MIASMATIC EVALUATION OF HYPERLIPIDEMIA

MIASMATIC EVALUATION OF HYPERLIPIDEMIA

by

Dr SHEENA K.N Dissertation Submitted to Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment of the requirements for the degree of

Doctor of Medicine in Organon of Medicine and Homoeopathic Philosophy Under the guidance of Dr ROSHAN PINTO DE PART ME NT OF O RGAN ON OF ME DICINE AND HOMOE OPAT HIC P HI LO SOP HY, FAT HE R M ULLE R HOMOE O PAT HIC ME DICA L COL LE GE , DE RA LAKAT T E , MANGAL ORE

2011 i

CERTIFICATE BY THE GUIDE This is t o cert ify t hat t he d issert at io n ent it led “MIASMATIC EVALUATION OF HYPERLIPIDEMIA” is a bo nafid e research wo rk do ne by Dr SHEENA K .N und er my gu id ance and sup er visio n dur ing t he year 2008 – 201 1, in part ia l fu lfillment o f t he requ ir ement fo r t he award o f t he degree o f “DO CTOR O F MEDICINE” (ORGANON OF MEDICINE AND HOMOEOPATH IC PH ILOSOPH Y) . I

have

sat isfied

myself

reg ard ing

t he

aut hent icit y

of

her

o bser vat io ns no t ed in t his d issert at io n and it co nfo r ms t o t he st and ards o f Rajiv Gand hi Univer sit y o f Healt h Sciences, Kar nat aka, Bang alo re. It has no t been su bmit t ed (p art ial o r fu ll) fo r t he award o f any o t her Degr ee o r Dip lo ma.

Dr ROSHAN PINTO Date : Place: Mang alo re

MD (HOM)

Pr of ess or , D epar tment of Or ganon of M edicine a nd Homo eopathic Philos op hy, Father Muller H omo eopathic M edica l College a nd H osp ital ,

Deralak at t e, Mangalo r e

ii

DECLARATION BY THE CANDIDATE

I

her eby declare t hat

t his d issert at io n

ent it led

“MIASMATIC

EVALUATION OF HYPERLIPIDEMIA” is a bo nafide and g enu ine research wo rk carr ied o ut by me, u nd er t he gu idance o f Dr ROSHAN PINTO, Pro fesso r, Philo so p hy,

Depart ment d ur ing

t he

o f Organo n year

of

med icine

20 08–20 11,

in

and

p art ial

Ho mo eo pat hic fu lfillment

of

requ ir ement fo r t he award o f DOCTOR OF MEDICINE (ORGANON O F MEDICINE AND HOMOEOPATH IC PH ILOSO PHY) . I have no t previo u sly su b mit t ed t his wo rk (part ial o r fu ll) t o an y ot her u niver sit y fo r t he award o f any o t her Degree o r Dip lo ma.

Date: Place: Mang alo re

Dr SHEENA K .N

iii

ENDORSEMENT BY THE HOD, PRINCIPAL/ HEAD OF THE INSTITUTION This is t o cert ify t hat t he d issert at io n ent it led “MIASMATIC EVALUATION OF HYPERLIPIDEMIA” is a bo nafid e research wo rk carr ied o ut by Dr SHEENA K .N u nder t he gu idance and super vis io n o f Dr ROSHAN PINTO d ur ing t he year 20 08 – 2011, in part ial fu lfillment o f t he req u irement fo r t he award o f t he degree o f “DO CTOR O F MEDICINE” (ORGANON O F MEDICINE AND HOMOEO PATH IC PHILOSO PHY). We have sat isfied reg ard ing t he aut hen t ic it y o f her o bser vat io ns no t ed in t his d issert at io n and it co nfo r ms t he st and ards o f Rajiv Gand h i Universit y o f Healt h S ciences, Kar nat aka, Bangalo re. It has no t been su bmit t ed (part ial o r fu ll) fo r t he award o f a ny o t her Degree o r Dip lo ma.

HEAD O F THE DEPARTMENT

PRINCIPAL

Dr SHIVAPRASAD K . BSc, M D (H OM ) Professor, HOD, Dept . o f Organo n o f Med ic ine and Ho mo eo pat hic P hilo so ph y, Fr. Muller Homoeopathic Medical College, Deralakatte, Mangalore

Dr SRINATH RAO

Dat e:

Dat e:

MD (HOM)

Professor, HOD, Dept.of Materia Medica, Fr. Mu ller Ho mo eo pat hic, Medical College, Deralakatte, Mangalore

iv

P lace: Manga lo re

P lace: Manga lo re

COPYRIGHT

Declaration by the Candidate

I hereb y declare t hat t he Rajiv Gand hi University of H ea lth Sciences, K arnata ka, Bangalo re shall have t he r ig ht s t o preserve, u se and d isseminat e t his d issert at io n / t hesis in pr int o r elect ro nic fo r mat fo r acad emic / research purpo se.

Date: Place: Mang alo re

Dr SHEENA K .N

© Rajiv Gandhi University o f Hea lth Sciences, K arnata ka

v

Acknowledgement

I consid er this as my privileg e to thank the Almight y God, who is responsible for ever ything in my life, an d give him all the glory for th e accom plishment of m y post graduat e studies. I thank him for h elping me t o achieve this task thro ugh the follo wing perso ns who have b een of imm ense hel p and source of enco uragem ent in my end eavor . I would like to expr ess m y sin cer e and h ear tfelt thanks to my resp ect ed teach er and guide Dr Rosha n Pinto, Prof essor, Department of Organon of Medicin e

and Homo eopathic Philosoph y f or providing me exp ert guidan ce,

constructive advi ce, freedom of thought, per sonal attention, timely support and encourag em ent throughout m y post graduat e course and during the diss ertation work. It is my good fortune to do this wor k under his guidance. It is m y pri vileg e to express sincere gra titude to R ev. Fr P atrick Rodrigues,

Director,

FMCI

and

Rev.

Fr

Wilfred

Prakash

D’souza,

Administrator of Fr. Muller Homo eopathic Medi cal coll ege, Man galore fo r providing m e an opportunity and ad equat e f acilities to carry out this wor k to my satisfaction in this reputed institution. I would like to expr ess my gratitude to Dr Shashi Kant Tiwari former principal, who is and was a real source of inspiration and also Dr Srinath Rao, Prin cipal, Father Muller Homo eopathic Med ical College for his support whil e persuing my studies. I express m y sincere than ks to Dr Shivapr asad K , Vice prin cipal and Head of the Departm ent of Organon of Medi cine and Homo eopathic Philosophy, for his constant support, care and encouragement. I also express my gratitud e to Dr M. K. Kamath, PG Co-ordinator an d Head of th e D epartm ent of M edicin e, wh o wa s the man behind most acti vities of the postgraduates, guiding us to perfection.

vi

I o we m y sin cer e gratitude for all the help, and coop eration that I have received from my coll eagues of various d epartments of FMH MC of whick I cannot withhold th e nam es of few li ke D r Jacint ha Mont eiro, Dr Deena Monteiro, Dr Deepa Rebello, Dr Prabhukira n and Dr Josep h Tho mas. I must than k all my batchmates es pecially Dr Shalini and Dr Rekha for their companions hip, co operation and tim ely help which considerabl y eas ed my task. I attribute part of my success and st rength to them. A wor d of gratitud e to Mr Suresh and D r Shripathi Kalluraya for t eachin g statistical

application

and

r esear ch

h elp ing

to

formulat e

th e

R esear ch

Methodologi es for my synopsis and carry ou t the statistical wor k of my thesis. I

thank

all

the

m emb ers

of

no n-t eaching

staff

of

Fr.

Mull er

Homoeopathi c M edical Colleg e, esp ecially library staff for th eir promp t service and th e staff o f out patient depart ment and clini cal laboratory who ha s provided m e with the cas e material requir ed for the study. I would hav e n ever a ccom plished my go al without th e encourag em ent an d prayers of my par ents Mr K. Naraya na n & Mrs Rajalakshmi Naraya na n and my brother Mr Sreejith who is a world of en couragement and un derstanding to me. Special reg ards I carr y in my heart for my husb and Mr Salin Kumar and my b eloved son Vaishak Salin for their love and co -operation in every aspect of my life. Last but not the least, my sin cer e tha nks to all th e Patients o n whom th e study was conduct ed and MicroBits, Kan kanady for takin g pains for the successful and timely compl etion of this wor k. I thank all th e p ersons who have directly or indirectly influ enced m e fo r the better outco me of this work.

