aus einer Hufrehe Klinik
03.06.2006, 07:26
Overview of Laminitis
From experimental studies, we now understand more about the changes which take place in the horse's hind gut following carbohydrate overload and the generally accepted view that laminal detachment is due to ischaemia (Hood et al 197 has been added to by the identification of MMP activators (Johnson 199 which may originate in the gut. Bailey et al provide an interpretation of this research which combines the two theories of ischaemia and basement membrane degradation, previously regarded by many to be incompatible. Nevertheless, applying these important findings to the clinical situation has not, as yet, yielded therapeutic improvements.
Harvey Cushing in 1932 described a fatal syndrome in humans characterised by unusual disposition of fat depots, osteoporosis, immune suppression, generalised weakness which was associated with basophilic adenoma of the pituitary gland. This syndrome we now know to be due to elevated concentrations of circulating cortisol of adrenal origin and hyperadrenocorticism has become known as Cushing's disease. In the horse Cushing's disease is always secondary to a pituitary adenoma or hyperplasia; pituitary dependent Cushing's disease (PDCD).
An important recent finding (Johnson 2002) has been the identification of a metabolic abnormality due to an abnormal activity of the 11 ß-hydroxysteroid dehydrogenase type 1 enzyme in integumentary tissue of laminitis cases. These cases differ in clinical presentation from PDCD cases in that animals of any age may be affected, they do not show the hirsuitism characteristic of advanced PDCD cases and contrastingly they all are, or have been, obese. Whilst the terms peripheral Cushing's disease and Equine Metabolic Syndrome have been suggested to describe hypercorticism not of adrenal origin, the term obesity dependent laminitis seems the most descriptive and least likely to avoid confusion with PDCD which may be better restricted to horses suffering hyperadrenocorticism.
Clinical experience has long indicated that keeping horses in a lean, fit bodily condition reduces the risk of their suffering laminitis. Indeed, dietary measures have for years often been sufficient to prevent laminitis in native ponies and cobs. Yet despite scrupulous dietary management some animals continued to suffer recurrent episodes of laminitis; Johnson's work has now provided an explanation. Laminitis is a disease of domestication. Cobs and warmbloods seem to have energy metabolism similar to that of native ponies and cannot cope with the improved pastures and calorific feeds they are exposed to. As we have strong evidence of the link between obesity and laminitis it defies understanding that those responsible for showing horses in the UK not only tolerate, but select for, obesity as a prerequisite for a champion. Whilst the average horse owner may mismanage their horses due to ignorance, laziness or lack of dieting facilities, the active promotion of obesity by show and breed societies is frank cruelty.
The presence of plasma endogenous ACTH concentrations greater than 50 pg/ml, elevated serum cortisol, insulin and glucose concentrations seems the best method of diagnosing PDCD at present. Cases with normal endogenous ACTH concentrations but with elevated serum insulin, cortisol and glucose are suggestive of insulin resistance and obesity dependent laminitis. To avoid erroneous results these tests should be made after an overnight fast and not if the horse is currently experiencing laminitis. The seasonality of PDCD, most cases suffering laminitis in the Autumn, suggests that the primary lesion may be of pineal rather than pituitary gland origin. Correlation between melatonin concentrations in PDCD cases and laminitis may be instructive when combined with histopathological examinations of the pineal gland.
Exogenous corticosteroid administration, particularly using long acting formulations has been associated with iatrogenic laminitis. The use of dexamethasone suppression testing to establish a diagnosis of Cushing's disease has been known to precipitate laminitis. Even the use of short acting corticosteroid preparations intra-articularly has resulted in laminitis. Clinical experience demonstrates that these are not inevitable sequelae of corticosteroid administration. Unfortunately, it seems impossible to predict which horses will suffer laminitis and founder following injection of corticosteroids. Nevertheless, clinicians should be aware of, and warn owners of these, sometimes fatal, sequelae to the use of corticosteroids, particularly if the animal is already at high risk of developing laminitis.
Clinicians are aware that the stress of conditions such as vaccination, worming, travelling and even proximity to low flying jets can trigger an attack of laminitis in some horses. The mechanisms in these cases are unknown but a causal association with elevated blood cortisol concentrations cannot be excluded. Laminitis is known to be predisposed to by PDCD and obesity dependent laminitis, both conditions resulting in hypercorticism. In vitro studies have demonstrated that the digital blood vessels exposed to cortisol show increased sensitivity to endogenous catecholamines (Eyre et al 1979).
