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Direct Effect of Hepatitis B Infection on Insulin Resistance

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Background: Dhatu Sarata is defined as the supreme quality & functional aspect of Dhatu. (2) Chakrapani described it as "Vishuddhatara Dhatu," which means the finest, purest & excellent state of Dhatu. It is the actual test to measure an individual's strength (physical and mental). On the other hand, Intelligence is a feature that is defined to describe a person's cognitive abilities concerning their Sarata. Aim: The Present study primarily deals with intelligence quotient (IQ) & its correlation with Dhatu Sarata through questionnaires & assessments with special reference to Rasa and Rakta Sarata. Material & methods: The present survey(Observational) study was conducted on apparently healthy individuals randomly selected from O.P.D/I.P.D. of Pt. Khushilal Sharma Government (Autonomous) Ayurvedic College and Institute, Bhopal (Madhya Pradesh), including students and staff of the college and people living in the surrounding areas. All the volunteers who have Rasa or Rakta Sarata evaluated by Ayursoft software were further assessed for IQ with the help of the Wechsler Adult intelligence scale online test with 20 questions. A non-parametric test (Spearman Correlation) was used to explore the correlation between the two variables, i.e., Rasa Sarta &IQ and Rakta Sarta & IQ, as at least one of the variables. Result & observations: Out of 300 individuals, a total of 290 persons were found to be of Rasa Sara and Rakta Sara. There was a moderate correlation between Rasa Sarata & IQ, while Rakta Sarta and IQ showed a strong positive correlation. These positive findings obtained through this study validate the classical reference about the clinical manifestation of Rasa & Rakta Dhatusarata. Conclusion: Furthermore study can be carried out to find out its relationship with recent laboratory parameters. All remaining Dhatu Sarata can also be studied & compared with IQ level.
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INTERNATIONAL JOURNAL OF RESEARCH IN MEDICAL SCIENCES & TECHNOLOGY
INTERNATIONAL JOURNAL OF RESEARCH IN MEDICAL
SCIENCES & TECHNOLOGY
e-ISSN:2455-5134; p-ISSN: 2455-9059
Direct Effect of Hepatitis B Infection on Insulin Resistance
*Moafak Ali Kamal, **Alaa Fadhel Ibrahem Cabhs,
#Hasan Salh Abbas Al-Naqeeb
* M. B. Ch. B. (Diploma Medicine), Ministry of Health, Karbala Health Directorate-
Department of Inspection and Complaint, Karbala, Iraq.
** MD, Ministry of Health, Baghdad Medical office-Al-Karkh, Al-Yarmouk
Teaching Hospital, Baghdad, Iraq.
# M. B. Ch. B. (Baghdad University), Diploma Medicine (Kufa University)
Ministry of Health, Karbala Health Directorate, Gynecology and
Obstetrical Teaching Hospital, Karbala, Iraq.
Paper Received: 19th February, 2021; Paper Accepted: 15th March, 2021;
Paper Published: 15th March, 2021
DOI: http://doi.org/10.37648/ijrmst.v11i01.002
How to cite the article:
Moafak Ali Kamal, Alaa Fadhel Ibrahem
Cabhs, Hasan Salh Abbas Al-Naqeeb,
Direct effect of hepatitis B infection on
insulin resistance, IJRMST, January-June
2021, Vol 11, 9-20, DOI:
http://doi.org/10.37648/ijrmst.v11i01.002
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INTRODUCTION
Hepatitis is an infection that causes
hepatitis/liver irritation. The most well-
known types of this infection are hepatitis
A, B and C. The hepatitis C infection,
which is communicated through the blood,
is riskier, in light of the fact and exist no
fortification for this infection. Hepatitis C
keeps the liver from doing its ordinary
capacities. An individual has diabetes
when the body experiences issues
engrossing (glucose). Glucose is a
wellspring of energy that additionally
influences all organs and muscles in the
body. Since glucose is handled through the
liver like different supplements, the
connection between hepatitis C and
diabetes ought not be astounding.
Hepatitis can cause diabetes in two
fundamental manners. Right off the bat,
diabetes can happen in light of the fact that
somebody has a background marked by
persistent hepatitis as the constant hepatitis
C infection at last makes it hard for the
liver to dispose of abundance glucose.
Whenever left untreated, the condition can
ultimately cause hyperglycemia. The
hepatitis C infection likewise builds
insulin obstruction. This is a significant
danger factor for type 2 diabetes.
