Type 1 diabetes is the most common form of diabetes in children: 90 to 95 per cent of under 16s with diabetes have this type.It is caused by the inability of the pancreas to produce the hormone insulin.Type 1 diabetes is classified as an autoimmune disease, meaning a condition in which the body's immune system 'attacks' one of the body's own tissues or organs.In Type 1 diabetes it's the insulin-producing cells in the pancreas that are destroyed.
As with adults, the cause of childhood diabetes is not understood. It probably involves a combination of genes and environmental triggers. The majority of children who develop Type 1 don't have a family history of diabetes.
The main symptoms are the same as in adults. They tend to come on over a few weeks:
Drinking more than usual, including overnight, frequent urination, including overnight, weight loss, tiredness.
Symptoms that are more typical for children include:
Tummy pains, headaches, behaviour problems.
Sometimes diabetic ketoacidosis occurs before diabetes is diagnosed, although this happens less often in the UK due to better awareness of the symptoms to look out for. Doctors should consider the possibility of diabetes in any child who has an otherwise unexplained history of illness or tummy pains for a few weeks. If diabetes is diagnosed, your child should be referred to the regional specialist in childhood diabetes.
The specialised nature of managing childhood diabetes means that most children are cared for by the hospital rather than by their GP. Most children with diabetes need insulin treatment. If this is the case, your child will need an individual insulin routine, which will be planned with the diabetes team.
Most now use frequent daily dosage regimes of fast-acting insulin during the day and slow-acting insulin at night.
Very small children normally don't need an injection at night, but will need one as they grow older.
Increasing numbers of children use continuous insulin pumps.
Often in the first year after diagnosis, your child may need only a small dose of insulin. This is referred to as 'the honeymoon period'.
As well as insulin treatment, good glucose control and avoidance of ‘hypos’ (low blood glucose attacks) is important.
This is because many of the complications of diabetes increase with the length of time diabetes has been present.
Type 1 diabetes is the most common form of diabetes in children: 90 to 95 per cent of under 16s with diabetes have this type.It is caused by the inability of the pancreas to produce the hormone insulin.Type 1 diabetes is classified as an autoimmune disease, meaning a condition in which the body's immune system 'attacks' one of the body's own tissues or organs.In Type 1 diabetes it's the insulin-producing cells in the pancreas that are destroyed.
As with adults, the cause of childhood diabetes is not understood. It probably involves a combination of genes and environmental triggers. The majority of children who develop Type 1 don't have a family history of diabetes.
The main symptoms are the same as in adults. They tend to come on over a few weeks:
Drinking more than usual, including overnight, frequent urination, including overnight, weight loss, tiredness.
Symptoms that are more typical for children include:
Tummy pains, headaches, behaviour problems.
Sometimes diabetic ketoacidosis occurs before diabetes is diagnosed, although this happens less often in the UK due to better awareness of the symptoms to look out for. Doctors should consider the possibility of diabetes in any child who has an otherwise unexplained history of illness or tummy pains for a few weeks. If diabetes is diagnosed, your child should be referred to the regional specialist in childhood diabetes.
The specialised nature of managing childhood diabetes means that most children are cared for by the hospital rather than by their GP. Most children with diabetes need insulin treatment. If this is the case, your child will need an individual insulin routine, which will be planned with the diabetes team.
Most now use frequent daily dosage regimes of fast-acting insulin during the day and slow-acting insulin at night.
Very small children normally don't need an injection at night, but will need one as they grow older.
Increasing numbers of children use continuous insulin pumps.
Often in the first year after diagnosis, your child may need only a small dose of insulin. This is referred to as 'the honeymoon period'.
As well as insulin treatment, good glucose control and avoidance of ‘hypos’ (low blood glucose attacks) is important.
This is because many of the complications of diabetes increase with the length of time diabetes has been present.