Exogenous corticosteroids possess both glucocorticoid and mineralocorticoid effects. It has been suggested that corticosteroids may predispose to laminitis by increasing the permeability to gut derived activators or mediators. The mineralocorticoid effect leading to altered mineral balance should not be ignored. Serum concentrations and creatinine clearance ratios of calcium, magnesium, sodium, potassium, chloride and phosphate are often found to be abnormal in laminitis cases (Eustace unpublished data) combined with an elevated mean corpuscular volume. An association between forage mineral status, fructan concentration and mineral status of laminitis cases deserves further investigation. Particular research into the magnesium status of both forage and horse may be worthwhile as this element is thought to be lowered in herbage treated with nitrogenous fertilizers (Frape 199 and is frequently low in blood samples from laminitis cases.
Our lack of understanding of the mechanism whereby either changes in the hind gut following carbohydrate overload, or hypercorticism induce such devastating damage in the feet restricts us in improving preventative or therapeutic regimes in dietary laminitis. Until the mechanisms of these main "causes" of laminitis are better understood, it is incumbent upon us to educate horse owners in the means of preventing laminitis by using high fibre low calorie diets, restricted grazing and body condition scoring which have for years stood the test of time as an effective means of preventing this crippling disease.
References
Cushing, H. (1932)
The basophil adenomas of the pituitary body and their clinical manifestations (Pituitary Basophilsim).
Bull Johns Hosp. Vol 50 Part 137-195.
Hood D.M., Amoss M.S., Hightower D., McDonald D.R., McGrath J.P., McMullan W.C. and Scrutchfield W.L. (197.
Equine Laminitis I; Radioisotopic Analysis of the Haemodynamics of the Foot During the Acute Disease.
Journal of Equine Medicine and Surgery 2, 439 444.
Eyre, P., Elmes, P.J., & Strickland, S. (1979)
Corticosteroid-potentiated vascular responses of the equine digit: a possible phamacological basis for laminitis.
American Journal of Veterinary Research 40, 135-138
Frape, D. (199
Equine Nutrition and Feeding
2nd Ed. Blackwell Science, Oxford. P324
Johnson, P.J., Tyagi, S.C., Katwa, L.C., Ganjam, V.K., Moore, L.A., Kreeger, J.M. and Messer, N.T. (199
Activation of extracellular matrix metalloproteases in equine laminitis.
Veterinary Record. 142, 392-396.
Johnson, P.J. (2002)
The equine metabolic syndrome Peripheral Cushing's syndrome.
Veterinary Clinics Equine Practice 18. 271-293
http://www.laminitisclinic.org/Overview ... nitis.html
From experimental studies, we now understand more about the changes which take place in the horse's hind gut following carbohydrate overload and the generally accepted view that laminal detachment is due to ischaemia (Hood et al 197 has been added to by the identification of MMP activators (Johnson 199 which may originate in the gut. Bailey et al provide an interpretation of this research which combines the two theories of ischaemia and basement membrane degradation, previously regarded by many to be incompatible. Nevertheless, applying these important findings to the clinical situation has not, as yet, yielded therapeutic improvements.
Harvey Cushing in 1932 described a fatal syndrome in humans characterised by unusual disposition of fat depots, osteoporosis, immune suppression, generalised weakness which was associated with basophilic adenoma of the pituitary gland. This syndrome we now know to be due to elevated concentrations of circulating cortisol of adrenal origin and hyperadrenocorticism has become known as Cushing's disease. In the horse Cushing's disease is always secondary to a pituitary adenoma or hyperplasia; pituitary dependent Cushing's disease (PDCD).
An important recent finding (Johnson 2002) has been the identification of a metabolic abnormality due to an abnormal activity of the 11 ß-hydroxysteroid dehydrogenase type 1 enzyme in integumentary tissue of laminitis cases. These cases differ in clinical presentation from PDCD cases in that animals of any age may be affected, they do not show the hirsuitism characteristic of advanced PDCD cases and contrastingly they all are, or have been, obese. Whilst the terms peripheral Cushing's disease and Equine Metabolic Syndrome have been suggested to describe hypercorticism not of adrenal origin, the term obesity dependent laminitis seems the most descriptive and least likely to avoid confusion with PDCD which may be better restricted to horses suffering hyperadrenocorticism.
