999\linewidth-2\tabcolsep}p{\dimexpr.34\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}\multicolumn{3}{p{\dimexpr(1\linewidth-2\tabcolsep)}}{\cAlignHack Drug prescribing pattern}\\
\tblmidrule 
Items &
    Drugs &
  \% \\
\multicolumn{1}{p{\dimexpr(.2868\linewidth-2\tabcolsep)}}{\multirow{6}{\linewidth}{Drug Groups}} &
  Antidiabetic &
  22\%\\
 &
  Antihypertensives &
  15.5\%\\
 &
  Multivitamins &
  12.72\%\\
 &
  Antiplatelet &
  9.9\%\\
 &
  Statins &
  4.31\%\\
 &
  Miscellaneous category &
  35.5\%\\
\multicolumn{1}{p{\dimexpr(.2868\linewidth-2\tabcolsep)}}{\multirow{5}{\linewidth}{Antidiabetic drugs}} &
  Metformin &
   43.14\%\\
 &
  Glimepiride &
   8.83\%\\
 &
  Vildagliptin &
   0.98\%\\
 &
  Sitagliptin &
   1.96\%\\
 &
  Insulin &
   42.16\%\\
Fixed Dose Combinations (FDCs) &
  Metformin + Glimepiride &
   3.9\%\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begingroup
\makeatletter\if@twocolumn\@ifundefined{theposttbl}{\gdef\TwoColDocument{true}\onecolumn\onecolumn}{}\fi\makeatother \setlength\LTcapwidth{\textwidth}
\begin{longtable}{p{\dimexpr.1443\linewidth-2\tabcolsep}p{\dimexpr.1894\linewidth-2\tabcolsep}p{\dimexpr.13370000000000001\linewidth-2\tabcolsep}p{\dimexpr.11510000000000005\linewidth-2\tabcolsep}p{\dimexpr.4175\linewidth-2\tabcolsep}}
\caption{\boldmath {Demographic Details of Study Population } }
\label{tw-bad6f3c84335}
\def\arraystretch{1.1}\\\endfirsthead \hline \noalign{\vskip3pt} \noalign{\textit{Table \thetable\ continued}} \noalign{\vskip3pt} 
\tbltoprule \rowcolor{kwdboxcolor}S.No & IP.No & Age & Sex & Reasons For Admission\\
\tblmidrule \endhead \hline \noalign{\vskip3pt} \noalign{\textit{\hfill Continued on next page}} \noalign{\vskip3pt} \endfoot \endlastfoot 
\tbltoprule \rowcolor{kwdboxcolor}S.No & IP.No & Age & Sex & Reasons For Admission\\
\tblmidrule 
1 &
  23751 &
  76 &
  M &
  low back pain, fever for 10 days, generalized body weakness\\
2 &
  28186 &
  57 &
  F &
  fever, redness 15 days, c/ o~diffuse swelling in the left foot.\\
3 &
  27467 &
  64 &
  M &
  sudden onset of weakness in left UL and LL\\
4 &
  26840 &
  35 &
  M &
  Giddiness \& profuse sweating\\
5 &
  25420 &
  60 &
  M &
  Acute abdominal pain, constipation, nausea \& vomiting, SOB\\
6 &
  28001 &
  54 &
  F &
  Fever with chills \& rigours \\
7 &
  28002 &
  47 &
  F &
  Fever with cold \& cough with sputum, abdominal pain loose stools\\
8 &
  27751 &
  78 &
  F &
  Giddiness increased with a change in head position,\\
9 &
  27791 &
  34 &
  M &
  Generalised weakness, difficulty in climbing up stairs\\
10 &
  28195 &
  40 &
  F &
  High-grade fever with chills, headache, vomiting pains\\
11 &
  28083 &
  43 &
  M &
  Fever associated with headache, generalised body pains\\
12 &
  26116 &
  77 &
  M &
  loss of speech with right UL weakness since 3D\\
13 &
  28213 &
  52 &
  M &
  unconscious state associated with sweating, loose stools, and fever for 1 day.\\
14 &
  28128 &
  36 &
  M &
  fever on \& off associated with expectoration, black stools.\\
15 &
  28109 &
  76 &
  M &
  vomiting, slurred, slurred speech, generalised weakness, and chest pain.\\
16 &
  28761 &
  68 &
  M &
  pain in the abdomen, previously had seizures\\
17 &
  27573 &
  48 &
  F  &
  chest pain, SOB associated with sweating, pain at left radiating.\\
18 &
  27333 &
  55 &
  M &
  Sudden onset of giddiness, fall at home, fever.\\
19 &
  26180 &
  57 &
  F &
  Abdominal pain at right hypochondria fever\\
20 &
  27765 &
  79 &
  F &
  left UL \& LL weakness, loose stools.\\
21 &
  27346 &
  58 &
  M &
  right-sided weakness in both UL \& LL associated with mouth deviation\\
22 &
  28275 &
  65 &
  M &
  jaundice, fever, coloured urine\\
23 &
  22491 &
  55 &
  M &
  retrosternal \& epigastric burning associated with sweating\\
24 &
  27922 &
  62 &
  F &
  generalizes weakness \& history of reduced sleep, and joint pains.\\
25 &
  28496 &
  50 &
  M &
  hoarseness in voice, walking at 3 a.m. to the toilet \& unconscious\\
26 &
  25680 &
  42 &
  F &
  abdominal distention, pain in abdomen\\
27 &
  27577 &
  47 &
  M &
  Black-coloured stools, vomiting\\
28 &
  21641 &
  38 &
  F &
  lower abdominal pain, chest discomfort, SOB, mild giddiness\\
29 &
  28992 &
  38 &
  F &
  severe knee joint pain (right side), fever, loose stools\\
30 &
  21660 &
  64 &
  M &
  Fever, cough with expectoration in the last 3-4 days\\
31 &
  27798 &
  75 &
  M &
  giddiness associated with LOC\\
32 &
  28640 &
  64 &
  M &
  weakness of left UL\&LL, slurring of speech with a deviation of the mouth\\
33 &
  23307 &
  65 &
  M &
  Fever with chills \& rigours, body aches in the last 3 months\\
34 &
  26781 &