I will add to what Marcelo has already included above, relating to a few points not touched upon:
There is unfortunately no "cure". Type 1 diabetes is only managed through exogenous insulin and unfortunately, needles are a big part of this management (in measuring glucose levels more than once a day and giving insulin shots). [There were few experimental designs at one point that forced the insulin jet through a very narrow bore at very high pressure into the skin - I'm not sure what came of them, they do not seem to commonly used.]
Insulin injections are not quite the replacement of precise and dynamic control beta cells provide. As alluded to in the previous post, using larger than necessary insulin creates a potentially far more dangerous situation of hypoglycemia, which can be fatal. Treatment with insulin is designed to err or the side of caution, accepting the cost of transient hyperglycemia to avoid hypoglycemia. Of course, these excursions on high side, in the long run have their cumulative consequences.
Organ transplant does provide a far better control but it entails a life-long immunosuppression and there is always a severe shortage of donor organs so this method is not available to everyone.
Consult a good diabetes clinic where trained nurses could be very good in dealing with children and gradually putting their fears of needles to rest.
In future, we hope to treat this disease through insulin gene therapy. Our expectation is that a single treatment cycle will adequately control blood glucose (dynamically) for more than a month, possibly a year... stay tuned!
well the quest goes on to develop oral insulin although till that time one has to deal with it and see to it that it is not part of a larger autoimmune syndrome where other organs like thyroid gland and pituitary etc may also be involved so the childs whole hormonal evaluation is needed also in such cases as one comes across such case reports where syndromes are there with these autoimmune phenomenon and right noe human insulin is the only answer till the child grows up and the other options as sauggested alkthough whether any herbs can work or not in an autoimmune phenomenon dr krishnan plwase provide some documented publiucations as as far as one knows only in type 2 diabetics such therapies work and if at all anything works the mechanism of action ans cab they affect the T cell phenomenon which is disturbed in these children and treg cells etc/
you are welcome and recently sanofi has come up with inhalable insulin which maybe of help for your patient who abhors injections if it is of any help .In thje meantime hopefully everything has been assessed regarding polyglandular involvement which can occasionally occur inthese young children .Idont know how just adding vitamins will affect the diabetes status but there is no harm in adding them .
ALTHOUGH IT IS KNOWN THAT TYPE 1 dm IS AN AUTOIMMUNE DISEAESE RESULTING FROM T Cell Mediated Destruction of beta cellz .Recently special invdstigations of role of MYd 88 WHICH IS USED BY MULTIPle TLR'S (INNATE PATTERN RECOG ITION RECEPTORS),showed that signaling through receptors which use MYd88 adaptor is critical for development of type 1 DM -NOD mice lacking TLR2/TLR4 were dispe nsable for dev of TIDM (OR PROTECTION FROM FREUNDS ADJUVANT)WHEN DELETEDINDIVIDUALLY ,in contrast the effect of complete protection from DM was asso ciated with MYD88-tHEASE FACTORS indicate indicate intestinal interactions of intestinal icriobes with innate immune system is a critical epigenetic factor modifying T1DM [redisposition and newer thrapies can be planned on this basis since MyD88 mice -negative mice with a defined microbial consortium representing human gut bacterial phyla normally present ,attenuates T1DM.
The role of innate immunity in many diseases is beginning to get appreciated, which underscores the pivotal role of intestinal (and to some degree lungs) microbes. Unfortunately, at this point our knowledge is very limited otherwise we wouldn't have been assuming that only a dead bacterium is a good bacterium.