Clinical experience has long indicated that keeping horses in a lean, fit bodily condition reduces the risk of their suffering laminitis. Indeed, dietary measures have for years often been sufficient to prevent laminitis in native ponies and cobs. Yet despite scrupulous dietary management some animals continued to suffer recurrent episodes of laminitis; Johnson's work has now provided an explanation. Laminitis is a disease of domestication. Cobs and warmbloods seem to have energy metabolism similar to that of native ponies and cannot cope with the improved pastures and calorific feeds they are exposed to. As we have strong evidence of the link between obesity and laminitis it defies understanding that those responsible for showing horses in the UK not only tolerate, but select for, obesity as a prerequisite for a champion. Whilst the average horse owner may mismanage their horses due to ignorance, laziness or lack of dieting facilities, the active promotion of obesity by show and breed societies is frank cruelty.
The presence of plasma endogenous ACTH concentrations greater than 50 pg/ml, elevated serum cortisol, insulin and glucose concentrations seems the best method of diagnosing PDCD at present. Cases with normal endogenous ACTH concentrations but with elevated serum insulin, cortisol and glucose are suggestive of insulin resistance and obesity dependent laminitis. To avoid erroneous results these tests should be made after an overnight fast and not if the horse is currently experiencing laminitis. The seasonality of PDCD, most cases suffering laminitis in the Autumn, suggests that the primary lesion may be of pineal rather than pituitary gland origin. Correlation between melatonin concentrations in PDCD cases and laminitis may be instructive when combined with histopathological examinations of the pineal gland.
Exogenous corticosteroid administration, particularly using long acting formulations has been associated with iatrogenic laminitis. The use of dexamethasone suppression testing to establish a diagnosis of Cushing's disease has been known to precipitate laminitis. Even the use of short acting corticosteroid preparations intra-articularly has resulted in laminitis. Clinical experience demonstrates that these are not inevitable sequelae of corticosteroid administration. Unfortunately, it seems impossible to predict which horses will suffer laminitis and founder following injection of corticosteroids. Nevertheless, clinicians should be aware of, and warn owners of these, sometimes fatal, sequelae to the use of corticosteroids, particularly if the animal is already at high risk of developing laminitis.
Clinicians are aware that the stress of conditions such as vaccination, worming, travelling and even proximity to low flying jets can trigger an attack of laminitis in some horses. The mechanisms in these cases are unknown but a causal association with elevated blood cortisol concentrations cannot be excluded. Laminitis is known to be predisposed to by PDCD and obesity dependent laminitis, both conditions resulting in hypercorticism. In vitro studies have demonstrated that the digital blood vessels exposed to cortisol show increased sensitivity to endogenous catecholamines (Eyre et al 1979).
Exogenous corticosteroids possess both glucocorticoid and mineralocorticoid effects. It has been suggested that corticosteroids may predispose to laminitis by increasing the permeability to gut derived activators or mediators. The mineralocorticoid effect leading to altered mineral balance should not be ignored. Serum concentrations and creatinine clearance ratios of calcium, magnesium, sodium, potassium, chloride and phosphate are often found to be abnormal in laminitis cases (Eustace unpublished data) combined with an elevated mean corpuscular volume. An association between forage mineral status, fructan concentration and mineral status of laminitis cases deserves further investigation. Particular research into the magnesium status of both forage and horse may be worthwhile as this element is thought to be lowered in herbage treated with nitrogenous fertilizers (Frape 199 and is frequently low in blood samples from laminitis cases.
Our lack of understanding of the mechanism whereby either changes in the hind gut following carbohydrate overload, or hypercorticism induce such devastating damage in the feet restricts us in improving preventative or therapeutic regimes in dietary laminitis. Until the mechanisms of these main "causes" of laminitis are better understood, it is incumbent upon us to educate horse owners in the means of preventing laminitis by using high fibre low calorie diets, restricted grazing and body condition scoring which have for years stood the test of time as an effective means of preventing this crippling disease.