Place: Mangalore Date:

Dr SHEENA K.N

vii

Affectionately Dedicated To… My Family

viii

LIST OF ABBREVIATIONS

<

:

Aggravation

>

:

Amelioration

α

:

Alpha

ACTH

:

Adrenocorticotrophic hormone

AMP

:

Adenosine mono phosphate

APD

:

Acid peptic disease

Apo

:

Apoprotein

ASCVD

:

Artherosclerotic cardio vascular disease

ATP

:

Adenosine Tri phosphate

Av

:

Aversion

β

:

Beta

CAD

:

Coronary artery disease

CETP

:

Cholesteryl ester transfer protein

Chol

:

Total cholesterol

Co A

:

Co enzyme A

CP

:

Characteristic particulars

Cr

:

Craving

CVA

:

Cerebrovascular accident

DALY

:

Disability adjusted life year

DM

:

Diabetes Mellitus

DM

:

Dominant miasm ix

FA

:

Fatty acid

F/H

:

Family history

FM

:

Fundamental miasm

HDL

:

High density lipoproteins

HMG

:

Hydroxy methyl glutaryl

HS

:

At bed time

IDL

:

Intermediate density lipoprotein

LCAT

:

Lecithin cholesteryl acyl transferase

LDL

:

Low density lipoprotein

LPL

:

Lipoprotein lipase

MG

:

Mental generals

NAD

:

No abnormality detected

NADPH

:

Nicotinamide adenine dinucleotide phosphate

PG

:

Physical generals

P/H

:

Past history

Pkt

:

Packet

PVD

:

Peripheral vascular disease

S

:

Same

SCR

:

Standardized case record

TG

:

Triglyceride

TAG

:

Triacyl glycerol

VLDL

:

Very Low density lipoprotein

WHO

:

World Health Organization x

ABSTRACT

Background: Hyperlipidemia is regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol on atherosclerosis. It results from genetic predisposition interacting with an individual diet & lifestyle. Any defect in the synthesis, transport or excretion of the lipids causes a rise in their level in plasma which becomes a risk factor for coronary heart disease which is one of the major cause of death in the present day. Objective : 1. To study the different types of hyperlipidemia 2. To assess the role of miasm in hyperlipidemia and know the effectiveness of

constitutional method of treatment which includes the miasmatic background of the individual. Methods: A total number of 30 cases were taken randomly for the study. The cases with deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL > 130mg/ dl or HDL 0.30 is consistent 32

with diagnosis of FDBL. Protein methods (apoE phenotyping) or DNA-based methods (apoE genotyping) can be performed to confirm homozygosity for apoE2. Other mutations in apoE can also cause this condition. Familial Hypercholesterolemia (FH) is very rare autosomal co dominant disorder caused by around 750 mutations in the LDL receptor gene causing no LDL receptors in the liver. This leads to delayed catabolism of LDL and its precursor particles from the blood, resulting in increased rates of LDL production. It is characterized by elevated plasma LDL-C with normal TG. Total cholesterol levels are usually 500 mg/dL - 1000 mg/dL. Most patients with homozygous FH present in childhood with cutaneous xanthomas on the hands, wrists, elbows, knees, heels, or buttocks. Arcus cornea is usually present and some patients have xanthelasmas. Accelerated atherosclerosis is a devastating complication of homozygous FH and can result in disability and death in childhood. The diagnosis can be confirmed by obtaining a skin biopsy and measuring LDL receptor activity in cultured skin fibroblasts or by quantifying the number of LDL receptors on the surfaces of lymphocytes using cell-sorting technology. Heterozygous FH caused by the inheritance of one mutant LDL receptor allele occurs in approximately 1 in 500 persons worldwide, making it one of the most common single gene disorders. It is characterized by elevated plasma LDL-C 200 to 400 mg/dL and normal TG levels. They present with hypercholesterolemia from birth, and can be detected in the cord blood. The disease is often detected in adulthood, on routine screening, appearance of tendon xanthomas, or the premature development of symptomatic coronary atherosclerotic disease. Since the disease is codominant in 33

inheritance and has a high penetrance 90% of parent and 50% of the patient’s siblings are usually hypercholesterolemic. The family history is frequently positive for premature ASCVD on one side of the family, particularly among male relatives. Corneal arcus is common, and tendon xanthomas involving the dorsum of the hands, elbows, knees, and especially the Achilles tendons are present in 75% of patients. FH heterozygotes with elevated plasma Lp(a)appear to be at greater risk for cardiovascular complications. Untreated men with heterozygous FH have a 50% chance of having MI before age 60. Although the age of onset of atherosclerotic heart disease is later in women with FH, coronary disease is significantly more common in women with FH than in the general female population. No definitive diagnostic test for heterozygous FH is available. Familial Defective ApoB-100 (FDB) is a dominantly inherited disorder. As a consequence of the mutation in LDL receptor–binding domain of apoB-100, LDL binds the LDL receptor with reduced affinity and is removed from the circulation at a reduced rate. The disease is characterized by elevated plasma LDL-C levels with normal TG, tendon xanthomas, and an increased incidence of premature ASCVD. Autosomal Recessive Hypercholesterolemia (ARH) is a rare disorder due to mutations in a protein involved in LDL receptor–mediated endocytosis in the liver. Clinically it is characterized by hypercholesterolemia, tendon xanthomas, and premature CAD. Wolman Disease is an autosomal recessive disorder caused by complete deficiency of lysosomal acid lipase. Failure to hydrolyze the neutral lipids, results in their accumulation within cells. The disease presents within the first weeks of life with hepatosplenomegaly, steatorrhea, adrenal calcification, and failure to thrive. The disease is usually fatal within

34

the first year of life and can be diagnosed by measuring acid lipase activity in fibroblasts or liver tissue biopsy specimens Cholesteryl Ester Storage Disease is a less severe form of genetic disorder in which there is low, but detectable, acid lipase activity. Patients with this disorder sometimes present in childhood with hepatomegaly and a mixed hyperlipidemia, due to elevations in the levels of plasma LDL and VLDL. Other patients present later in life with hepatic fibrosis, portal hypertension, or with premature atherosclerosis. Sitosterolemia is a rare autosomal recessive disease caused by mutations in one of two members of the ATP - binding cassette transporter family. Due to mutation in these genes the intestinal absorption of plant sterols is increased and biliary excretion of the sterols is reduced, resulting in increased plasma levels of sitosterol and other plant sterols. Patients with sitosterolemia can have either normal or elevated plasma levels of cholesterol. Irrespective of the plasma cholesterol level, these patients develop cutaneous and tendon xanthomas as well as premature atherosclerosis. Episodes of hemolysis, presumably secondary to the incorporation of plant sterols into the red blood cell membrane, are a distinctive clinical feature of this disease. Sitosterolemia is confirmed by demonstrating an elevated plasma sitosterol level. Primary

disorders

of

ApoB-containing

lipoprotein

metabolism

(Unknown

etiology)9,13 Familial Hypertriglyceridemia (FHTG,) is a relatively common (1 in 500) autosomal dominant disorder of unknown etiology.

An increased VLDL production, impaired

VLDL catabolism, or a combination of the two causes elevation of VLDL (Type IV hyperlipoproteinemia). Some patients with FHTG have a more severe form of 35

hyperlipidemia in which both VLDL and chylomicrons are elevated (type V hyperlipidemia), as these two classes of lipoproteins compete for the same lipolytic pathway. Increased intake of simple carbohydrates, obesity, insulin resistance, alcohol use, or estrogen treatment, all of which increase VLDL synthesis, can precipitate the development of chylomicronemia, severe hypertriglyceridaemia and pancreatitis It is characterized by moderately elevated plasma TG with more modest elevations in cholesterol. FHTG does not appear to be associated with increased risk of ASCVD in many families. Clinically xanthomas are lacking. The diagnosis of FHTG is suggested by the triad of elevated plasma TG 250 to 1000 mg/dL, normal or only mildly increased cholesterol levels

> 250 mg/ dL, and reduced plasma HDL-C. Plasma LDL-C is

generally not increased and is often reduced due to defective metabolism of the TG-rich particles. The identification of other first-degree relatives with hypertriglyceridemia is useful in making the diagnosis. Familial

Combined

Hyperlipidemia

(FCHL)

multiple

lipoprotein-type

hyperlipidaemia, It is of an autosomal dominant inherence. The molecular etiology of FCHL is unknown but is likely to involve defects in several different genes. FCHL is the most common primary lipid disorder, occurring in approximately 1 in 200 persons. Approximately 20% of patients who develop CAD before age 60 have FCHL. It is characterized by moderate elevation of plasma TG and cholesterol and reduced plasma HDL-C. The affected family members typically have one of three possible phenotypes: (1) elevated plasma LDL-C, (2) elevated plasma TG and VLDL-C, or (3) elevated plasma LDL-C and VLDL-C. A classic feature of FCHL is that the lipoprotein phenotype can switch among these phenotypes with changing patterns of lipids in the blood. 36

FCHL has no typical physical signs. They can manifest in childhood but is sometimes not fully expressed until adulthood. Visceral obesity, glucose intolerance, insulin resistance, hypertension, and hyperuricemia are often present. These patients do not develop xanthomas The levels of apoB are disproportionately high relative to plasma LDL-C due to the presence of small dense LDL. A mixed dyslipidemia with plasma TG levels between 200 and 800 mg/dL, cholesterol levels between 200 and 400 mg/dL, and HDL-C levels >40 mg/dL and a family history of hyperlipidemia and or premature CAD suggests the diagnosis of FCHL. An elevated plasma apoB level supports this diagnosis. Polygenic

Hypercholesterolemia

This

is

the

most

prevalent

form

of

hypercholesterolaemia. It is characterized by hypercholesterolemia with a normal plasma TG in the absence of secondary causes of hypercholesterolemia. Only 10% of firstdegree relatives are hypercholesterolemic. Xanthomas are absent. Genetic disorders of HDL metabolism Mutations in certain genes encoding critical proteins in HDL synthesis and catabolism cause marked variations in plasma HDL-C levels. Genetic forms of hypoalphalipoproteinemia (low HDL-C) are not always associated with accelerated atherosclerosis. ApoA-I Deficiency and ApoA-I Mutations is seen with complete genetic deficiency of apoA-I due to mutations in the apoA-I gene resulting in the virtual absence of HDL from the plasma. Because apoA-I is required for LCAT function, plasma and tissue levels of free cholesterol are increased, leading to development of corneal opacities and plantar

37

xanthomas. Clinically apparent coronary atherosclerosis typically appears between the fourth and seventh decade. Mutations in the apoA-I gene has low plasma HDL . But are rare. Other than corneal opacities, most of them have no clinical sequelae. A few specific mutations in apoA-I cause systemic amyloidosis and the mutant apoA-I has been found as a component of the amyloid plaque. Tangier Disease is a rare autosomal codominant form of low plasma HDL-C caused by mutations in the gene encoding ATP-binding cassette transporter 1 gene (ABCA1), a cellular transporter that facilitates efflux of unesterified cholesterol and phospholipids from cells to apoA-I and plays a critical role in the generation and stabilization of the mature HDL particle. In its absence, HDL is rapidly cleared from the circulation. Patients with Tangier disease have plasma HDL-C levels < 5 mg/dL and extremely low circulating levels of apoA-I. The disease is associated with cholesterol accumulation in the reticuloendothelial system, resulting in hepatosplenomegaly and pathognomonic enlarged, grayish yellow or orange tonsils. An intermittent peripheral neuropathy (mononeuritis multiplex) or a sphingomyelia like neurologic disorder can also be seen in this disorder. Tangier disease is associated with premature atherosclerotic disease, but the risk is not very high which may be attributed to the low plasma LDL-C seen in this condition. LCAT Deficiency is a rare disorder caused by mutations in LCAT enzyme which mediates the esterification of cholesterol ,the deficiency of which impairs the formation of mature HDL particles and leads to rapid catabolism of circulating apoA-I causing great increase in the proportion of free cholesterol in circulating lipoproteins. 38