Having said that, it is also true that a great many things that seem to work beautifully in mice utterly or largely fail in men. Various groups have shown substantial to full protection against development of mouse version of type 1 diabetes by many specific maneuvers. They are all useful tools in improving our understanding about various possibilities but due to a tremendous amount of redundancies of our immune system, I suspect that protection/prevention of T1D in men may take a while. But I must confess that it would be a fantastic progress when it happens.
dear tausif although till today i used to look down on rodent studies even of GnRH studies till i realized we dont even have models of studying GREEN FLUORESCENT PROTEIN LABELLED gNrh NEURONS except in rodents and allelectrophysiological studies which have come in making us uncderstand the neurophydsiology of reproduction or be it negative ot positive feedback has come from these and all earlier studies were practically useless where they were just studying electrical activity in mediobasal hypothalamus and hypothesize various roles and all data on kisspeptins,neurokinin B etc haave come from rodent models although there are three isoforms of GnRH neuros and in man some are obsolete and to study kallmanngebne one couldnt reproduce it in rodent models the kalman gene and one had to use other animalo models but one has to use the closest models available .and anyhow it is this healthy plaform which stimulates our brains to do some new work and it is not to insult or abuse anyone but learn from each ot5her -thanks once again for your input-kulvinder
aS WITH Marcels answer it is not clear but it is consisered an autoimmune disease where a combination of genes are considered responsible for its causation and usually in some cases it is a part of multiorgan autoimmune disorder like thyroid ,pancreas ,pituitary etc beig involved along with sjogrens syndrome and recently the role of PD1 and PDL1 and PROGRAMMED DEATH LIGANDS hae come to throw some light in such autoimmune syndromes with being found 9involved in T1d,RH ARTHRITIS,NMULTIPLE SCLEROSIS ANSD A particular polymorphism has been associated which is being investigated and might provide answers regarding further treatment of the disorder,and as with the discussion of tausif and mine we discussed local i9nnate immunity in detail -as far as variose i dont understand what you mean by that but i dony think simple psychosomatic disorders can lead to T1D-and as far s cold why should it lead to as so many people live in extreme cold countries without developng T1D UNLESSSWOME COLD PRECIPITATING ANTIBODI8ES-And hopefully one day we will get rid of the injectable insulin understanding the pathophysiology well
Over the years we have accumulated considerable fragmented knowledge about type 1 diabetes (T1D). However, we do not know everything about it. For example, we know that inheriting certain variant (alleles) genes increases the likelihood of getting T1D, just as having other alleles reduces the possibility of getting the disease. We also know that having the alleles associated with T1D only increases the possibility of getting the disease but it does not confer a certainty. In that context, two identical twins, sharing the genetic makeup, both may or may not get the disease.
The involvement of environmental factor(s) is implicit from such observations as described above. What tips the balance, has been debated. There are indications for many things, such as shortage of vitamin D3 in the upper northern hemisphere residents (not enough sun light), triggering by viral infection, even milk or milk by-products, just to name a few potential candidates.
in the case of T1D, generally speaking, the autoimmune destruction is quite targeted and not generalized, as in some other cases mentioned by Kulvinder. T1D patients tend to have no systemic autoimmune damage to other organs as long as their blood glucose is adequately controlled. Secondary complications, such as renal failure, neuropathy, vasculopathy etc. are directly associated with hyperglycemia. Poorer the control, worse the secondary complication!
The immunologists are also making progress and hoping that the aberrant immune system, which mistakenly begins destroying "self" cells, could be controlled or re educated to begin ignoring its own cells, as it does normally. Recognition of self and foreign is a dynamic and what is proving to be quite a complex process. At this point it unclear if in near future, we would be able to fully manipulate this system. When we do, that will provide an ideal solution in the form of stopping the continued damage before complete destruction of beta cells.
But until the ideal treatment is devised, we need a better treatment than what is currently available. Insulin injections and glucose level testing (multiple, daily) impacts quality of life and even with due diligence, long-term damage is not fully prevented. Pancreas transplant works well but it requires life-time use of immunosuppression. The drugs used are not trivial in terms of side effects. Furthermore, there just aren't enough donor organs for everyone.
Few groups, including mine, have focussed our efforts on gene-therapy based approach where insulin synthesis is tied to glucose level for a dynamic (self-regulated) control. By the very nature, such as system cannot respond to increase in blood glucose within a minute, as beta cells do, but a delay of 15-20 min (in our system using animal models) but it still offers a far better regulation than injectable insulin.