  53 &
  F &
  pain in the left hip, bed sores grade 2 on the right gluteal region\\
35 &
  26661 &
  68 &
  F &
  breathlessness on exertion, fatigue, dull, intermediate palpitation \\
36 &
  28368 &
  68 &
  M &
  giddiness,1-episode seizure\\
37 &
  28357 &
  55 &
  M &
  non-healing ulcer over left toe in the last 1 month\\
38 &
  28625 &
  64 &
  M &
  multiple episodes of loose stools, cramps\& abdominal pain\\
39 &
  26722 &
  55 &
  M &
  sudden onset of left half-body paraesthesia decreased sensation\\
40 &
  27572 &
  78 &
  F &
  slurring of speech, mouth deviated to the right side\\
41 &
  27368 &
  50 &
  F &
  sudden giddiness\& chest discomfort \\
42 &
  28188 &
  38 &
  M &
  F/U/C of post left URSL+ DJS\\
43 &
  28056 &
  56 &
  M &
  High-grade fever, bleeding manifestation like rashes \& joint pains\\
44 &
  26367 &
  70 &
  F &
  Low-grade fever, cough, loss of appetite\\
45 &
  28013 &
  36 &
  M &
  nephrotic syndrome, old PTE, came for renal biopsy.\\
46 &
  26655 &
  70 &
  F &
  fever, dry cough, and body pains since 10D\\
47 &
  26667 &
  34 &
  M &
  Worsening, weakness, difficulty in sitting and walking, weight loss:10kgs\\
48 &
  27602 &
  58 &
  F &
  uncontrolled sugar, leg pain, heaviness in chest.\\
49 &
  27673 &
  44 &
  M &
  loose stools, pain in the abdomen, post renal transplant.\\
50 &
  28043 &
  36 &
  M &
  came for a renal biopsy\\
51 &
  28994 &
  68 &
  M &
  Fever, Left leg pain\\
52 &
  29016 &
  25 &
  M &
  right radio cephalic fistula\\
53 &
  28289 &
  56 &
  M &
  AV fistula constriction\\
54 &
  28732 &
  60 &
  F &
  SOB, orthopnoea, chest discomfort\\
55 &
  28955 &
  58 &
  F &
  Headache, generalised weakness, Dysarthria.\\
56 &
  28676 &
  56 &
  M &
  Fell at his home and sustained injury over his Left face, Chest and Knee\\
57 &
  26736 &
  58 &
  F &
  SOB, Vomiting, Typical Chest Pain.\\
58 &
  28696 &
  61 &
  F &
  AV fistula constriction\\
59 &
  28337 &
  48 &
  M &
  Pain and weakness in right ankle, painful flexion\\
60 &
  28004 &
  36 &
  F &
  Left-sided chest pain radiating to Arm.\\
61 &
  28843 &
  66 &
  M &
  SOB and Bilateral Pedal Edema.\\
62 &
  28344 &
  53 &
  M &
  Hematemesis,Malena,SOB Grade II\\
63 &
  28930 &
  85 &
  M &
  Weakness, unresponsiveness, sensorium.\\
64 &
  28849 &
  54 &
  M &
  Abdominal Pain.\\
65 &
  28056 &
  56 &
  M &
  High-Grade fever.\\
66 &
  28274 &
  55 &
  F &
  High-grade fever with chills and rigours, Dry Cough.\\
67 &
  27981 &
  66 &
  M &
  Unconscious\\
68 &
  28991 &
  70 &
  M &
  Fever with chills, rigours, giddiness.\\
69 &
  28936 &
  68 &
  F &
  SOB, vomiting, Epigastric discomfort.\\
70 &
  28489 &
  64 &
  M &
  Fever, Burning Micturition admitted for cystoscopy.\\
71 &
  28858 &
  57 &
  F &
  Chest discomfort, SOB, Orthopnoea.\\
72 &
  28429 &
  61 &
  M &
  Pain in the right shoulder.\\
73 &
  28857 &
  56 &
  M &
  Orthopnoea, chest discomfort.\\
74 &
  28619 &
  65 &
  F &
  unresponsive state, sensorium\\
75 &
  28956 &
  58 &
  M &
  headache. generalizes weakness, and dysarthria.\\
76 &
  28675 &
  49 &
  M &
  admitted for AV fistula constriction\\
77 &
  28799 &
  59 &
  M &
  complete body ache, abdominal discomfort, low back pain\\
78 &
  28716 &
  53 &
  M &
  bilateral oedema, abdominal distention, scrotal swelling\\
79 &
  27854 &
  53 &
  M &
  upper abdominal pain associated with vomiting, and fever.\\
80 &
  27361 &
  61 &
  M &
  acute urinary retention, dysuria\\
81 &
  26245 &
  61 &
  F &
  fever, cough with sputum, weakness, SOB on excretion.\\
82 &
  27502 &
  57 &
  F &
  Syncope with sweating, palpitation\\
83 &
  28064 &
  67 &
  M &
  Unresponsive state, not moving limbs.\\
84 &
  26612 &
  78 &
  M &
  SOB on exertion, cough with sputum, oedema on both legs.\\
85 &
  28083 &
  38 &
  M &
  Fever with chills, General body pains, Headache.\\
86 &
  28635 &
  54 &
  F &
  Recurrent attacks of pyelonephritis\\
87 &
  27989 &
  61 &
  F &
  Fever, chest pain, lower back pain, vomiting, Right cheek swelling.\\
88 &
  27575 &
  65 &
  M &
  SOB.\\
89 &
  27460 &
  60 &
  F &
  Fever, cough, weakness, headache, LOC.\\
90 &
  27745 &
  60 &
  M &
  Fever, SOB, Sleep disturbance.\\
91 &
  27705 &
  53 &
  M &
  pain in the abdomen, radiating to right loin, vomiting 2 episodes.\\
92 &
  26604 &
  71 &
  M &
  cough with sputum, pain in the lower abdomen\\
93 &
  26661 &
  68 &
  M &
  difficulty in breathing.low abdominal pain, dark stools\\
94 &
  21733 &
  52 &
  M &
  fever, swelling of feet, generalised weakness, loss of appetite\\
\tblbottomrule 
\end{longtable}
\endgroup
\makeatletter\@ifundefined{TwoColDocument}{}{\twocolumn}\makeatother 