References
Cushing, H. (1932)
The basophil adenomas of the pituitary body and their clinical manifestations (Pituitary Basophilsim).
Bull Johns Hosp. Vol 50 Part 137-195.
Hood D.M., Amoss M.S., Hightower D., McDonald D.R., McGrath J.P., McMullan W.C. and Scrutchfield W.L. (197.
Equine Laminitis I; Radioisotopic Analysis of the Haemodynamics of the Foot During the Acute Disease.
Journal of Equine Medicine and Surgery 2, 439 444.
Eyre, P., Elmes, P.J., & Strickland, S. (1979)
Corticosteroid-potentiated vascular responses of the equine digit: a possible phamacological basis for laminitis.
American Journal of Veterinary Research 40, 135-138
Frape, D. (199
Equine Nutrition and Feeding
2nd Ed. Blackwell Science, Oxford. P324
Johnson, P.J., Tyagi, S.C., Katwa, L.C., Ganjam, V.K., Moore, L.A., Kreeger, J.M. and Messer, N.T. (199
Activation of extracellular matrix metalloproteases in equine laminitis.
Veterinary Record. 142, 392-396.
Johnson, P.J. (2002)
The equine metabolic syndrome Peripheral Cushing's syndrome.
Veterinary Clinics Equine Practice 18. 271-293
http://www.laminitisclinic.org/Overview ... nitis.html
Zuletzt geändert von Eddi am 17.03.2007, 10:29, insgesamt 1-mal geändert.
03.06.2006, 07:27
Pituitary Dependent Cushing's Disease (PDCD)
Harvey Cushing in 1932 described a fatal syndrome in humans characterised by unusual disposition of fat depots, osteoporosis, immune suppression, generalised weakness which was associated with basophilic adenoma of the pituitary gland. This syndrome we now know to be due to elevated concentrations of circulating cortisol of adrenal origin and hyperadrenocorticism has become known as Cushing's disease. In the horse Cushing's disease is always secondary to a pituitary adenoma or hyperplasia; pituitary dependent Cushing's disease (PDCD).
An important recent finding (Johnson 2002) has been the identification of a metabolic abnormality due to an abnormal activity of the 11 ß-hydroxysteroid dehydrogenase type 1 enzyme in integumentary tissue of laminitis cases. These cases differ in clinical presentation from PDCD cases in that animals of any age may be affected, they do not show the hirsuitism characteristic of advanced PDCD cases and contrastingly they all are, or have been, obese. Whilst the terms Peripheral Cushing's disease and Equine Metabolic Syndrome have been suggested to describe hypercorticism not of adrenal origin, the term obesity dependent laminitis (ODL) seems the most descriptive and least likely to avoid confusion with PDCD which term may be better restricted to horses suffering hyperadrenocorticism.
PDCD in horses appears to be due to insufficient DOPamine being released from the hypothalamus. DOPamine inhibits the pars intermedia of the pituitary gland. Therefore when there is less DOPamine there is less inhibition of the pars intermedia which then increases in size.
Equine PDCD cases always develop laminitis if they live long enough. They may become immunosuppressed and subject to a variety of parasitic or infectious agents such as helminthiasis or pneumonia. Many cases show muscle loss and become polydipsic and polyphagic; they may be diabetic. A supra-orbital swelling, due to the deposition of a fat depot, is commonly seen giving the eyes a protuberant appearance.
To the trained observer, these cases can be diagnosed on clinical appearance and history alone. The clinical signs include;
Failure to shed their coat in Spring, the coat becomes long, thick and matted.
Affected animals tend to sweat more than normal, they lose weight despite an increased appetite.
They may become diabetic, either diabetes mellitus, (sugar diabetes) or diabetes insipidus. They therefore drink excessively, and if stabled you will notice their bedding is quickly soaked.
They show filling above the eyes. This is fat deposition in the supra-orbital fossae. [Normal horses have depressions above the eyes, you can see these depressions moving when a horse chews].
They become depressed and ill-looking, with dull eyes and they lose the shine on their coat.
They all develop laminitis eventually.
Their body shape changes so that they lose muscle mass, developing a dipped back, poorly muscled neck and quarters with a pendulous abdomen. There is a re-distribution of fat depots. The horse looking thin ("ribby" but gaining a rather "blocky" appearance. This is particularly evident if it has been dieted in the mistaken belief that it's laminitis is due to obesity.