Progressive corneal opacification due to the deposition of free cholesterol in the lens, very low plasma HDL-C

< 10 mg/dL, and variable hypertriglyceridemia are

characteristic of both complete deficiency (classic LCAT deficiency) and partial deficiency (fish-eye disease) types. Complete LCAT deficiency is characterized by a hemolytic anemia and progressive renal insufficiency that eventually leads to end-stage renal disease. Despite the extremely low plasma levels of HDL-C and apoA-I, premature ASCVD is not a feature of either complete or partial LCAT deficiency. The diagnosis can be confirmed by assaying LCAT activity in the plasma. CETP Deficiency occurs with mutations in the gene encoding CETP which facilitates the transfer of cholesteryl esters among lipoproteins, especially from HDL to apoBcontaining lipoproteins in exchange for triglycerides causing a high HDL-C condition. Homozygous deficiency of CETP, results in very high plasma HDL-C > 150 mg/dL due to accumulation of large, cholesterol-rich HDL particles while heterozygotes for CETP deficiency have only modestly elevated HDL-C. The relationship of CETP deficiency to risk of ASCVD remains a matter of debate. Primary disorders of HDL metabolism 9,11 The gene defect is not known Primary Hypoalphalipoproteinemia / Familial hypoalphalipoproteinemia is the most common inherited cause with a low plasma HDL-C level with relatively normal cholesterol and TG levels. It is an autosomal dominant disease. The metabolic etiology of this disease appears to be primarily accelerated catabolism of HDL and its apolipoproteins. Several cases have been described in association with an increased incidence of premature ASCVD

39

Familial Hyperalphalipoproteinemia Familial hyperalphalipoproteinemia has a dominant inheritance pattern. Plasma HDL-C is usually > 80 mg/dL in affected women and

>

70

mg/

dL

in

affected

men.

The

genetic

basis

of

primary

hyperalphalipoproteinemia is not known, and the condition may be associated with decreased risk of CAD. Secondary disorders of lipoprotein metabolism9, 11 Significant changes in plasma levels of lipoproteins are seen in a variety of diseases. These constitute the vast majority of cases with hyperlipidaemia met in clinical practice. Change-over to modern low-fibre, high-fat and refined carbohydrate diet is probably the major cause for the high prevalence of Type IV and Type IIb hyperlipidaemias seen in urban societies of India which are highly atherogenic and thus are considered as the first reversible risk factor of ASCVD. Dietary control of fat intake along with n-3FA supplementations is necessary to alleviate this type of hyperlipidaemia.13 Obesity is frequently, though not invariably, accompanied by hyperlipidemia. The increase in adipocyte mass and accompanying decrease in insulin sensitivity associated with obesity have multiple effects on lipid metabolism. More free FA are delivered from the expanded adipose tissue to the liver where they are re-esterified in hepatocytes to form TG, which are packaged into VLDL for secretion into the circulation. High dietary intake of simple carbohydrates also drives hepatic production of VLDL, leading to increases in VLDL and or LDL in some obese individuals. Plasma HDL-C tends to be

40

low in obesity. Weight loss is often associated with a reduction of plasma apoBcontaining lipoproteins and an increase of plasma HDL-C. Diabetes Mellitus Patients with type 1 diabetes mellitus are generally not hyperlipidemic if they are under good glycemic control. Diabetic ketoacidosis is frequently accompanied by hypertriglyceridemia due to increased hepatic influx of free FA from adipose tissue. The hypertriglyceridemia responds dramatically to administration of insulin. Patients with type 2 diabetes mellitus are usually dyslipidemic, even if under relatively good glycemic control. The high levels of insulin and insulin resistance associated with type 2 diabetes causes (1) a decrease in LPL activity resulting in reduced catabolism of chylomicrons and VLDL, (2) an increase in the release of free FA from the adipose tissue, (3) an increase in FA synthesis in the liver, and (4) an increase in hepatic VLDL production. They have several lipid abnormalities, including elevated plasma TG (due to increased VLDL and lipoprotein remnants), elevated dense LDL, and decreased HDL-C. In some diabetic patients, especially those with a genetic defect in lipid metabolism, the TG can be extremely elevated. Elevated plasma LDL-C level in diabetic indicate the development of diabetic nephropathy. Patients with lipodystrophy, who have profound insulin resistance, have markedly elevated VLDL and chylomicrons. Thyroid Disease Hypothyroidism is associated with elevated plasma LDL-C primarily due to a reduction in hepatic LDL receptor function and delayed clearance of LDL. Thyroxin has a permissive role in stimulating the key enzymes like LPL and LCAT in circulation. Therefore in patients with hypothyroidism there is decreased catabolism of VLDL and IDL which causes accumulation of cholesterol and TG in circulation, having an increased circulating IDL. Some are mildly hypertriglyceridemic > 300 mg/dL. Type 41

IIa and sometimes Type IIb with lower levels of HDL2 is the dyslipidaemia seen in untreated patients with hypothyroidism. The profile is highly atherogenic.13 Renal Disorders Nephrotic syndrome is associated with hyperlipoproteinemia, which is usually mixed but can manifest as hypercholesterolemia or hypertriglyceridemia alone. It appears to be due to a combination of increased hepatic production and decreased clearance of VLDL, with increased LDL production. TG lipolysis and remnant clearance are both reduced in patients with renal failure.

Patients

with

renal

transplants

are

usually

hyperlipidemic

due

to

immunosuppression drugs Liver Disorders: Liver being the principal site of formation and clearance of lipoproteins, liver diseases can profoundly affect plasma lipid levels in a variety of ways. Hepatitis due to infection, drugs, or alcohol is often associated with increased VLDL synthesis and mild to moderate hypertriglyceridemia. Cholestasis is associated with hypercholesterolemia as it blocks the major excretory pathway by which cholesterol is excreted.But in chronic liver disease an abnormal lipoprotein is synthesised and secreted by the liver, called lipoprotein X, over and above diversion of cholesterol to the systemic circulation, producing a peculiar type of hypercholesterolaemia. However, in acute liver cell failure, there is decreased synthesis of LCAT and so slower catabolism of VLDL producing Type IV hyperlipidaemia.13 Severe hepatitis and liver failure are associated with dramatic reductions in plasma cholesterol and TG due to reduced lipoprotein biosynthetic capacity. Alcohol: Regular alcohol consumption has a variable effect on plasma lipid levels. The most common effect of alcohol is to increase plasma TG levels. Excess of alcohol intake 42

induces FA synthesis in the liver causing suppression of FA oxidation. Excess of free FA combines with glycerol and thus excess of VLDL is secreted. Further, there is also slower degradation of Chylomicron and so Type V hyperlipidaemia occurs in these patients.13 The usual lipoprotein pattern seen with alcohol consumption is type IV (increased VLDL), but persons with an underlying primary lipid disorder may develop severe hypertriglyceridemia (type V) if they drink alcohol. Regular alcohol use is also associated with a mild to moderate increase in plasma levels of HDL-C Glycogen Storage Diseases Other rarer causes of secondary hyperlipidemias include glycogen storage diseases such as von Gierke’s disease, which is caused by mutations in glucose-6-phosphatase. The inability to mobilize hepatic glucose during fasting results in hypoinsulinemia and increased release of free FA from adipose tissue. Hepatic FA synthesis is also increased, resulting in fat accumulation in the liver and increased VLDL secretion. The hyperlipidemia associated with this disease can be very severe Autoimmune diseases (SLE, dysglobulinaemias) produce autoantibodies which form complexes with either the enzymes like LPL or with the Apo of the circulating lipoprotein and slows down their catabolism, producing varieties of dyslipidaemias. 13 Cushing Syndrome: Glucocorticoid excess is associated with increased VLDL synthesis and hypertriglyceridemia causing mild elevations in plasma LDL-C in Cushing Syndrome. Drugs A variety of drugs have been identified to interfere with lipid metabolism either directly or indirectly and cause dyslipidaemias. The most important are the oestrogencontaining OCP which can enhance VLDL production from liver and produce hypertriglyceridaemia This problem gets aggravated if the woman has some undetected metabolic, hormonal or genetic defect related to lipid metabolism.13 43

MANAGEMENT OF HYPERLIPIDEMIA Early detection and early control of high cholesterol in a person is an important step in reducing the development and progression of coronary heart disease and atherosclerosis. Lowering plasma cholesterol by diet and drugs slows and may even reverse the progression of atherosclerotic lesions and the complications they cause The demonstration that lipid-lowering therapy significantly reduces the clinical complications of ASCVD has brought the diagnosis and treatment of these disorders into the domain of the general internist. The metabolic consequences associated with changes in diet and lifestyle have increased the number of hyperlipidemic individuals who could benefit from lipid-lowering therapy.13 Most patients with hyperlipidaemia are asymptomatic and have no clinical signs. Many are discovered during the screening of high-risk individuals 11 Guidelines for the screening and management of lipid disorders have been provided by an expert Adult Treatment Panel (ATP) convened by the National Cholesterol Education Program (NCEP) of the National Heart Lung and Blood Institute. The NCEP ATPIII guidelines published in 2001 recommend that all adults over age 20 have plasma levels of cholesterol, TG, LDL-C, and HDL-C measured after a 12-hr overnight fast.9 Selective screening of people at high risk of cardiovascular disease should be undertaken, to include those with: 