\begingroup
\makeatletter\if@twocolumn\@ifundefined{theposttbl}{\gdef\TwoColDocument{true}\onecolumn\onecolumn}{}\fi\makeatother \setlength\LTcapwidth{\textwidth}
\begin{longtable}{p{\dimexpr.2267\linewidth-2\tabcolsep}p{\dimexpr.25\linewidth-2\tabcolsep}p{\dimexpr.23009999999999998\linewidth-2\tabcolsep}p{\dimexpr.2932\linewidth-2\tabcolsep}}
\caption{\boldmath {Demographic details of the study population} Drug Interactions }
\label{tw-a994bb0b238a}
\def\arraystretch{1.1}\\\endfirsthead \hline \noalign{\vskip3pt} \noalign{\textit{Table \thetable\ continued}} \noalign{\vskip3pt} 
\tbltoprule \rowcolor{kwdboxcolor}IP No & Drug Interactions & DI Effects & Severity\\
\tblmidrule \endhead \hline \noalign{\vskip3pt} \noalign{\textit{\hfill Continued on next page}} \noalign{\vskip3pt} \endfoot \endlastfoot 
\tbltoprule \rowcolor{kwdboxcolor}IP No & Drug Interactions & DI Effects & Severity\\
\tblmidrule 
23751 &
  Azithromycin + Ondansetron &
  both increase Qt, CHF, bradycardia, and electrolyte imbalance &
  Serious\\
28186 &
  Linezolid + Tramadol &
  both increase serotonin levels, monitor CNS \& renal toxicity &
  Serious\\
27467 &
  Labetalol + Amlodipine &
  both increase antiHTN channel blocking &
  Significant\\
26840 &
  Biseprolol+ Amlodipine/Biseprolol+ Kcl &
  anti-HTN blocking/increases Sr. K+ &
  Significant\\
25420 &
  Ofloxacin + Metformin &
  increases the effect of metformin by the PD effect. &
  Significant\\
28001 &
  Pantoprazole + Clopidogrel &
  decreases the effect of clopidogrel by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
28002 &
  NO &
  NO &
  No\\
27751 &
  Losartan + Aspirin &
  increases Sr.K+ levels, renal function deterioration &
  Significant\\
27791 &
  NO &
  NO &
  No\\
28195 &
  Azithromycin + Ondansetron &
  both increase Qt, CHF,  bradycardia, and electrolyte imbalance &
  Serious\\
28083 &
  Escitalopram + Clopidogrel &
  risk of bleeding &
  Significant\\
26116 &
  NO &
  NO &
  Minor\\
28213 &
  NO &
  NO &
  No\\
28128 &
  Clarithromycin + Amlodipine &
  increases the effect of Amlodipine enzyme CYP3A4 metabolism &
  Significant\\
28109 &
  Cinnarizine + Prochlorperazine &
  increases sedation &
  Significant\\
28761 &
  NO &
  NO &
  No\\
27573 &
  Ceftriaxone + Enoxaparin &
  increases anticoagulant of enoxaparin &
  Serious\\
27333 &
  Pantaprazole + Clopidogrel &
  decreases the effect of clopidogrel by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
26180 &
  NO &
  NO &
  No\\
27765 &
  Telmisartan + Atorvastatin &
  increases myopathy &
  Significant\\
28275 &
  Metronidazole + Acetaminophen &
  increases PD effect &
  Minor\\
22491 &
  Heparin + Aspirin &
  increases anticoagulant &
  Significant\\
27922 &
  Aspirin + Glimepiride &
  increases the effect of glucose by an unknown mechanism &
  Significant\\
27922 &
  Aspirin + Glimepiride &
  increases the effect of glucose by an unknown mechanism &
  Significant\\
28496 &
  NO &
  NO &
  No\\
25680 &
  NO &
  NO &
  No\\
27577 &
  Fluconazole + Ondansetron &
  increases QTC interval &
  Serious\\
21641 &
  NO &
  NO &
  No\\
27798 &
  Bisoprolol + Amlodipine &
  both increase antiHTN channel blocking &
  Significant\\
28640 &
  Telmisartan + Atorvastatin &
  increases toxicity of atorvastatin &
  Significant\\
23307 &
  Hydrocortisone + Levofloxacin &
  both increase the synergism. &
  Significant\\
26781 &
  NO &
  NO &
  No\\
26661 &
  Levofloxacin + Metformin &
  increases the effect of metformin by PD synergism &
  Significant\\
28368 &
  NO &
  NO &
  No\\
28357 &
  Ofloxacin + Metformin &
  increases the effect of metformin by the PD effect. &
  Significant\\
28625 &
  Pantoprazole + Clopidogrel &
  decrease the effect of clopidogrel by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
26722 &
  Pantoprazole + Clopidogrel &
  decrease the effect of clopidogrel by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
27572 &
  Losartan + Carvedilol &
  both increase serum potassium &
  Significant\\
27368 &
  Pantoprazole + Clopidogrel &
  decrease the effect of clopidogrel by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
28188 &
  NO &
  NO &
  No\\
28056 &
  Sodium Bicarbonate + Azithromycin &
  decreases the level of azithromycin by inhibition of GI absorption &
  Significant\\
26367 &
  Pantoprazole + Dabigatran &
  increases the level of dabigatran by P-Glycol protein(MDR1) &
  Significant\\
28013 &
  Aspirin + Furosemide &