Worldwide, and the absence of a rapid and
expanded response, is expected to remain a
ABSTRACT
The aim of this research is to find out the targeted effect between insulin resistance and
viral hepatitis B (CVHB) Insulin resistance - a blood sugar disorder that precedes
diabetes mellitus - is a hallmark of chronic hepatitis C infection, regardless of the severity
of the virus or other "metabolic" factors.
Method: 100 samples were collected and a medical examination was performed on the
patients. The second step is described as aiming to find out the factors in relation to the
metabolism and liver B antigen. As for the determinants that were used in order to know
insulin sensitivity, the determinants were HOMA, QUICKI and Mffm.
Conclusion: Our test exhibits that CVHB is related with IR. CVHB may should be
observed for event of IR and diabetes mellitus
Keywords: Hepatitis, IR, Aminotransferase, CVHB, HOMA
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number People living with hepatitis B
virus:
Its current high levels are the same
throughout the 40 years or so the next
fifty, as is the cumulative number of deaths
that will occur Between 2015 and 2030
there will be 20 million deaths. As for the
number People living with the hepatitis C
virus are: Really increased, although there
is an effective treatment for it. It was no
longer possible Postpone strengthening of
the global response the five hepatitis
viruses (A, B, C, D and E) differ. Great
difference between them, and
characterized by different transmission
patterns, and affect in different
populations, which results in a difference
Health outcome. An effective response
requires a combination of Standardized
procedures, with tailored interventions
offered for each One of the five viruses at
the same time.
Elimination of hepatitis epidemics as one
of the major public health threats is
possible using:
Currently available tools and approaches
are under development and exist
Opportunities to improve and expand the
response by investing in five Areas for
basic interventions, namely
1. Vaccines - effective vaccines are
available to prevent infection Each
of the viral hepatitis A, B, and E
where they operate A group of
countries is already implementing
large-scale programs It is
inexpensive to vaccinate children
against hepatitis B virus
2. Prevention of mother-to-child
transmission of hepatitis B virus
Child - timely vaccination at birth
with a dose Hepatitis B virus
vaccine is an essential intervention
for preventing hepatitis B virus
Transmission of the virus from
mother to child at birth, which is
possible Improve it through
prenatal screening and use
Antiviral drugs.
3. Reduced harm for injecting drug
users - can be guaranteed Access to
sterile injection tools and addiction
treatment services Drug, to prevent
epidemics of hepatitis B And
combating them among drug users
who inject drugs as part of a
package A comprehensive range of
interventions for the prevention,
treatment and care of the injured
with human immunodeficiency
virus and viral hepatitis and other
blood-borne infections of drug
user’s injection
4. To treat - new oral medications can
be tolerated patients well and
administered regimens to infected
patient’s Chronic hepatitis virus
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achieving cure rates of over 90% is
also available effective treatment
for those with chronic infection
with hepatitis B virus, provided
treatment continues throughout life
for most of those infected
Often prevention programs and especially
for certain population groups, which are
the most affected and exposed to risks,
limited in scope and coverage And
between 2000 and 2010, there was a
decrease of 91% in Hepatitis B virus
infection, 83% reduction in infection
Hepatitis C virus resulting from unsafe
injections However, it is estimated that
medical injections and is still responsible
for 1.7 million new infections With
hepatitis B virus annually and between
157,000 and 315,000 cases New hepatitis
C infection annually. The coverage
decreases Global harm reduction programs
for people who inject drugs, including
That's about needle and syringe programs,
about 10% by the year In 2014, global
HIV vaccination coverage increased Liver
B in childhood to more than 82%, but
vaccination With a dose of vaccine at
birth, hepatitis B virus retarded Far behind
its coverage did not exceed 3 And Because
of the lack of testing strategies and tools
Simple and effective, less than 5% of
infected people are known Chronic
hepatitis ordered their infection. For this
reason, the diagnosis It often comes late,
and appropriate tests are rarely available
for evaluation Liver disease guides
treatment decisions, including directing
them when Starting treatment.
The possibility that liver fat causes insulin
resistance in the body, which causes a
decrease in its effect on blood sugar, and
then type 2 diabetes occurs. Professor
Michael Roden of the Austrian Hanus
Hospital in the capital, Vienna, explained
that liver fat is one of the common
consequences of weight gain, noting that
medical studies have shown that these fats
play a pivotal role in the development of
metabolic syndrome, which results from
weight gain in the abdominal area in
particular and high cholesterol. In addition,
blood sugar, and because of high blood
pressure, this syndrome may lead to early
arteriosclerosis resulting from calcification
of blood vessels, heart attacks or strokes.