A family history of coronary heart disease (especially below 50 years of age)



A family history of lipid disorders



The presence of a xanthoma 44



The presence of xanthelasma or corneal arcus before the age of 40 years



Obesity



Diabetes mellitus



Hypertension



Acute pancreatitis



Those undergoing renal replacement therapy Serum cholesterol concentration does not change significantly after a meal and as

a screening test, a random blood sample is sufficient. If the total cholesterol concentration is raised, HDL cholesterol, TG, and LDL cholesterol concentrations should be quantitated on a fasting sample. If a test for hypertriglyceridaemia is needed, a fasting blood sample is mandatory 11 Multiple epidemiologic studies have demonstrated a strong relationship between serum cholesterol and CAD. Randomized controlled clinical trials have unequivocally documented that lowering plasma cholesterol reduces the risk of clinical events due to atherosclerosis. Since both hypertriglyceridemia and low plasma levels of HDL-C confer higher ASCVD risk, the NCEP ATPIII recommends more aggressive therapy to lower the plasma LDL-C in patients with these dyslipidemias.9 Hyperlipidaemia results from genetic predisposition interacting with an individual's diet.11 Studies show the role of the environment rather than the genetic makeup of a population. Data from The Multiple Risk Factor Intervention Trial (MRFIT) have shown that although cardiovascular risk rises progressively as total cholesterol concentration increases the risk increase is modest for individuals with no other

45

cardiovascular risk factors. With each additional risk factor the effect produced by the same difference in cholesterol concentration becomes greatly magnified.11 Reference values 14,15 Normal values vary with age, diet, sex and geographic regime. Recommended levels of lipoproteins in Indian population are : Total cholesterol

:

40mg/dL

Triglycerides

:

Sunrise to sunset, Change of position, Abnormal discharge. Winter, Cold weather

Suppression of pathological elimination Psychosis, incidence of suicide, CVA, MI Repeated abortion, IUD. Infertility, Degenerative diseases

Constitutional Appearance

Lean thin, Active

Obese.Flabby, sluggish. Stout, Overnourished.

Lean thin. Narrow chest

Thin, wrinkled, looks old for his age.

Face

Inverted pyramid Yellow sallow, pale, earthy complexion. Eyes sunken

Dropsical. Oily skin

Pale ,round, fair smooth, clear skin & waxy smooth complexion. Sunken eyes, flushed cheeks. Thin lips.

Greasy. High cheek bones & rough skin. Dry & wrinkled like old person.Thick lips

Thermal

Generally chilly

Hot

Extremely chilly

Sensitive to changes either heat or cold

Perspiration

Profuse, offensive, during sleep

On forehead during sleep. Copious.

Profuse

Offensive < all complaints

Appetite

Insatiable hunger

Discomfort after eating

Increased

Decreased

Craving

Sweet, Sour, Spicy, Salty. Oily, Fried, Indigestible Unnatural substances like chalk, clay, Hot food.

Alcohol, Beer, Pungent, Well Indigestible things, Potatoes, seasoned, Salty food. Tea, Tobacco, Meat, Salt, Greasy, fatty food. Things which make them sick. Very hot / really cold

Stimulants like alcohol, tea, coffee, very spicy. Indigestible.Cold food

Aversion

Milk, cold food

Meat, milk, wine, spices

Meat

Meat, animal food, less spicy food

Bowels

Constipation

Diarrhoea

Alternating diarrhea and constipation

Dysentry

72

Particulars of Hyperlipidemia Family history May or may not have a F/H of hyperlipidemia

Etiology

Unknown cause Increased intake of fat, Secondary to alcoholism, drugs, hepatic infections

Pathology

Defective metabolism of fat Deficiency in apoprotein or enzymes.

Clinical Manifestations

No manifestations with only serum changes Pancreatitis. Reversible with diet & life style changes

F/H of hyperlipidemia, atherosclerosis, CAD etc

F/H of hyperlipidemia

Strong F/H of hyperlipidemia, early CAD, stroke etc.

Mutation in gene. Hepatic cholestasis. Enzyme disorders Secondary to auto immune disease like SLE, endocrine disorders like DM, hypothyroidism, Cushing’s syndrome. Defect in receptors, enzyme activity. Deposition of cholesterol & lipoprotein in the wall of blood vessels

Mutation in gene

Mutation in gene Secondary to nephritic syndrome

Defect in receptors, enzymes

Lipemia retinalis Hepatomegaly, Hepatic fibrosis, Spleenomegaly, hypertension, Xanthoma, Xanthelesma, Atherosclerosis, Enlarged tonsils

Recurrent pancreatitis. Intermittent peripheral neuropathy

Lack of apoprotein, receptors, enzyme activity Atheromatous plaque resulting in complication of haemorrhage, thromboembolic phenomena Accelerated atherosclerosis Premature CAD, Stroke, PVD Haemolysis

73

HYPERLIPIDEMIA IN REPERTORY The rubrics specifically related to hyperlipidemia seen in repertories are SYNTHESIS 9.1 40 Generals – Hyperlipidemia - all-s, aur, calc, calc-f, chel, chin, chion, chr-ac, colch, cortiso, ferr-i, hydr, lec, med, nux-v, perh-mal, tarax, thuj, thyreotr, vanad, zing Generals – Arteriosclerosis - adren. Am-i. am-van. aml-ns. ant-ar. arg-n. Arn. ars. Ars-i. asar. aster. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-ren. Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac. fuc. Glon. hed. hyper. iod. kali-bi. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mand. naja Nat-i. nitac. phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. spartin-s. Stront-c. Stront-i. strophh. sumb. syph. Tab. thlas. thyr. Vanad. Visc. zinc-p. -

Old people in – bar-c, stroph-h

Generals – Diabetis mellitus – accompanied by arteriosclerosis – aur, chlorpr,plb, syzyg Mind – memory weakness – arteriosclerotic disease with - plb. MURPHY’S REPERTORY 41 Blood - Blood vessels, general – atheroma- aur-m. bell. brom. Calc. Calc-f. caps. Graph. kali-i. Lac-ac. Lach. lyc. phos. Plb. Sil. sulph. - elderly people, in Lach. - morbus brightii, in ph-ac. - obese persons, in- caps.

Blood – Blood vessels, general – arteriosclerosis - adren. am-i. am-van. aml-ns. ant-ar. argn. Arn. ars. Ars-i. Aur. aur-br. Aur-i. aur-m-n. Bar-c. bar-i. bar-m. bell-p. benz-ac. cact. cal-

74

ren. Calc. calc-ar. calc-f. card-m. chinin-s. chlol. con. crat. Cupr. ergot. fl-ac. form. form-ac. fuc. Glon. hed. hyper. iod. Kali-i. kali-sal. kres. lach. lith-c. mag-f. mang. naja Nat-i. nit-ac. phos. Plb. Plb-i. Polyg-a. rad-br. rauw. Sec. sil. solid. Stront-c. Stront-i. stroph-h. sumb. Tab. thlas. thyr. Vanad. Visc. zinc-p. BOERICKE’S REPERTORY 42 Circulatory system - Arteries - Atheroma of arteries - adren. Am-i. am-van. ant-ar. arn. ars. Ars-i. aur. Aur-i. aur-m-n. Bar-c. bar-m. cact. calc-f. chinin-s. con. crat. ergot. Glon. Kalii. kali-sal. lach. lith-c. Nat-i. phos. plb. Plb-i. Polyg-a. sec. stront-c. Stront-i. stroph-h. sumb. thyroiod. Vanad. SPECIFIC THERAPEUTICS

42,43.

As in any other disease, the remedy that encompasses

the diseased state of the constitutional expression at all levels, body, mind and spirit, termed as constitutional remedy which necessarily coincides with the miasmatic expression of the individual is the approach to hyperlipidemia. Inspite there are certain remedies specifically related to hyperlipidemia clinically proven to bring down serum lipid levels as well as remove the pathological deposition of lipids on arterial walls. Allium Sativum – Adapted to fleshy subjects. Patients who eat a great deal more especially meat than they drink. Arnica – Marked effect on blood. Fatty heart and hypertrophy. Arsenicum iodatum – Senile heart, fatty degeneration, Arteriosclerosis. Aurum metallicum – Develops in the organism by attacking the blood. Deterioration of body fluids. Arteriosclerosis with high blood pressure. Baryta carb – Useful in general degenerative changes, especially in coats of arteries.Acts on the muscular coats of heart and vessels. Arterial fibrosis. Blood vessels soften and degenerate.

75

Calc flour – Arteriosclerosis. Cardus marianus – Has specific relation to vascular system. Abuse of alcoholic beverages especially beer. Cholesterinum – Obstinate hepatic engorgements. Gallstones. Crataegus – Arteriosclerosis. Said to have a solvent power upon crustaceous and calcareous deposits in arteries. Glonoine – Sciatica in atheromatous subjects. Graphites – Tendency to obesity. Aids absorption of cicatricial tissue. Plumbum metallicum – A great drug of general sclerotic condition. Hypertension and arteriosclerosis. Plumbum iodatum - Arteriosclerosis Polygonum aviculare – In material doses of tincture found useful especially in arteriosclerosis Strontia – Arteriosclerosis. High blood pressure with flushed face, pulsating arteries Strontia iodat - Arteriosclerosis Tabacum – Produces high tension and arteriosclerosis of coronary arteries Vanadium – Arteriosclerosis. Fatty heart. Atheroma of arteries of brain and liver

76

Methodology 76

METHODOLOGY

Source of data This study was conducted on the patients who reported to the outpatient department of Fr. Muller Homoeopathic Medical College and Hospital, Deralakatte, as well as from Kankanady and peripheral centres. Patients belonging to age group of 25 to 75 years were considered for the study. Both the sexes were included belonging to various socioeconomic group. A total number of 30 cases were taken randomly for the study. The cases with elevated serum Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL > 130mg/ dl or HDL Amelioration of clinical features 0 – Disappearance of clinical features G – good N – Normal R – Regular etc.