  increases and decreases serum potassium &
  Significant\\
26655 &
  Pantoprazole + Budesonide &
  decreases the effect of budesonide by increasing gastric Ph &
  Significant\\
28043 &
  Metformin + Furosemide &
  decreases the level of Furosemide by an unspecified mechanism &
  Minor \mbox{}\protect\newline \\
28289 &
  Clonidine + Metoprolol &
  increases the risk of bradycardia &
  Serious\\
28732 &
  Telmisartan+Atorvastatin &
  increases the risk of myopathy &
  Significant\\
28676 &
  Pantaprazole+Cyanocobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Minor\\
26736 &
  Na Bicarbonate+Levofloxacin &
  decreases the level of levofloxacin by inhibition of GI absorption &
  Serious\\
28696 &
  No &
  NO &
  No\\
28337 &
  Rantidine+Cyanocobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Minor\\
28004 &
  Olmisartan+Aspirin &
  increases serum potassium levels &
  Significant\\
28843 &
  Aspirin+Prasugrel &
  increases the toxicity by PD synergism &
  Significant\\
28344 &
  Octreotide+Ondansetron &
  both increase the QT interval &
  Serious\\
28930 &
  Carvedilol+ Hydralazine &
  increases the effect of carvedilol by PD synergism &
  Significant\\
28849 &
  Isoniazide+Ondansetron &
  CYP-450 inhibitor may decrease the clearance of ondansetron &
  Significant\\
28056 &
  Azithromycin + Ondansetron &
  increases QTC interval &
  Serious\\
28274 &
  Pantaprazole+Cyanacobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Minor\\
27981 &
  Pantaprazole+Clopidogrel &
  decreases the effect by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
28991 &
  No &
  NO &
  No\\
28936 &
  Pantaprazole+Cyanacobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Significant\\
28489 &
  Piperacillin+Amikacin &
  increases the effect of amikacin by PD synergism &
  Minor\\
28858 &
  Olmisartan+Telmisartan &
  increases serum potassium levels &
  Significant\\
28429 &
  Metoprolol+Cyanocobalamine &
  decreases the level of cyanocobalamin by an unexpected mechanism &
  Minor\\
28857 &
  No &
  NO &
  No\\
28619 &
  Atorvastatin+Azithromycin &
  increases the level of azithromycin by P-Glycol protein(MDR1) &
  Significant\\
28956 &
  Telmisartan+Atorvastatin &
  increases the risk of myopathy &
  Significant\\
28675 &
  Biseprolol+ Amlodipine/Biseprolo+ Kcl &
  increases and decreases serum potassium &
  Significant\\
28799 &
  No &
  NO &
  No\\
28716 &
  Aspirin+Furosemide &
  increases and decreases serum potassium &
  Significant\\
27854 &
  No &
  NO &
  No\\
27361 &
  Diclofenac+Budesonide &
  increases toxicity by PD synergism &
  Significant\\
26245 &
  Pantaprazole+Clopidogrel &
  decreases the effect by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
27502 &
  Azelastine+Cinnerizine &
  increases sedation &
  Significant\\
28064 &
  Pantaprazole+Cyanacobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Significant\\
26612 &
  Pantaprazole+Clopidogrel &
  decreases the effect by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
28083 &
  Atorvastatin+Azithromycin &
  increases the level of azithromycin by P-Glyco protein (MDR1) &
  Significant\\
28635 &
  Metformin+Furosemide &
  decreases the level of furosemide by an unknown mechanism &
  Minor\\
27989 &
  Pantaprazole+Clopidogrel &
  decreases the effect by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
27575 &
  Telmisartan+Furosemide &
  increases and decreases serum potassium &
  Significant\\
27460 &
  Azithromycin + Ondansetron &
  both increase the QTc interval &
  Serious\\
27745 &
  Budesonide+Hydrocortisone &
  decreases the level of hydrocortisone by affecting CYP3A4 metabolism &
  Significant\\
27705 &
  Pantaprazole+Clopidogrel &
  decreases the effect by affecting the hepatic enzyme CYP2C19 metabolism &
  Significant\\
26604 &
  Ceftizoxime+Furosemide &
  increases the toxicity of furosemide by PD synergism &
  Minor\\
26661 &
  Ramipril+Glimeperide &
  increases the effect of glimepiride by PD synergism &
  Significant\\
21733 &
  Pantoprazole + Cyanocobalamine &
  decreases the level of cyanocobalamin by inhibiting GI absorption &
  Significant\\
22474 &
  Levodopa+Amlodipne &
  increases the effect of amlodipine by PD synergism &
  Significant\\
26304 &
  No &
  NO &
  No\\
27822 &
  Telmisartan+Metoprolol &
  both decrease the serum potassium level &
  Significant\\
\tblbottomrule 
\end{longtable}
\endgroup
\makeatletter\@ifundefined{TwoColDocument}{}{\twocolumn}\makeatother 