Insulin resistance is a condition in the
body characterized by a decrease in the
sensitivity of tissues to the effects of
insulin, which leads to an elevated level of
insulin in the blood. Increased insulin
levels, in turn, have a pathological effect
on the vascular wall, which contributes to
the formation of atherosclerotic lesions.
Moreover, insulin resistance is a
significant risk factor for complications,
which increases mortality from
cardiovascular disease to 65% In addition,
prolonged hyperinsulinemia leads to
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depletion of the isolated system of the
pancreas, leading to type 2 diabetes in
addition. In addition, this study is relevant
to patients with chronic viral hepatitis - a
number of recent studies show an
insufficient effect of antiviral therapy if the
patient has an increased level of insulin
resistance.
MATERIAL AND METHOD
All the necessary tests and requirements
for the patients were performed with
opinions on them all the medical
examinations and all the participants had
all the required conditions and met all the
accompanying measures: age 18 years,
without history of diabetes and
hypertension that significant prescription,
negative for hepatitis C neutralizer serum
aspartate Aminotransferase or alanine
aminotransferase (ALT) <80 IU/L, serum
gamma glutamyl transferase (GGT) <80
mg/dL, serum creatinine <1.5 mg dL, The
success assessment that gave our
evaluation data interweaved a certified
appraisal, anthropometric examinations,
and blood tests. Height and weight were
surveyed to the closest 0.1 cm and 0.1 kg
utilizing the standard show for subjects
wearing a light outfit and without shoes.
Weight list (BMI) was settled as weight
(kg) isolated by the square of tallness
(m2). Waist circuit was evaluated at the
most invulnerable point between the lower
line of the rib keep and the iliac top,
toward the finishing of a standard sneak
past of breathing and to the closest 0.1 cm.
Muscle versus fat extent and all out-fat
mass were evaluated by bioelectric
impedance appraisal. Heartbeat was
evaluated utilizing the correct arm of
individuals who were in an orchestrated
condition, after they had rested for at any
rate 10 minutes.
The centralizations of lipid, uric corrosive
and GGT were estimated utilizing an
autolyser utilizing the enzymatic
chromatography strategy, Cystatin C was
estimated by turn around immunoassay,
and it was estimated by the hepatitis B
antigen-connected immunosorbent test
technique.
STATISTICAL ANALYSIS
100 samples were collected and the
statistical analysis required finding the p-
value and find a value was conducted
MEAN ±SD and the statistical analysis
was performed using a program SPSS25
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RESULTS
Table 1- Baseline characteristics
Variables
Men
Women
60
40
AGE (YR)
50.2 ± 11.8
49.7± 11.1
BMI (KG/M2)
25.6 ± 2.9
24.9 ± 2.7
PERCENTAGE BODY FAT (%)
23.5 ± 5.5
31.7 ± 6.1
SYSTOLIC BP (MMHG)
128.1 ± 16.1
122.3 ± 15.4
AST (IU/L)
24.1 ± 8.2
21.1 ± 11.1
ALT (IU/L)
27.8 ± 17.1
20.0 ± 11.1
GAMMA-GLUTAMYL TRANSFERASE
37.1 ± 20.3
20.0 ± 12.6
FASTING PLASMA GLUCOSE (MG/DL)
92.2 ± 15.5
89.3 ± 15.3
F.NSULIN (ΜU/ML)
5.50 ± 3.43
5.1 ± 3.22
TC (MG/DL)
198.3 ± 33.1
198.8 ± 35.2
TRI (MG/DL)
140.0 ± 81.1
102.9 ± 65.1
HIGH-DENSITY LIPOPROTEIN (MG/DL)
51.1 ± 12.5
58.8 ± 14.1
LOW-DENSITY LIPOPROTEINS (MG/DL)
125.1± 30.3
123.2 ± 32.2
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Table 2- Means ±SD of metabolic hazard influence relationship with hepatitis B virus
Negative
Recovery from hepatitis B
Chronic hepatitis B)
43.2 ± 10.9
50.9 ± 10.1
50.8 ± 10.7
25.2 ± 2.8
25.1 ± 2.9
24.9 ± 2.6
87.0 ± 7.5
87.3 ± 7.1
87.7 ± 7.3
23.4 ± 5.6
23.7 ± 4.5
23.9 ± 4.9