Their resistance to infections or worm burdens is reduced.
With the plethora of tests used to confirm hypercorticism, which ones are safe for the laminitic and which give most information relating to both forms of "Cushing's disease"?
Whilst the dexamethasone suppression test or the combined ACTH stimulation / DX suppression tests are regarded as providing a definitive diagnosis of hyperadrenocorticism, I have known horses either develop laminitis, or suffer a deterioration in a pre-existing laminitis, following their use. Neither test provides any diagnostic information about hypercorticism not of adrenal origin (Obesity Dependent Laminitis; ODL).
Whilst a Thyroid Releasing Hormone response test is safe, it is only of value if the horse shows a baseline cortisol concentration within the normal range. Additionally, this test provides too many equivocal results to be reliable as a PDCD test and again is non diagnostic for ODL.
A combined Dx suppression / TRH response test has the disadvantages noted for both tests above.
The test I use these days is a measurement of endogenous ACTH, cortisol, insulin and glucose. The test is safe for the laminitic, involves one blood sample and is relatively inexpensive.
The test should ideally be performed first thing in the morning after the horse has been stabled overnight with no food provided. It is inadvisable to use any of the above tests if the horse is currently suffering from laminitis, the stress of which is likely to cause erroneous results.
A transport kit should be obtained from Cambridge Specialist Laboratory Services (Tel 01223-493400) and placed in a freezer overnight. A 2ml blood sample should be taken by syringe and needle (not glass vacutainer) and placed in the EDTA tubes provided. These should ideally be centrifuged immediately and the plasma drawn off and placed in the frozen sample tube provided. However, if the EDTA tubes are kept upright and placed in a cold refrigerator to settle, the plasma can be drawn off later in the day and transferred to the transport kit.
The presence of plasma endogenous ACTH concentrations greater than 50 pg/ml, elevated serum cortisol, insulin and glucose concentrations is diagnostic of PDCD. Cases with normal endogenous ACTH concentrations (< 30 pg/ml) but with elevated serum insulin, cortisol and glucose concentrations are diagnostic of of insulin resistance and obesity dependent laminitis.
Treatment options - PDCD
Periactin. Small white tablets (4mg Cyproheptadine) Effective in about 80% of cases.
Periactin 0.6 mg/kg BW/day¾ increasing over 8 weeks
Periactin dosage for a 300 kg Pony.
Week 1
70 tablets total
(10/day)
Week 2
77
11
Week 3
84
12
Week 4
98
14
Week 5
112
16
Week 6
112
16
Week 7
120
17
Week 8
140
20
Thereafter 20 tablets/day
Periactin dosage for a 400 kg Pony
Week 1
105 tablets total
(15/day)
Week 2
112
16
Week 3
119
17
Week 4
133
19
Week 5
147
21
Week 6
154
22
Week 7
161
23
Week 8
182
26
Thereafter 26 tablets/day.
Periactin dosage for a 500 kg Horse.
Week 1
133 tablets total
(19/day)
Week 2
140
20
Week 3
154
22
Week 4
168
24
Week 5
175
25
Week 6
189
27
Week 7
203
29
Week 8
217
31
Thereafter 31 tablets/day.
Celance (Small greenish lozenges 250 µg Pergolide)
This drug comes in three strengths so be sure which ones you are using and check the dosage prescribed. The drug is expensive so if you use it make sure the horse eats it ! The surest way is to feed it from the hand either in a titbit or a sandwich. . BE AWARE THAT BOTH PERIACTIN AND CELANCE CAN INITIATE OR AGGRAVATE LIVER DISEASE - your vet can check on this by measuring liver related enzyme and bile acid concentrations in clotted blood samples.
Dosage 0.25 to 2mg daily as a continuing treatment. This drug is much more expensive than Periactin but seems a little more reliable in achieving a positive response.
Trilostane (Modrenal) 0.5 mg/kg daily
Aminoglutethimide up to 4mg/kg daily
Vitex 40 to 100ml of solution or tincture per day
Melatonin 1mg/day in the evening
Treatment options - ODL
No specific treatments are proven, use of cortisol blockers could theoretically help. Strict control of management and diet are presently our only practical treatments.