\begin{table*}[!htbp]
\caption{\boldmath {Based on Gender} }
\label{tw-0f8761575a11}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.2735\linewidth-2\tabcolsep}p{\dimexpr.38650000000000006\linewidth-2\tabcolsep}p{\dimexpr.34\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Gender & No of patients & Percentage\\
\tblmidrule 
Male &
  62 &
  60.30\%\\
Female &
  32 &
  32.90\%\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Based on Age} }
\label{tw-430c1836c299}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.2802\linewidth-2\tabcolsep}p{\dimexpr.37980000000000004\linewidth-2\tabcolsep}p{\dimexpr.34\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Age & No of patients & Percentage\\
\tblmidrule 
25-35 &
  5 &
  5.00\%\\
35-45 &
  11 &
  11.00\%\\
45-55 &
  22 &
  23.00\%\\
55-65 &
  33 &
  33.00\%\\
65-75 &
  16 &
  16.00\%\\
75-85 &
  7 &
  7.00\%\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Based on Common Comorbidity} }
\label{tw-4520b115bb00}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.50\linewidth-2\tabcolsep}p{\dimexpr.50\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Common Comorbidity & No of Patients\\
\tblmidrule 
Hypoglycemia &
  4\\
UTI &
  10\\
RTI &
  4\\
CAD &
  9\\
CVA &
  4\\
Hypothyroidism &
  15\\
CKD &
  17\\
HTN &
  77\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Based on Common Oral Hypoglycemics} }
\label{tw-cce5dee3183c}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.4535\linewidth-2\tabcolsep}p{\dimexpr.5465\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Drugs & No of Patients\\
\tblmidrule 
Metformin &
  44\\
Glimepiride &
  10\\
Sitagliptin &
  3\\
Vildagliptin &
  2\\
Metformin +Glimepiride &
  5\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Based on types of Insulin used in Type 2 DM} }
\label{tw-ffc4934a2d12}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.5133\linewidth-2\tabcolsep}p{\dimexpr.4867\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Insulin & No of Patients\\
\tblmidrule 
Sanctus &
  2\\
Human Mixtard insulin &
  26\\
Human Actrapid insulin &
  16\\
HMI+HAI &
  3\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\begin{table*}[!htbp]
\caption{\boldmath {Based on Severity of Drug Interaction} }
\label{tw-de52f5db4311}
\def\arraystretch{1.1}
\ignorespaces 
\centering 
\begin{tabulary}{\linewidth}{p{\dimexpr.4834\linewidth-2\tabcolsep}p{\dimexpr.5166\linewidth-2\tabcolsep}}
\tbltoprule \rowcolor{kwdboxcolor}Severity & No of Cases\\
\tblmidrule 
Significant &
  52\\
Serious &
  9\\
No &
  24\\
Minor &
  9\\
\tblbottomrule 
\end{tabulary}\par 
\end{table*}