127.3 ± 16.4
127.3 ± 15.1
127.1 ± 16.6
197.0 ± 34.1
197.3 ± 34.6
196.6 ± 35.6
143.1 ± 85.2
136.2 ± 80.2
136.1 ± 79.1
52.0 ± 11.9
51.3 ± 12.5
51.3 ± 12.5
90.7 ± 15.3
92.1 ± 14.4
91.9 ± 14.4
5.47 ± 3.38
5.29 ± 3.10
5.9 ± 4.11
1.24 ± 0.86
1.22 ± 0.80
1.43 ± 1.24
0.31 ± 0.077
0.34 ± 0.055
0.362 ± 0.132
9.31 ± 2.43
9.45 ± 3.44
8.33 ± 3.11
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Figure 1- P Value for risk factors
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CORRELATION
Table 3- insulin affect reactivity
BMI
WC
BFP
FPG
0.144
0.166
0.123
Insulin
0.334
0.431
0.452
HOMA index
0.442
0.452
0.231
QUICKI index
-0.224
-0.331
-0.491
Mffm index
-0.258
-0.446
-0.399
Table 4 - Logistic regression test
P
IR
HOMA
QUICKI
β
SE
(95% CI)
β
SE
(95% CI)
Hepatitis B virus status
Negative
1.000
1.000
Recovery from hepatitis B
-0.032
0.198
0.81 (0.625-1.025)
-0.066
0.143
0.897 (0.644-1.15)
Chronic hepatitis B
0.42
0.120
1.569 (1.108-2.031)
0.347
0.154
1.745 (1.211-2.282)
DISCUSSION
In this test, CVHB apparently was
connected with IR in subjects without past
diabetes. CVHB self-sufficiently foreseen
a clinically enormous development in the
odds extent for IR improvement. These
outcomes show that patients with CVHB
may require close checking for the rate of
infrared radiation and diabetes. Since the
ebb and flow, test reports benchmark data
on the connection among CVHB and IR in
an enormous people, these results maintain
past suggestions that CVHB illness is
connected with IR It is an in part
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abandoned twofold infection that
utilizations switch replication in the
replication cycle. CVHB contamination is
a medical issue that influences around
3.7% of the complete populace with
constant hepatitis B. The greater part of
them were contaminated straightforwardly
from the mother during labor or through
contact between the youngsters. CVHB
disease may expand the rate of cirrhosis,
cirrhosis, and hepatocellular carcinoma. In
addition, CVHB contamination is related
with sicknesses like PAN, GN, and joint
inflammation besides, there is exploratory
proof that CVHB disease expands the
presence of both IR and related diabetes
mellitus. A new creature study
demonstrated that HBx weakens the
insulin-flagging pathway, The infrared
radiation is thought to be brought about by
inadequate glucose digestion limit which
prompts the discharge of more insulin to
accomplish a similar organic reaction and
hyperinsulinemia may prompt a huge
assortment of anomalies in the veins,
kidneys and muscles, which is the
principle infection related with metabolic
condition. Diabetes and metabolic
condition are likewise free danger factors
for atherosclerosis, and in this manner,
early screening of high-hazard bunches is
vital for fruitful wellbeing advancement.
The best quality level for deciding insulin
affectability is the insulin hyperglycemia
procedure. The HOMA model, QUICKI
list, and Mffm utilized in this investigation
exhibit a decent relationship with the
neural connection strategy and can be
effectively utilized in introductory
practice.
CONCLUSION
Insulin opposition (IR) is the important
sign for improvement of metabolic
condition and type 2 diabetes. Constant
viral hepatitis B (CVHB) is quite possibly
the most widely recognized medical
conditions and past clinical examinations
additionally propose that hyperinsulinemia
happens in CVHB. Notwithstanding, the
impact of hepatitis B infection (HBV)
contamination on human insulin
affectability stays disputable. The creators
subsequently examined the theory that
HBV disease may connect with IR and
metabolic condition, by contrasting
occurrence of IR between HBV-
contaminated subjects and solid gathering.