Exogenous corticosteroid administration, particularly using long acting formulations has been associated with iatrogenic laminitis. The use of dexamethasone suppression testing to establish a diagnosis of Cushing's disease has been known to precipitate laminitis. Even the use of short acting corticosteroid preparations intra-articularly has resulted in laminitis. Clinical experience demonstrates that these are not inevitable sequelae of corticosteroid administration. Unfortunately, it seems impossible to predict which horses will suffer laminitis and founder following injection of corticosteroids. Nevertheless, clinicians should be aware of, and warn owners of these, sometimes fatal, sequelae to the use of corticosteroids, particularly if the animal is already at high risk of developing laminitis
http://www.laminitisclinic.org/PDCD.html
Harvey Cushing in 1932 described a fatal syndrome in humans characterised by unusual disposition of fat depots, osteoporosis, immune suppression, generalised weakness which was associated with basophilic adenoma of the pituitary gland. This syndrome we now know to be due to elevated concentrations of circulating cortisol of adrenal origin and hyperadrenocorticism has become known as Cushing's disease. In the horse Cushing's disease is always secondary to a pituitary adenoma or hyperplasia; pituitary dependent Cushing's disease (PDCD).
An important recent finding (Johnson 2002) has been the identification of a metabolic abnormality due to an abnormal activity of the 11 ß-hydroxysteroid dehydrogenase type 1 enzyme in integumentary tissue of laminitis cases. These cases differ in clinical presentation from PDCD cases in that animals of any age may be affected, they do not show the hirsuitism characteristic of advanced PDCD cases and contrastingly they all are, or have been, obese. Whilst the terms Peripheral Cushing's disease and Equine Metabolic Syndrome have been suggested to describe hypercorticism not of adrenal origin, the term obesity dependent laminitis (ODL) seems the most descriptive and least likely to avoid confusion with PDCD which term may be better restricted to horses suffering hyperadrenocorticism.
PDCD in horses appears to be due to insufficient DOPamine being released from the hypothalamus. DOPamine inhibits the pars intermedia of the pituitary gland. Therefore when there is less DOPamine there is less inhibition of the pars intermedia which then increases in size.
Equine PDCD cases always develop laminitis if they live long enough. They may become immunosuppressed and subject to a variety of parasitic or infectious agents such as helminthiasis or pneumonia. Many cases show muscle loss and become polydipsic and polyphagic; they may be diabetic. A supra-orbital swelling, due to the deposition of a fat depot, is commonly seen giving the eyes a protuberant appearance.
To the trained observer, these cases can be diagnosed on clinical appearance and history alone. The clinical signs include;
Failure to shed their coat in Spring, the coat becomes long, thick and matted.
Affected animals tend to sweat more than normal, they lose weight despite an increased appetite.
They may become diabetic, either diabetes mellitus, (sugar diabetes) or diabetes insipidus. They therefore drink excessively, and if stabled you will notice their bedding is quickly soaked.
They show filling above the eyes. This is fat deposition in the supra-orbital fossae. [Normal horses have depressions above the eyes, you can see these depressions moving when a horse chews].
They become depressed and ill-looking, with dull eyes and they lose the shine on their coat.
They all develop laminitis eventually.
Their body shape changes so that they lose muscle mass, developing a dipped back, poorly muscled neck and quarters with a pendulous abdomen. There is a re-distribution of fat depots. The horse looking thin ("ribby" but gaining a rather "blocky" appearance. This is particularly evident if it has been dieted in the mistaken belief that it's laminitis is due to obesity.
Their resistance to infections or worm burdens is reduced.
With the plethora of tests used to confirm hypercorticism, which ones are safe for the laminitic and which give most information relating to both forms of "Cushing's disease"?
Whilst the dexamethasone suppression test or the combined ACTH stimulation / DX suppression tests are regarded as providing a definitive diagnosis of hyperadrenocorticism, I have known horses either develop laminitis, or suffer a deterioration in a pre-existing laminitis, following their use. Neither test provides any diagnostic information about hypercorticism not of adrenal origin (Obesity Dependent Laminitis; ODL).