\bgroup
\fixFloatSize{images/a615c29a-65db-40c6-96f0-57d1ab680c80-upicture2.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/a615c29a-65db-40c6-96f0-57d1ab680c80-upicture2.png}{\includegraphics{images/a615c29a-65db-40c6-96f0-57d1ab680c80-upicture2.png}}{\includegraphics{a615c29a-65db-40c6-96f0-57d1ab680c80-upicture2.png}}
\makeatother 
\caption{\boldmath {Based on Gender}}
\label{f-735d3b8826a3}
\end{figure}
\egroup

\bgroup
\fixFloatSize{images/aa6e4118-0cd4-44ce-b8ee-9b667db8022d-upicture3.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/aa6e4118-0cd4-44ce-b8ee-9b667db8022d-upicture3.png}{\includegraphics{images/aa6e4118-0cd4-44ce-b8ee-9b667db8022d-upicture3.png}}{\includegraphics{aa6e4118-0cd4-44ce-b8ee-9b667db8022d-upicture3.png}}
\makeatother 
\caption{\boldmath {Based on Age}}
\label{f-41c79280a5ac}
\end{figure}
\egroup

\bgroup
\fixFloatSize{images/7f16567d-1bb1-4a2c-b74e-883d0a95f3e3-upicture4.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/7f16567d-1bb1-4a2c-b74e-883d0a95f3e3-upicture4.png}{\includegraphics{images/7f16567d-1bb1-4a2c-b74e-883d0a95f3e3-upicture4.png}}{\includegraphics{7f16567d-1bb1-4a2c-b74e-883d0a95f3e3-upicture4.png}}
\makeatother 
\caption{\boldmath {Based on Common Comorbidities}}
\label{f-a6bb21e6ddd6}
\end{figure}
\egroup

\bgroup
\fixFloatSize{images/290caeff-2b0e-49c3-9c53-6d3a4169e546-upicture5.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/290caeff-2b0e-49c3-9c53-6d3a4169e546-upicture5.png}{\includegraphics{images/290caeff-2b0e-49c3-9c53-6d3a4169e546-upicture5.png}}{\includegraphics{290caeff-2b0e-49c3-9c53-6d3a4169e546-upicture5.png}}
\makeatother 
\caption{\boldmath {Based on common Oral Hypoglycemics}}
\label{f-4da683148997}
\end{figure}
\egroup

\bgroup
\fixFloatSize{images/4338522a-3987-41a4-af1e-743a493519b0-upicture6.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/4338522a-3987-41a4-af1e-743a493519b0-upicture6.png}{\includegraphics{images/4338522a-3987-41a4-af1e-743a493519b0-upicture6.png}}{\includegraphics{4338522a-3987-41a4-af1e-743a493519b0-upicture6.png}}
\makeatother 
\caption{\boldmath {Based on types of Insulin used in Type 2 DM}}
\label{f-957578877e6e}
\end{figure}
\egroup