Diet and Regimen All the patients were explained and educated about the importance of low calorie diet and physical exercises as per the need. Instructions were given to avoid other medicinal agents during the treatment.

Assessment of Effectiveness Effectiveness of the treatment was assessed on the basis of 1. Serum lipid profile 2. For the effective assessment and evaluation, disease intensity scores were also maintained.

79

After completion of treatment, disease intensity of the post treatment scores were compared with the pre treatment disease intensity score and statistically evaluated. Notes: For disease intensity scores refer appendix: 1

Plan for Data Analysis Data has been analysed by using descriptive statistics and the results have been presented by using frequency table, percentage, pie diagram, and graphs. The significance of treatment effect based on different homoeopathic therapeutic strategies are tested using ‘t’ test.

80

Results 80

RESULTS Table 3: Distribution of cases according to age group Age group

No. of cases

Percentage

25-35

7

23.33

35-45

10

33.3

45-55

4

13.3

55-65

7

23.3

65-75

2

6.6

In this study maximum prevalence of Hyperlipidemia were found in the age group of 35 to 45 years (10 cases – 33.33%). Followed by 25 to 35 and 55 to 65 years of age group (7 case in each group – 23.33%) and 45 to 55 years of age group (4 cases – 13.3%). Minimum prevalence is found in 65 to 75 years age group (2 cases 6.6%). Table 4: Distribution of cases according to sex

Sex

No. of case

Percentage

Male

12

40

Female

18

60

Total

30

100

Out of 30 patients studied, 12 cases (40%) were males and 18 cases (60%) were females.

81

Case distribution according to age group 33.3

35 30 23.33

25

23.3

20 15 10

No. of cases

13.3

Percentage

10 7

7 4

5

6.6 2

0 25-35

35-45

45-55

55-65

65-75

Age group Fig.11: Case distribution according to age group

Distribution of cases according to sex Males 12 40% Females 18 60%

Fig.12: Case distribution according to sex

82

Table 5: Case distribution according to religion Religion

No of cases

Percentage

Hindu

8

26.6

Christian

14

46.6

Muslim

8

26.6

Total

30

100

Out of 30 cases maximum prevalence of Hyperlipidemia was found in Christians (14 cases – 46.66%). Hindus and Muslims shared equal prevalence of (8 cases each26.66%).

Table 6: Case distribution according to physical activity Physical activity

No of cases

Percentage

Sedentary

16

53.33

Moderate

14

46.6

Severe

0

0

Total

30

100

Among 30 patients included in this clinical study, majority 16 cases (53.3 %) were found to have sedentary life with minimal physical activity. The rest were patients with moderate physical activity 14 cases (46.6%). There were no patients with severe physical activity.

83

Case distributions according to religion

26.6

Muslim

8

Percentage No of cases 46.6

Christian

14 26.6

Hindu

8

0

20

40

60

Fig.13: Case distribution according to religion

Case distribution according to physical acitivity 53.33 46.6

60

No of cases

40

Percentage 20

16

14

0

0 0

Sedentary

Percentage No of cases

Moderate

Severe

Fig.14: Case distribution according to physical activity

84

Table 7: Case distribution according to fundamental miasm Miasm

Fundamental miasm No. of cases

Percentage

Psora

0

0

Sycosis

16

53.3

Syphilitic

1

3.3

Tubercular

1

3.3

Sycosyphilitic

11

36.6

Psora syco

1

3.3

Total

30

100

Table 8: Case distribution according to dominant miasm Dominant miasm Miasm

No. of cases

Percentage

Psora

8

26.6

Sycosis

16

53.3

Syphilitic

0

0

Tubercular

1

3.3

Psorasyco

5

16.6

Total

30

100

Sycotic expression is well marked and found to be dominating in both fundamental and dominant miasm with 16 cases (53.3%). Syco syphilitic expression stands next with 11 (36.6%) in fundamental miasm and

Psora with 8 (26.6%) in

dominant miasm. Tubercular, Syphilitic and Psora-sycotic comprises 1 each (3.3%) in fundamental miasm. Psora comprises 8 (26.6%) and Psorasycotic 5 (16.6%) cases in 85

dominant miasm. Only one case gives Tubercular expression (3.3%) in dominant miasm. There is no expression from Psoric miasm in fundamental miasm and syphilitic miasm in dominant miasm

Case distribution according to fundamental miasm 100

100

100

53.3 50 16

3.3 1

0

3.3

36.6 30

0

No of cases 0 3.3

30

Percentage o No of cases 0

Fig.15: Case distribution according to fundamental miasm

Case distribution according to dominant miasm 1 3%

5 17%

8 27%

Psora Sycosis Syphilitic Tubercular Psorasyco

16 53%

Fig.16: Case distribution according to dominant miasm 86

Table 9: Case distribution according to the type of hyperlipidemia Type of Hyperlipidemia

No of cases

Percentage

Familial hyper cholesterolemia

4

13.3

Polygenic hypercholesterolemia

7

20

10

33.3

CETP deficiency

1

3.3

Familial chylomicronemia

1

3.3

Hepatic lipasedeficiency

2

6.6

Secondary hyperlipidemia

5

16.6

30

100

Familial combined hyperlipidemia

Total

Among 30 patients included in this clinical study, majority (10 cases-33.3 %) were found to be having Familial combined hyperlipidemia. Polygenic hyperlipidemia was next with 7 cases (23.3%).This was followed by Secondary hyperlipidemia and Familial hypercholesterolemia with 5(16.6%) and 4 (13.3%) cases respectively. The rest were of Hepatic lipase deficiency (2cases – 6.6%), CETP deficiency (1case – 3.3%) and Familial chylomicronemia(1case – 3.3%) .

87

Table 10: Case distribution according to constitutional remedies

Name of the remedy

No of cases

Percentage

Calcarea carb

4

13.3

Lycopodium

10

33.3

Medorrhinum

1

3.3

Natrum mur

2

6.6

Nux Vomica

1

3.3

Phosphorus

4

13.3

Pulsatilla

4

13.3

Sepia

2

6.6

Sulphur

2

6.6

Total

30

100

Out of 30 cases, Lycopodium was used as a constitutional remedy in 10 cases (33.3%). Calcarea carb, Phosphorous and Pulsatilla were used as constitutional remedy in 4 cases (13.3%) each. Sepia, Sulphur and Natrum mur were used as constitutional in 2 cases (6.6%) each.1 case (3.3%) each was treated with Nux vomica and Medorrhinum.

88

Fig.17: Case distribution according to the type of hyperlipidemia

Case distribution according to constitutional remedies 33.3

35 30 25

No of cases 20 13.3

15

13.3

10

6.6

10

6.6

3.3

5

2

1 0

2

6.6

3.3

4

0

Percentage

13.3

4

4

4

2

1 6

8

2 10

Fig.18: Case distribution according to constitutional remedies 89

Table 11: Case distribution according to the effectiveness of treatment Effectiveness

No of cases

Percentage

Improved

26

86.6

Not improved

4

13.3

Total

30

100

86.6 90 80 70 60 50 40 30

No of cases 26

percentage

13.3

20

percentage

10

4

0

No of cases Improved

Not improved

Fig.19: Case distribution according to the effectiveness of treatment

Out of 30 cases, 26 ( 86,6%) showed improvement in the serum lipid profile. Following the guidelines all through the proforma, the status of the patient is assessed and substantiated under two criteria according to the score, based on serum lipid level.

90

THE EXPLANATION OF THE STATISTICAL TOOLS AND TECHNIQUES Table 12: Statistical analysis table

Sl.No

X

Y

(X - Y)=Z

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

15 11 6 11 12 17 16 22 15 15 14 23 9 7 18 7 19 14 13 19 29 20 6 10 15 14 15 17 9 4 Mean X =422

5 7 1 4 15 4 11 31 13 10 6 17 5 7 14 2 12 4 0 16 16 15 1 4 9 13 13 13 2 4 Mean Y = 274

10 4 5 7 -3 13 5 -9 2 5 8 6 4 0 4 5 7 10 13 3 13 5 5 6 6 1 2 4 7 0 Mean Z =148

X - Score before treatment Z - Mean difference Y - Score after treatment Mean X = 422/30 = 14.07 Mean Y = 274/30 = 9.13 Mean Z = 148/30 = 4.93 91

_ Z 5.07 -0.93 0.07 2.07 -7.93 8.07 0.07 -13.93 -2.93 0.07 3.07 1.07 -0.93 -4.93 -0.93 0.07 2.07 5.07 8.07 -1.93 8.07 0.07 0.07 1.07 1.07 -3.93 -2.93 -0.93 2.07 -4.93

_ (Z – Z)2 25.70 0.86 0.00 4.28 62.88 65.12 0.00 194.04 8.58 0.00 9.42 1.14 0.86 24.30 0.86 0.00 2.28 25.70 65.12 3.72 65.12 0.00 0.00 1.14 1.14 15.44 8.58 0.86 4.28 24.30 Mean _ (Z – Z)2 = 617.87

A. Question to be answered: is there any significant difference between the scores taken before and after the treatment. B. Null hypothesis: there is no significant difference between the scores before and after the treatment. C. Standard error of the mean differences: the mean of the differences Z = Z/n = 148/30 = 4.93 The estimation of the population standard deviation is given by the formula SZ = √ (Z –Z) 2 / n-1 = √ 617.87 / 29 = √ 21.31 = 4.62 The estimation of the standard error is calculated by using the formula = SZ /√n = 4.62 /√30 = 4.62/ 5.47 = 0.84 D. Critical ratio is calculated using the formula : t = Z /Sz /√n = 4.93 / 0.84 = 5.85

92

E. Compare with the tabled values:

The test statistic ‘t’ follows student ‘t’ distribution with n-1(29) degrees of freedom. Here, tabled value of ‘t’ at 5% level of significance is 2.045 and 1% level of significance is 2.756 for 29 degrees of freedom. Since the calculated value is 5.85 which is greater than the tabled at 5% &1%, we reject the Null Hypothesis. Inference: This study provides an evidence to say that there is reduction in the disease intensity scores after the homoeopathic treatment based on constitutional treatment and general management. Therefore the Homeopathic constitutional medicines are effective in treating hyperlipidemia.