Whilst a Thyroid Releasing Hormone response test is safe, it is only of value if the horse shows a baseline cortisol concentration within the normal range. Additionally, this test provides too many equivocal results to be reliable as a PDCD test and again is non diagnostic for ODL.
A combined Dx suppression / TRH response test has the disadvantages noted for both tests above.
The test I use these days is a measurement of endogenous ACTH, cortisol, insulin and glucose. The test is safe for the laminitic, involves one blood sample and is relatively inexpensive.
The test should ideally be performed first thing in the morning after the horse has been stabled overnight with no food provided. It is inadvisable to use any of the above tests if the horse is currently suffering from laminitis, the stress of which is likely to cause erroneous results.
A transport kit should be obtained from Cambridge Specialist Laboratory Services (Tel 01223-493400) and placed in a freezer overnight. A 2ml blood sample should be taken by syringe and needle (not glass vacutainer) and placed in the EDTA tubes provided. These should ideally be centrifuged immediately and the plasma drawn off and placed in the frozen sample tube provided. However, if the EDTA tubes are kept upright and placed in a cold refrigerator to settle, the plasma can be drawn off later in the day and transferred to the transport kit.
The presence of plasma endogenous ACTH concentrations greater than 50 pg/ml, elevated serum cortisol, insulin and glucose concentrations is diagnostic of PDCD. Cases with normal endogenous ACTH concentrations (< 30 pg/ml) but with elevated serum insulin, cortisol and glucose concentrations are diagnostic of of insulin resistance and obesity dependent laminitis.
Treatment options - PDCD
Periactin. Small white tablets (4mg Cyproheptadine) Effective in about 80% of cases.
Periactin 0.6 mg/kg BW/day¾ increasing over 8 weeks
Periactin dosage for a 300 kg Pony.
Week 1
70 tablets total
(10/day)
Week 2
77
11
Week 3
84
12
Week 4
98
14
Week 5
112
16
Week 6
112
16
Week 7
120
17
Week 8
140
20
Thereafter 20 tablets/day
Periactin dosage for a 400 kg Pony
Week 1
105 tablets total
(15/day)
Week 2
112
16
Week 3
119
17
Week 4
133
19
Week 5
147
21
Week 6
154
22
Week 7
161
23
Week 8
182
26
Thereafter 26 tablets/day.
Periactin dosage for a 500 kg Horse.
Week 1
133 tablets total
(19/day)
Week 2
140
20
Week 3
154
22
Week 4
168
24
Week 5
175
25
Week 6
189
27
Week 7
203
29
Week 8
217
31
Thereafter 31 tablets/day.
Celance (Small greenish lozenges 250 µg Pergolide)
This drug comes in three strengths so be sure which ones you are using and check the dosage prescribed. The drug is expensive so if you use it make sure the horse eats it ! The surest way is to feed it from the hand either in a titbit or a sandwich. . BE AWARE THAT BOTH PERIACTIN AND CELANCE CAN INITIATE OR AGGRAVATE LIVER DISEASE - your vet can check on this by measuring liver related enzyme and bile acid concentrations in clotted blood samples.
Dosage 0.25 to 2mg daily as a continuing treatment. This drug is much more expensive than Periactin but seems a little more reliable in achieving a positive response.
Trilostane (Modrenal) 0.5 mg/kg daily
Aminoglutethimide up to 4mg/kg daily
Vitex 40 to 100ml of solution or tincture per day
Melatonin 1mg/day in the evening
Treatment options - ODL
No specific treatments are proven, use of cortisol blockers could theoretically help. Strict control of management and diet are presently our only practical treatments.
Exogenous corticosteroid administration, particularly using long acting formulations has been associated with iatrogenic laminitis. The use of dexamethasone suppression testing to establish a diagnosis of Cushing's disease has been known to precipitate laminitis. Even the use of short acting corticosteroid preparations intra-articularly has resulted in laminitis. Clinical experience demonstrates that these are not inevitable sequelae of corticosteroid administration. Unfortunately, it seems impossible to predict which horses will suffer laminitis and founder following injection of corticosteroids. Nevertheless, clinicians should be aware of, and warn owners of these, sometimes fatal, sequelae to the use of corticosteroids, particularly if the animal is already at high risk of developing laminitis
http://www.laminitisclinic.org/PDCD.html
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