\bgroup
\fixFloatSize{images/180c1742-0b3f-4acc-804d-cdcb4a97759b-upicture7.png}
\begin{figure}[!htbp]
\centering \makeatletter\IfFileExists{images/180c1742-0b3f-4acc-804d-cdcb4a97759b-upicture7.png}{\includegraphics{images/180c1742-0b3f-4acc-804d-cdcb4a97759b-upicture7.png}}{\includegraphics{180c1742-0b3f-4acc-804d-cdcb4a97759b-upicture7.png}}
\makeatother 
\caption{\boldmath {Based on Severity of Drug Interaction}}
\label{f-a327341e554b}
\end{figure}
\egroup
The challenges a physician treating diabetes patients faces are exacerbated by both the unique and general characteristics of these patients, such as the dose forms that are available, the unanticipated administration of medications to patients, reported drug interactions, and typical co-morbidities encountered in diabetic patients. The study was created to aid in reducing prescription errors, providing safe dosage regimens, teaching the patients by closely monitoring the patients' glycaemic control and other responses to medication, and ultimately promoting the judicious and sensible use of pharmaceuticals [Tables~\ref{tw-0013a2adc047} and~\ref{tw-54717dae9f17}].

\textbf{Method and Collection of Data}

\textbf{Study site}

The study conducted at Medicine ward of Gleneagles Aware Global Hospital LB. Nagar.

\textbf{Study duration}

The study was conducted for six months from October 2017 to March 2018 \unskip~\cite{2106768:29287993}.

\textbf{Study design}

It is a prospective observational study conducted on diabetes mellitus patients.

\textbf{Study criteria}

The following study is carried out using the following factors,

\textbf{Inclusion criteria }


  
  \begin{enumerate}
  \item \relax Patients with diabetes for at least 1 year.
  \item \relax Patients with diabetic complications.
  \item \relax Patients with other co-morbid conditions \unskip~\cite{2106768:29288003,2106768:29287998}.
  \end{enumerate}
  \textbf{Exclusion criteria }

\textbf{Pregnant women and nursing mothers.}

\textbf{Study Procedure}

This is a prospective observational study conducted over six months. The study was conducted at Medicine ward of Gleneagles Aware Global Hospital LB. Nagar. Patients who were admitted to the Medicine ward of the hospital and those visiting OPD for six months from October 2017 to March 2018 are enrolled. Diabetic patients visiting the endocrinologist are evaluated, diagnosed, and prescribed suitable therapy. Using a suitable data collection form, the following details collected are patient demographics, prescription charts, lab data, progress charts, medical records, doctor's notes, and nursing notes \unskip~\cite{2106768:29288005}.
    
\section{Results}
This investigation was carried out in a tertiary care hospital's IPDs for diabetesology as well as general medicine. Participants in this study had to have type 2 diabetes for at least a year and be between the ages of 25 and 85, regardless of their gender. Patients older than 85 years old were eliminated due to the increasing occurrence of other co-existing illness conditions. Data were gathered from 98 diabetic patients' profile sheets who visited the OPD and IPD over the study's six-month period, from October 2017 to March 2018 [Tables~\ref{tw-58e4fe9da37f} and~\ref{tw-2a0c6505418b}].

Records are used to gather information on patient demographics, blood glucose and HbA1C levels, diagnoses, and medications administered [Tables~\ref{tw-bad6f3c84335} and~\ref{tw-a994bb0b238a}].

Patients were categorised as having controlled fasting blood sugar (FBS) 110 mg/dL/HbA1C 7 or having uncontrolled diabetes (FBS {\textgreater}110 mg/dL/HbA1C {\textgreater}7) based on the blood glucose levels and HbA1C. The prescription patterns for medicines in managed and uncontrolled diabetics with additional co-morbid illnesses were discovered using a descriptive analysis of the data. 62 (64.3\%) of the 94 patients were men, and 32 (35.7\%) were women, with respective mean ages of 58.06 11.13 as well as 57.08 12.58 years. 37 patients in our study population had diabetes that was under control, while 57 patients were not [Tables~\ref{tw-0f8761575a11} and~\ref{tw-430c1836c299}].

In the population that was under control, the meantime that type 2 diabetes persisted was 5.57 2.98 years, but in the uncontrolled group, it was 7.18 5.8 years [Tables~\ref{tw-4520b115bb00} and~\ref{tw-cce5dee3183c}]. 

The most prevalent cardiovascular comorbidity among diabetes patients was systemic hypertension, with a frequency of 78.6\%. Among these individuals, 22\% had IHD as well as 4\% had dyslipidemia concomitant.IHD (49\%) and dyslipidaemia (21\%) came after systemic hypertension. In patients, 18.35\% have hypothyroidism and 20\% have CKD [Tables~\ref{tw-ffc4934a2d12} and~\ref{tw-de52f5db4311}].

Additionally, aspirin was given to 4.1\% of IHD patients, while 5.1\% of patients also received clopidogrel. Statins were prescribed for all dyslipidemic individuals.