93

35

30

25

20 Scoring before Scoring after

15

10

5

0 1 2 3

4 5 6

7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

Fig.20: Distribution of all cases according to pre and post treatment analysis using scoring char 94

Discussion 95

DISCUSSION Hyperlipidemia, which is the raised or abnormal levels of lipids & lipoproteins in the blood has become a great health hazard, especially in developed countries which has turned out to be a challenge to the physician. It contributes to high morbidity and remains a major cause of high mortality in our country. The current study is done for the better understanding of different types of hyperlipidemia, to assess the role of miasm in hyperlipidaemia and its management through general and constitutional homoeopathic treatment. This study was conducted in patients who reported to the outpatient department of Fr. Muller Homoeopathic Medical College and Hospital at Deralakatte, as well as from Kankanady and peripheral centres. A total number of 30 cases were taken randomly for the study. The cases with deviated serum lipid i.e. Cholesterol > 200mg/ dl, Triglycerides > 150mg/dl, LDL > 130mg/ dl or HDL 175

10



4 >

5 -

6 <

7

8

PRESCRIPTION 9

10

RX 1. SL pkt (1P) HS 2. No 40 pills 4–0–4 x 2 wks

1

2

> 24.07.10

4

5

6

>

>

-

<

7

8

9

10

Serum cholesterol – 226 mg/dl TG – 138mg/dl LDL – 123 mg/dl HDL – 35 mg/dl 1

7. 08. 10

3

2

3

4

5

6

> >

>

>

-

-

7

8

9

10

RX 1. Phos 200 (1P) H S2. No 2 . No 40 pills 4–0–4 x 2 wks . RX 1. SL pkt (1P) HS

Generally feels better 2 . No 40 pills 4–0–4 x 2 wks 1

2

3

4

5

6

> >

>

>

-

<

7

8

9

10

RX 1. SL pkt (1P) HS

Generals – good 2. No 40 pills

21. 08. 10

4–0–4 x 2 wks

115

4.09-10

1

2

3

4

5

6

>

>

>

>

-

-

7

8

9

10

RX 1. SL pkt (1P) HS 2. No 40 pills 4–0–4 x 2 wks

18.09.10

1

2

3

4

5

6

>

>

>

>

-

-

7

8

9

10

RX 1. SL pkt (1P) HS

Generals – good 2. No 40 pills

4–0–4 x 4 wks

SCORING

Sl No

Serum lipid levels

Scoring before treatment

Scoring after treatment

1.

Cholesterol

4

2

2.

Triglycerides

1

0

3.

LDL

6

0

4.

HDL

4

3

Total

15

5

116

INVESTIGATIONS REPORTS BEFORE AND AFTER TREATMENT

117

ANNEXURE 3 MASTER CHART

Sl. no

1

2

Particulars Of the Patient

Clinical Diagnosis

Name: Mr S B Age : 41 yrs Sex : M Occu : Govt employee Relegion :Hindu Add : Neeleshwar SCR No : 57123

Familial hypercholest erolemia External Haemorrhoid s Alopecia area’ta

Name: Mrs K M Age :40 yrs Sex:F Occu: Housewife Relegion: Muslim Add :Kumbla SCR No: 43325

Familial combined hyperlipidem iaAllergic rhinitis

Past And Family History

Mother – Hypercholes terolemia, Haemorrhoi ds Father – Expired due to liver disease Brother Haemorrhoi ds Mother – Epilepsy Father – Bronchial asthma, DM, Died following Renal failure Brother DM

Investigations

Before

After

Chol – 282mg/ dl TG166mg/ dl LDL – 156mg/ dl HDL32mg/ dl Chol255mg/ dl TG – 138mg/ dl LDL – 168mg/ dl HDL 47mg/ dl

Chol – 226mg/ dl TG – 138mg/ dl LDL – 123mg/ dl HDL – 35mg/ dl Chol – 232mg/ dl TG 106mg/ dl LDL155mg/ dl HDL56mg/ dl

Totality

Miasms

FM

Remedy

Duration of treatment

DM

Result Scoring B

A

MG: Fear of dark, Likes company, Doesn’t like contradiction, Doesn’t like to share, weak memory PG: Stocky appearance Cr –Sweets, meat Chilly patient CP: Bleeding < spicy food Hairfall< summer

SycoSyphil

Tub

Phos 200

3 mths

15

5

Improved

MG – Brooding, Suppressed emotion, Weeping when alone, Hasty, Doesn’t like company, Good confidence PG – Stocky appearance Cr – Fish Av – Sweets, Ice cream, Hot patient CP – Sneezing < Dust, Cold air, Morning. Breathlessness < lying down, Night

SycoSyphil

Psora

Natrum Mur 30

5 mths

11

7

Improved

118

Sl. no

3

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

Duration of treatment

Scoring

DM

B

Result

A

Name: Mrs Y Age : 41 yrs Sex: F Occu: Housewife Relegion: Hindu Add :Ullal SCR No: 14392

CETP deficiency Osteoarthritis Calcanean spur Hypertension

Mother – Osteoarthr itis Father – Expired of MI

Chol250mg/ dl TG – 66mg/ dl LDL – 148 mg/ dl HDL89mg/ dl

Chol – 225mg/ dl TG – 60mg/ dl LDL – 128mg/ dl HDL – 85mg / dl

MG: Mild, Likes company, Likes consolation Weak memory PG: Stocky appearance Decreased appetite Perspiration increased in general, Cr – Fish, Spicy Av – Veg Chilly patient CP: Joint pains pricking < before menses, exertion >Warmth, pressure Giddiness < getting up from sitting position

SycoSyphil

Syco

Puls 200, 1M

4mths

6

1

Improved

Name: Mr M Age : 35yrs Sex: M Occu: Driver Relegion: Muslim Add : Payyannur SCR No: 48619

Familial chylomicronem ia LRTI Tension headache Hypertension

Mother – Bronchial asthma Father – Died of MI

Chol – 223mg/ dl TG425mg/ dl LDL – 129mg/ dl HDL50mg/ dl

Chol – 198mg/ dl TG – 280mg/ dl LDL – 101mg/ dl HDL – 41mg/ dl

MG: Suppressed emotion, Arrogant, Introvert, Likes company, Sympathetic PG: stocky appearance Appetite decreased Thirst decreased Perspiration increased in general Cr- Shellfish Av- Meat Hot patient CP: Dry cough < after fried food, headache pricking < Tension, after sleep> pressure Chest burning < heavy food

SycoSyphil

Psora

Sulph 200

5mths

11

4

Improved

119

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

DM

Duration of treatment

Scoring

B

Result

A

5

Name: Mr J P Age : 27 Yrs Sex:M Occu: Attendar Relegion :Christian Add : Manjeshwar SCR No: 9154

Polygenic hypercholester olemia Sinusitis APD

P/H Appendici tis Father – Hypertens ion

Chol – 235mg/ dl TG 86mg/ dl LDL176mg/ dl HDL42mg/ dl

Chol324mg/ dl TG122mg/ dl LDL234mg/ dl HDL46mg/ dl

MG: Anxiety about future Sensitive, Intolerant to contradiction. PG: Stocky appearance Cr - Non Veg, cold drinks. Av – Veg Hot patient CP: < Tension Abdomen fullness < spicy, Non Veg Head ache < Sun, exertion > Tight bandage

Syco

Psora

Lyco 200

4 mths

12

15

Not Improved

6

Name: Mrs N Age : 37 Sex: F Occu Housewife: Relegion: Hindu Add : Bejai SCR No: 54279

Polygenic hypercholester olemia Varicose veins

P/H Bronchial asthma, Chikungu nya Mother – DM Expired

Chol – 310mg/ dl TG – 130mg/ dl LDL – 157mg/ dl HDL – 27mg/ dl

Chol – 149mg/ dl TG – 113mg/ dl LDL – 95mg/ dl HDL– 31mg/ dl

MG – Shy, Sensitive, Obstinate, Likes to be in company PG – stocky appearance Perspiration increased on face,Hard stool, once in two days Av – Chicken Sour food disagrees Hot patient CP – Extremities pain, Burning < Exertion, morning > warmth, Massage

Syco

Syco

Puls 200

3 mths

17

4

Improved

120

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

Duration of treatment

DM

Scoring

B

Result

A

7

Name: Mrs L R Age :42yrs Sex: F Occu: Lecturer Relegion: Christian Add : Bendore SCR No:54604

Polygenic hypercholester olemia Hypertension

P/H Eczema Bronchial asthma since 15 yrs Father – DM, Hypertens ion Mother – DM, Hypertens ion

Chol – 271mg/ dl TG – 124mg/ dl LDL – 212mg/ dl HDL – 35mg/ dl

Chol – 239mg / dl TG – 112mg / dl LDL – 174mg / dl HDL– 41mg/ dl

MG – Relegious, Emotional stress, Anxiety about children, Sympathetic, Suicidal thoughts PG – Obese Perspiration on face Cr – Sweets, fried food Av – Sour Hot patient

Syco

Syco

Lyco 200

4mths

16

11

Improved

8

Name: Mr H Age : 32yrs Sex: M Occu: Clerk Relegion: Muslim Add :Urumanai SCR No: 9504

Familial combined hyperlipidemia Functional impotency

Mother DM

Chol – 465mg/ dl TG – 180mg/ dl LDL – 374mg/ dl HDL – 55mg/ dl

Chol – 448mg /dl TG – 170mg / dl LDL – 394mg / dl HDL– 20mg /dl

MG: Fear of dogs, Likes company PG: Stocky appearance Increased thirst, Scanty perspiration Cr – Veg Av – Fish, sweet Chilly patient CP: Premature ejaculation, Xanthoma Headache < evening, > sleep