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Previous studies of polyarteritis nodosa (PAN) included patients with microscopic polyangiitis, because these entities were not distinguished prior to the Chapel Hill Consensus Conference (CHCC). This study was undertaken to describe the main characteristics of and long-term outcomes in patients with well-characterized PAN diagnoses. We conducted a systematic retrospective study of 348 patients who were diagnosed as having PAN between March 1963 and October 2005, were registered in the French Vasculitis Study Group database, and satisfied the American College of Rheumatology and CHCC criteria. Patient characteristics and outcomes were analyzed and compared according to hepatitis B virus (HBV) status. At diagnosis, the mean +/- SD age was 51.2 +/- 17.3 years. The most frequent findings were general symptoms (93.1%), neurologic manifestations (79%), skin involvement (49.7%), abdominal pain (35.6%), and hypertension (34.8%); 66.2% had renal artery microaneurysms; 70.1% had histologically proven PAN. Patients with HBV-related PAN (n = 123) had more frequent peripheral neuropathy, abdominal pain, cardiomyopathy, orchitis, and hypertension compared with patients with non-HBV-related PAN (n = 225). During a mean +/- SD followup of 68.3 +/- 63.5 months, 76 patients (21.8%) relapsed (63 with non-HBV-related PAN [28%] versus 13 with HBV-related PAN [10.6%]; P < 0.001); 86 patients (24.7%) died (44 with non-HBV-related PAN [19.6%] versus 42 with HBV-related PAN [34.1%]; P = 0.003). Five-year relapse-free survival rates were 59.4% (95% confidence interval [95% CI] 52.6-67.0) versus 67.0% (95% CI 58.5-76.8) for non-HBV-related PAN and HBV-related PAN, respectively. Multivariate analysis retained age >65 years, hypertension, and gastrointestinal manifestations requiring surgery or at least consultation with a surgeon as independent predictors of death, whereas patients with cutaneous manifestations or non-HBV-related PAN had a higher risk of relapse. Our findings indicate that the rate of mortality from PAN remains high, especially for the elderly, and relapses do occur, particularly in patients with non-HBV-related PAN with cutaneous manifestations.
Article
Recent evidence indicates that viral hepatitis is sometimes associated with the production of extrahepatic tissue injury. Hepatitis B virus (HBV) infection is most commonly incriminated but non-type B hepatitis may also be involved. Three types of syndromes have been recognized. First, a serum sickness-like prodrome consisting of skin eruptions, urticaria and polyarthralgias or arthritis may occur from one to six weeks prior to the onset of hepatitis in 15 to 20 per cent of patients and usually disappears by the time the patient becomes jaundiced. There is extensive evidence that circulating immune complexes are responsible for these symptoms. Second, about 30 to 40 per cent of patients with typical polyarteritis nodosa have persistent hepatitis B surface antigenemia (HBs Ag). Circulating immune complexes composed of HBs Ag, antibody, and complement have been demonstrated together with deposits of immune complexes at sites of vascular injury. Third, an immune complex type of glomerulonephritis may occur following hepatitis B virus infection, usually in association with chronic active hepatitis. Thus there is impressive evidence that hepatitis viruses, especially HBV, may produce a variety of extrahepatic manifestations in which the mechanism of pathogenesis involves an immunologic process rather than direct viral invasion and cytopathogenicity.
Article
The natural course of adult hepatitis B virus (HBV)-related membranous nephropathy in areas where HBV infection is endemic (characterized by vertical and horizontal transmission of HBV in early childhood) has not been fully defined. We evaluated the clinical features, pathological findings, serologic profiles, therapeutic responses, and prognoses of 21 patients with adult-onset HBV-related membranous nephropathy. The patients were followed for a mean of 60 months (range, 12 to 108). Only patients with evidence of glomerular capillary deposition of hepatitis B e antigen (HBeAg) in a renal-biopsy specimen were included. The clinical features and serologic studies suggested that the patients had acquired chronic HBV infection in early childhood; moreover, other causes of membranous nephropathy had been excluded. All were seropositive for hepatitis B surface antigen and had high titers of antibody to hepatitis B core antigen at first clinical presentation. HBeAg was detected in the serum of 17 patients (81 percent), yet only 3 had even slightly increased plasma alanine aminotransferase levels. The clinical response to therapy with interferon alfa was disappointing; only one of the five patients treated had a complete remission with seroconversion to antibody to HBeAg. Contrary to reports of studies in children, spontaneous remission of the nephrotic syndrome or proteinuria was uncommon in the adults with HBV-related membranous nephropathy whom we studied. Proteinuria and HBV antigenemia persisted in untreated patients. During the follow-up period, 29 percent of the patients had progressive renal failure and 10 percent required maintenance dialysis therapy. The course of HBV-related membranous nephropathy in adults in areas where HBV is endemic is not benign. Regardless of treatment, the disease has a slowly but relentlessly progressive clinical course in approximately one third of patients.
Article
The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
Article
The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to <7.0 mmol l(-1); whole blood > or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.