The patients with managed diabetes received higher CCB prescriptions. More individuals with uncontrolled diabetes than those with managed diabetes used combination antihypertensive medications. Only patients with uncontrolled diabetes received prescriptions for AT1 receptor blockers. individuals with uncontrolled diabetes received more prescriptions for clopidogrel, whereas individuals with managed diabetes received more prescriptions for aspirin. 

The mean number of cardiovascular medications was found to be 1.12 0.58 among diabetics who were under control, compared to 1.52 1.10 in those who were not. The greater rate of uncontrolled diabetic patients may be a result of patients' poor adherence to therapy, lack of knowledge, and education. This could result in the need for extra medications or drug combinations to manage them. 

\textbf{Comorbid Conditions}

Throughout the trial, 450 different medications were prescribed. Prescriptions for 101 (22\%) anti-diabetics, 70 (15.5\%) anti-hypertensives, 55 (12.72\%) multivitamins, 44 (9.9\%) anti-platelets, 18 (4.31\%) statins, and 162 (35.5\%) other medications were written. 42 (43.14\%) of the patients receiving antidiabetics were administered metformin, 8 (8.83\%) were prescribed glimepiride, 2 (1.96\%) were prescribed sitagliptin, 1 (0.98\%) were prescribed vildagliptin, and 41 (42.16\%) were prescribed insulin. The most frequently administered FDC (4, 3.9\%) was metformin plus glimepride.


    
\section{DISCUSSION}
Males (62.30\%) and females (32.90\%), respectively, made up the study's gender and age distributions. The age ranges were 25{\textendash}35 years (5\%), 35{\textendash}45 years (11\%) 45{\textendash}55 years (23\%) 55{\textendash}65 years (33\%) 65{\textendash}75 years (16\%), and 75{\textendash}85 years (7\%). The comorbid illnesses identified in the 94 instances in total were hypertension, hypothyroidism, chronic renal disease, urinary tract infections, and coronary artery disease.

Throughout the trial, 450 different medications were prescribed. Prescriptions for 101 (22\%) anti-diabetics, 70 (15.5\%) anti-hypertensives, 55 (12.72\%) multivitamins, 44 (9.9\%) anti-platelets, 18 (4.31\%) statins, and 162 (35.5\%) other medications were written.

42 (43.14\%) of the patients receiving antidiabetics were administered metformin, 8 (8.83\%) were prescribed glimepiride, 2 (1.96\%) were prescribed sitagliptin, 1 (0.98\%) were prescribed vildagliptin, and 41 (42.16\%) were prescribed insulin. The most frequently administered FDC (4, 3.9\%) was metformin plus glimepride. In addition, aspirin was given to 4.1\% of IHD patients, while 5.1\% of patients received both clopidogrel and aspirin. Statins were given to every patient with dyslipidemia. Individuals with uncontrolled diabetes were more likely to be administered clopidogrel, whereas individuals with managed diabetes were more likely to be prescribed aspirin. 

In patients with managed diabetes, CCBs were more frequently prescribed. those with uncontrolled diabetes used combination antihypertensive medications more frequently than those with managed diabetes. Only those patients with uncontrolled diabetes received prescriptions for AT1 receptor blockers. The greater proportion of uncontrolled diabetes patients may be a result of their poor adherence to therapy, lack of knowledge, and education. To treat their comorbid diseases, extra medications or drug combinations can be required as a result.

The drug interactions that were discovered were categorised according to their severity as follows: 24 study population patients did not experience any drug interactions, 52 significant interactions, 9 serious interactions, and 9 mild interactions.

Standard treatment, which demonstrated effective control of the disease Diabetes + Hypertension, was as follows: 


  
  \begin{enumerate}
  \item \relax \ensuremath{\beta }-Blockers (15.31\%) e.g. Metoprolol 
  \item \relax Ca\ensuremath{^{+2 }} channel blockers (22.45\% usage) e.g. Amlodipine 
  \item \relax Biguanides (43\%) e.g. Metformin
  \item \relax Human Mixtard Insulin (25\%)
  \end{enumerate}
  
    
\section{CONCLUSION}
In the final report, which was compiled from 94 patients with diabetes mellitus type II as the primary illness, hypertension was identified as the most common co-morbid condition (74 instances). 
    
\section{ACKNOWLEDGEMENT}
The corresponding author desires to express gratitude to Dr. G. Rajeswari (Principal), Department of Pharmacology, Saastra College of Pharmaceutical Education \& Research, Jwalamukhi temple, Varigonda, Nellore,  India for her guidance and constant support in completing this research work.

\textbf{Conflict of Interest}

The author declares there is no conflict of interest.

\textbf{Funding Support}

The author declares there is no funding support.
    
\balance 

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