Syco

Psora - Syco

Phos 200, 1M

5mths

22

31

Not Improved

121

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

DM

Duration of treatment

Scoring

B

Result

A

9

Name:Mrs G M Age :44yrs Sex:F Occu: Housewife Relegion: Christian Add :Kannur SCR No:57489

Polygenic hypercholester olemia Osteoarthritis Sinusitis

P/H Bronchial asthma, Chikungu nya Father Bronchial asthma

Chol – 287mg/ dl TG175mg/ dl LDL210mg/ dl HDL42mg/ dl

Chol269mg / dl TG146mg / dl LDL195mg / dl HDL45mg/ dl

MG – Mild, Indecisive, Weepy, Fear of thunderstorm, likes consolation PG – Stocky appearancePerspiration generally decreased, Thirst decreased Cr – Rice, Fish Av- Milk Hot patient CP – Joint pains < First movement > Rest Headache < Sun, Travelling, Afternoon > Tight bandage

Syco

Psora - Syco

Puls 200

3 mths

15

13

Improved

10

Name: Mrs R D Age :58yrs Sex:F

Secondary hyperlipidemia Diabetic cataract APD

P/H- DM since 14 yrs Night blindness at 5yrs Mother – DM, Hypertens ion, Stroke

Chol234mg/ dl TG200mg/ dl LDL – 161mg/ dl HDL – 33mg/ dl

Chol228mg / dl TG – 163mg / dl LDL – 156mg / dl HDL– 40mg/ dl

MG – Workaholic, Relegious, Mild, Sympathetic, Perfectionist, Fear of thunder & lightning, Anxiety about health PG – Stocky appearance, Perspiration increased generally Av – Spicy, Bitter Chilly patient CP – Distension of abdomen < Non Veg, Sweets

SycoSyphil

Syco

Phos 200

5 mths

15

10

Improved

Occu: Housewife Relegion: Christian Add : Kulshekar SCR No:52832

122

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

Duration of treatment

DM

Scoring

B

Result

A

11

Name: Mr K Age : 44 yrs Sex: M Occu: Executive officer Relegion: Hindu Add : Mangalore SCR No: 56928

Familial combined Hyperlipidemia Cholecystolithi asis

Father died of peptic ulcer Mother died of Tuberculo sis

Chol – 258mg/ dl TG – 203mg/ dl LDL – 168mg/ dl HDL – 50mg/ dl

Chol – 226mg / dl TG – 182mg / dl LDL – 139mg /dl HDL– 51mg/ dl

MG – Workaholic, Punctual, Leadership, Confident, Superiority, Bold PG – Stocky appearance Thirst increased Addiction – occasionally Alcohol Chilly patient CP – Right hypochondriac pain < after food

Tub

Syco

Nux Vom 200

3 mths

14

6

Improved

12

Name :Mr B Age : 58 yrs Sex: M Occu: Railway Guard Relegion: Hindu Add : Ottappalam SCR No: 55073

Secondary hyperlipidemia Hypertension Acute Bronchitis

P/H- DM since 18 yrs Chicken pox, 3yrs back Father – Died of Renal failure following DM Mother – Died of MI

Chol – 300mg/ dl TG – 147mg/ dl LDL – 248mg/ dl HDL – 23mg / dl

Chol238mg / dl TG – 129mg / dl LDL – 183mg / dl HDL– 30mg/ dl

MG – Workoholic, Perfectionist, Irritable, Reacts for anger PG – Lean, Perspiration increased, Appetite increased, Thirst increased, Cr – Fish, Av – Meat, Hard Stools Hot patient CP – Dry cough < Night Breathlessness on distension of abdomen

Syco Syphil

Syco

Lyco200

8 mths

23

17

Improved

123

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

13

Name: Mrs L S Age : 48 yrs Sex: F Occu: Housewife Relegion: Christian Add : Bantwala SCR No: 57290

Familial combined hyperlipidemia Cholecystolithi asis

Mother Hypertens ion

14

Name: Sr T Age : 43yrs Sex: F

Familial combined hyperlipidemia Allergic rhinitis, Arthritis Calcanean spur

P/H Fibroid uterus Mother – DM Father – DM, Hypertens ion Grand father – DM, Hypertens ion

Occu: Accountant Relegion: Christian Add :Deralakatte SCR No: 14010

Investigations

Miasms

Remedy

Totality Before

After

Chol241mg/ dl TG222mg/ dl LDL149mg/ dl HDL48mg/ dl Chol267mg/ dl TG – 197mg/ dl LDL – 139mg/ dl HDL – 89mg/ dl

Chol224mg / dl TG – 207mg / dl LDL – 130mg / dl HDL– 53mg/ dl Chol – 257mg / dl TG – 187mg / dl LDL – 138mg / dl HDL– 82mg/ dl

FM

Duration of treatment

Scoring

DM

B

Result

A

MG – Loquacious, Irritable, Gets angry fast, Likes consolation,Likes to share , Helps others, Memory weak PG- Obese, Perspiration increased in general Cr – Sweets, Ice cream Av- Spicy Pleasant dreams Chilly patient CP -

Syco

Syco

Phos 200

3 mths

9

5

Impeoved

MG: Suppressed emotion, Likes company, fear of snakes & worms ,Irritable, Anger – reacts PG: Stocky appearance Cr – Sweets Av – Pungent,sour Perspiration on back Chilly patient CP: Sneezing < morning, dust Headache > Pressure, Night Joint pain < first movement

Syco

PsoraSyco

Sepia 200

5 mths

7

7

Not Improved

124

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

15

Name: Mr M Age : 44 yrs Sex:M Occu: Airlines officer Relegion: Christian Add : Panjim SCR No: 33269

Familial hypercholester olemia Migraine

Grand father – DM, Hypertens ion, Osteoarthr itis Father Hypertens ion

16

Name: Sr M B Age : 67 yrs Sex:F Occu: Teacher Relegion: Christian Add : Mangalore SCR No:56632

Hepatic lipase deficiency Osteoarthritis with Osteopenia

P/H – Filariasis Hypertens ion since 15yrs Fibroid uterus Mother Hypertens ion

Investigations

Miasms

Remedy

Totality Before

After

Chol273mg/ dl TG197mg/ dl LDL199mg/ dl HDL34mg/ dl Chol212mg/ dl TG 166mg/ dl LDL – 134mg/ dl HDL – 36mg/ dl

Chol268mg / dl TG – 156mg / dl LDL179 mg/ dl HDL– 42mg/ dl Chol – 198mg / dl TG – 152mg / dl LDL – 127mg / dl HDL– 40mg/ dl

MG – Stress , Anxiety,Irritable, Controls anger, Contradiction Hot application

125

Duration of treatment

Scoring

B

Result

FM

DM

A

Syco

Psora

Lyco30, 200

12mths

18

14

Improved

Syco

Syco

Lyco 200

7 mths

7

2

Improved

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Miasms

Investigations

Remedy

Totality

Before

After

17

Name: Mrs K H Age: 57 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Valencia SCR No: 56804

Familial combined hyperlipide mia Migraine, Cholelithia sis

P/H – Fibroid uterus Mother – Cardiac failure Brother Renal failure Sister - DM, Hypertension

Chol281mg/ dl TG349mg/ dl LDL163mg/ dl HDL50mg/ dl

Chol – 256mg / dl TG – 297mg / dl LDL – 143mg / dl HDL– 54mg/ dl

18

Name: Mr C Age : 63 yrs Sex: M Occu: Lab assistant Relegion: Hindu Add : Mangalore SCR No: 55419

Secondary hyperlipide mia Grade I Renal parenchym al disease, Cholecystol ithiasis Grade II BPH

P/H – Hydrocoele at the age of 28 yrs, Hypertension since 5 yrs FatherHypertension Mother- DM, Hypertension, Osteoarthritis BrotherHypertension

Chol247mg/ dl TG – 127mg/ dl LDL – 183mg/ dl HDL – 37mg/ dl

Chol209mg / dl TG113mg / dl LDL144mg / dl HDL44mg/ dl

MG – Brooding of past, Weepy, Grief, Anger on contradiction, Does not like consolation, likes company PG- Stocky appearance, Perspiration increased in general Cr- Fish Hot patient CP – Headache Burning, Radiadting to neck, Vomiting, Lachrymation < Sun, Travelling, Crowd, Tension, Talking Incontinence of urine MG- Perfectionist, Confident PG – Stocky appearance Profuse general perspiration, offensive, yellow staining Cr- Fish Addiction – Smoking till 28yrs, Beer occasionally Chilly patient CP – Pricking pain in loin < Exertion

126

Duration of treatment

Scoring

Result

FM

DM

SycoSyphil

PsoraSyco

Lyco 200

4 mths

19

12

Improved

Syco

Syco

Calc carb 10 M

10mths

14

4

Improved

B

A

Sl. No

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Miasms

Investigations

Remedy

Totality

Before

After

19

Name: Mrs A M Age : 50 yrs Sex: F Occu: Lab assistant Relegion: Christian Add : Surathkal SCR No: NITK 06

Polygenic hyperchole sterolemia Varicose veins Osteoarthrit is Cervical spondylosis

P/H – Eczema in childhoodBro nchial asthma since 20 yrs Cerebral infarction

Chol251mg/ dl TG102mg/ dl LDL186mg/ dl HDL44mg/ dl

Chol176mg / dl TG70mg/ dl LDL106mg / dl HDL56mg/ dl

20

Name: Mrs B Age :60yrs Sex: F Occu: Housewife Relegion: Muslim Add : Kasargod SCR No: 5535

Polygenic hyperchole sterolemia CAD APD

P/H – Haemorrhoids since 25 yrs Low back ache since 6 yrs Mother & 2 brothers died of cancer Brother died of MI Brother Haemorrhoids

Chol412mg/ dl TG – 98mg/ dl LDL – 349mg/ dl HDL – 44mg/ dl

Chol330mg / dl TG68mg/ dl LDL 275mg /dl HDL42mg/ dl

FM MG – Mild, Weak memory, Inadequate confidence PG – Stocky appearance Appetite increased Thirst decreased profuse Perspiration Cr-Tea, Icecream, Sweets, Hot food, Fish, Spicy but disagreesAv- Oily food Ambhithermal CP – Aching pain of legs < Exertion, Standing Pricking pain & stiffness of joints < first movement > wam application MG – Irritable, Does not express /share, Suppressed emotion, Anxious about health, Weeps alone, Anger on contradiction, Fear of Snakes, Darkness, Robbers, Being alone, Weak memory PG – Stocky appearance Appetite decreased, Thirst decreased Cr- Fish, Sweet, Sour, Meat Unsatisfied stool Sleep disturbed Ambithermal CP- Breathlessness < Lying, Tension, Exertion Distension of abdomen < Early morning

127

Syco Syphil

Syphil

Duration of treatment

DM Syco

Syco

Scoring

B

Result

A

Puls 200

10mths

13

0

Improved

Nat Mur 200

8mths

19

16

Improved

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

21

Name: Mrs P B Age : 61 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Padil SCR No: 1727

Familial hyperchole sterolemia Osteoarthrit is Cervical spondylosis

P/H – Fibroid uterus, Hypertension since 14 yrs Hypothyroidis m since 5yrs Ganglion

Chol – 346mg/ dl TG 206 mg/ dl LDL – 287mg/ dl HDL18 mg/ dl

Chol276mg / dl TG 194mg / dl LDL196mg / dl HDL42 mg/ dl

22

Name: Mr M S Age : 30yrs Sex: M Occu: Business Relegion: Muslim Add : Adur SCR No: 7994

Familial combined hyperlipide miaTension headache Flatulent dyspepsia Arthritis

FatherHypertension MotherHypertension, DM, Gastritis

Chol390mg/ dl TG – 178mg/ dl LDL – 315mg/ dl HDL – 41mg/ dl

Chol296mg / dl TG – 156mg / dl LDL – 229mg / dl HDL– 46mg/ dl

FM MG – Grief, Consolation Hot drinks

128

Duration of treatment

DM

Scoring

B

Result

A

Syco

Syco

Medorrhin 200

12 mths

29

16

Improved

Syco

Psora

Lyco 200, 1M

5mths

20

15

Improved

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

23

Name: Mr A Age : 52 yrs Sex: M Occu: Bus conductor Relegion: Christian Add : Deralakatte SCR No: 8424

Secondary Hyperlipidemia Diabetis Mellitus

P/H – Jaundice, Lipoma

Chol – 217mg/ dl TG – 146mg/ dl LDL – 148mg/ dl HDL – 40mg/ dl

Chol – 200mg / dl TG – 139mg / dl LDL – 128mg / dl HDL– 45mg/ dl

24

Name: Mrs J Age :36 yrs Sex: F Occu: Housewife Relegion: Muslim Add : Arkula SCR No: 3647

Secondary hyperlipidemia Osteoarthritis Cervical spondylosis Varicose veins Hypertension Diabitis Mellitus

P/H – Malaria, Tonsillitis Nasal polyp, Cervical lymphade nopathy, Valvular stenosis MotherDM BrotherDM, Cardiac disease

Chol240mg/ dl TG208mg/ dl LDL – 151mg/ dl HDL48mg/ dl

Chol – 218mg / dl TG – 160mg / dl LDL – 138mg / dl HDL– 48mg/ dl

FM MG – Stress, Perfectionist Likes company, Sensitive, Weepy, Irritable PG – Stocky appearance Perspiration decreased, Thirst increased Cr- Chicken, Fried, meat, fatty food, Pickle, milk Addiction – Alcohol, Smoking Chilly patient CP – Tingling & numbness of extremities < Night MG- Anxious about health, Perfectionist, Weepy, Yielding, Fear of being alone, Irritable, Short tempered, Shouts back, Likes company & Consolation PG – Obese Profuse, offensive perspiration, Thirst decreased, Cr- Chicken, Meat, Spicy Sleep disturbed, Dreams frightful, snakes Hot patient CP – Knee joint pricking pain < Exertion, Sitting > Continued motion Back pain < lying on back

129

Duration of treatment

Scoring

DM

B

Result

A

Syco

Syco

Lyco 200

5mths

6

1

Improved

Syco

Syco

Lyco 200., 1M

5mths

10

4

Improved

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

FM

DM

Duration of treatment

Scoring

B

Result

A

25

Name: Mrs A N Age : 35 yrs Sex: F Occu: Housewife Relegion: Hindu Add : Ballalbagh SCR No: 17102

Familial combined hyperlipidemia Tension headache Haemorrhoids Enterobiasis

P/H – Malaria , Still birth delivery Mother – Hypertens ion FatherHypertens ion, Epilepsy

Chol260mg/ dl TG – 198mg/ dl LDL – 177mg/ dl HDL – 44mg/ dl

Chol – 237mg / dl TG – 179mg / dl LDL – 155mg / dl HDL– 49mg/ dl

MG – Courageous, Cannot tolerate insults, Irritale, Shouts back. Dipressed, Fear of snakes, Tensed on silly matters PG – Stocky appearance Perspiration increased on neck & back, Thirst increased, Cr- Leafy veg, Sweets Dreams of falling down, Escaping Chilly patient CP – Headache throbbing < Crowd, Noise, Tension > Warmth, Rest Hard stool Burning < Chicken

Syco Syphil

PsoraSyco

Calc Carb 200

5mths

15

9

Improved

26

Name: Mrs C G Age : 55 yrs Sex: F Occu: Housewife Relegion: Christian Add : Ladyhill SCR No: 10548

Familial hypercholester olemia Migraine, Allergic rhinitis

P/H – Chickenp ox MotherHypertens ion, Hyperchol esterolemi a, MI FatherExpired of Carcinom a thyroid

Chol270mg/ dl TG – 147mg/ dl LDL – 203mg/ dl HDL – 38mg/ dl

Chol – 253mg / dl TG – 140mg / dl LDL – 183mg / dl HDL– 42mg/ dl

MG – Suppressed emotion, Grief, Relegious, Anxious about health, Fastidious, Likes company & consolation PG – Lean, Perspiration increased in general, Thirst increased, Cr- Warm Sleep unrefreshing Hot patient CP – Sneezing < Morning, Nose & eye itching Watery coryza Head heaviness < Morning > Vomiting

SycoSyphil

Psora

Sulphur 200

3mths

14

13

Improved

130

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

Investigations

Miasms

Remedy

Totality Before

After

27

Name: Mrs J D Age : 70 yrs Sex: F Occu: Housewife Relegion: Christian Add : Konaje SCR No: 16373

Familial combined hyperlipidemia Osteoarthritis

P/H – Hypertens ion since 10 yrs Father – Carcinom a throat Sister IHD

Chol272mg/ dl TG186 mg/dl LDL – 191mg/ dl HDL44mg/ dl

Chol259mg / dl TG – 170mg / dl LDL – 174mg / dl HDL– 51mg/ dl

28

Name: Sr S Age : 58 yrs Sex: F Occu: Teacher Relegion: Christian Add :Mangalore SCR No: 18316

Familial combined hyperlipidemia Flatulent dyspepsia Cervical spondylosis Uterine fibroid

P/H – Typhoid Pneumoni a Mother – Fibroid uterus, Hypertens ion Fatherhypertensi on

Chol299mg/ dl TG208mg/ dl LDL207mg/ dl HDl51mg/ dl

Chol260mg / dl TG97mg/ dl LDL183mg /dl HDL58mg/ dl

FM MG – Mild, Weepy, Consolation >, Memory weak PG – Stocky appearance Appetite decreased, Thirst decreased Perspiration increased on head Cr- Salt. Hard stools, Burning micturition Hot patient CP- Knee joint pain < Morning, walking, > Rest Pressure incontinence of urine MG – Forsaken feeling, Insecurity, Sympathetic, Irritable, hates contradiction, Does not like consolation, Suppressed emotion, Fear of disease PG – Stocky appearance Perspiration increased on upper part of body, yellow staining Thirst increased Cr- Veg Av- Salt, Milk Hard difficult stool once in 2 days Urine difficult to control. Sleep disturbed Hot patient CP – Fullness in abdomen < Pork, Dal, Fish Neck pain < movement, Sitting straight

131

Duration of treatment

DM

Scoring

B

Result

A

SycoSyphil

Syco

Calcarea carb 200

4mths

15

13

Improved

Syco

Syco

Sepia 200

12mths

17

13

Improved

Sl. no

Particulars Of The Patient

Clinical Diagnosis

Past And Family History

29

Name: Mr A R Age : 30 yrs Sex: M Occu: Contractor Relegion: Muslim Add : Kallappu SCR No: 12984

Hepatic Lipase deficiency Obesity

Mother – Filariasis, DM

30

Name: Mr P M Age : 29 yrs Sex: M

Polygenic hypercholester olemia Obesity Tension headache

Father – Hypertens ion, DM

Occu: Merchant navy Relegion: Christian Add : Kulai SCR No: 17226

Investigations

Miasms

Remedy

Totality Before

After

Chol212mg/ dl TG200mg/ dl LDL140mg/ dl HDL32mg/ dl Chol205mg/ dl TG91mg/ dl LDL143mg/ dl HDL45mg/ dl

Chol188mg /dl TG171mg / dl LDL114mg / dl HDL40mg/ dl Chol200mg / dl TG90mg/ dl LDL141mg / dl HDL41mg dl

MG- Irritable, Quarrelsome, Obstinate, Anxious, Contradiction Rest Eye redness < Exposure to heat

132

Duration of treatment

Scoring

B

Result

FM

DM

A

PsoraSyco

Psora

Lyco 200

3mths

9

2

Improved

Syco

Psora

Calc carb 200

3mths

4

4

Not improved

133