4My2Greys
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FiveRoooooers I give a little less than a tsp, but I've read a tsp is what is recommended.
mychip1 I hope you will give it a try for Dustin. I really believe it would help him.
Ravenchilde I can't specifically speak for an IBD flare up, but Nadir has had numerous bouts of gurgly stomach, loss of appetite, along with diarrhea, often times which was bloody. He's been put on Metronidazole. Now whenever the gurglies start and I notice stools loose I give him some Manuka honey for about 3-4 meals and that usually does the trick. I've had stools firm up in a day, but depending how bad the flare up is it could take longer. I am only giving it to treat flare ups, but I think in cases of IBD it wouldn't be a bad idea to give the teaspoon before meals during flare up, but also continue to give maybe a 1/2 tsp daily for continued treatment for a while.
2dogs4cats and Fullmetalfrank thanks for posting positive about this. I think the more good experiences people read from people they know will help them. What's really interesting is Sulfasalazine is what is used often times to treat IBD, but it was giving you problems Fullmetalfrank and the Manuka honey helped with that. 2dogs4cats I treated a very nasty wound on Nadir with great success using this stuff.
manawatugal thank you for mentioning UMF rating. I've mentioned it in other threads when I've brought up Manuka honey but had not done here. I have 2 Manuka honeys I use, one with a 15+ rating and another that has a 16+ rating. I paid $28 for a 17.6 oz. jar of 16+ Wedderspoons 100% Raw Manuka honey. It says it's a product of New Zealand. I'm going to have to read the company's website and see if that's the case. How much would you pay for a honey with the same UMF?
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PubMed is terrific, thank you for this post.
I had toyed with giving Manuka honey to one of my boys, and tonight on my way home from work I picked up a jar and offered some to him. With peanut butter, which he loves. I've never seen such stinkeye.
Congratulating myself on buying the small jar ... I would love to hear from others who have a more positive experience than we did.
Maybe the combination is what tasted bad to him. I give to all mine straight off a spoon and they lick it all off with no problem. I have to admit it does have an odd odor, kinda smells like sweaty gym socks. If your pup gets the gurglies this stuff really helps and is much healthier than giving Pepcid and has more benefits overall.
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My order arrived Wednesday. I have to say I am very happy with the quality of these bullysticks, from a visual standpoint that is. The large 6" ones I ordered here are every bit as big diameter wise as the jumbo ones I got from the other company. Best thing I did too was ordering the No Odor ones as compared to the Low Odor ones I ordered from the orther company, these do not smell at all. I also ordered 2 lbs of lamb lung that my dogs are absolutely C-R-A-Z-Y over. I will definately be ordering from this company again.
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First my apologies to the rats whose lives were taken in this case to help prove the benefits of Manuka honey and to those who oppose all animal testing for that matter, as do I. But I thought that those with IBD dogs or those suffering from colitis would find this helpful. I've mentioned Manuka honey before for digestive problems and I do understand the hesitancy in trying anything with a dog diagnosed with IBD unless something has been tested and shown to have positive effects. This study shows that the use of Manuka honey does help in cases of IBD.
http://www.ncbi.nlm.nih.gov/pubmed/18688794
Effect of different doses of Manuka honey in experimentally induced inflammatory bowel disease in rats.
Prakash A, Medhi B, Avti PK, Saikia UN, Pandhi P, Khanduja KL.
Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh-160012, India.
Abstract
To evaluate the effect of different doses of Manuka honey in experimentally induced inflammatory bowel disease in rats. Adult Wistar rats of either sex were used (n = 30). Colitis was induced by a single intracolonic administration of TNBS dissolved in 35% ethanol. The rats (n = 30) were divided into five groups (n = 6) and were treated with vehicle (ethanol), TNBS, Manuka honey (5 g/kg, p.o.), Manuka honey (10 g/kg, p.o.) or sulfasalazine (360 mg/kg, p.o.) body weight for 14 days. After completion of treatment, the animals were killed and the following parameters were assessed: morphological score, histological score and different antioxidant parameters. Manuka honey at different doses provided protection against TNBS-induced colonic damage. There was significant protection with Manuka honey 5 g/kg as well as with 10 g/kg body weight compared with the control (p < 0.001). All the treated groups showed reduced colonic inflammation and all the biochemical parameters were significantly reduced compared with the control in the Manuka honey treated groups (p < 0.001). Manuka honey at different doses restored lipid peroxidation as well as improved antioxidant parameters. Morphological and histological scores were significantly reduced in the low dose Manuka honey treated group (p < 0.001). In the inflammatory model of colitis, oral administration of Manuka honey 5 g/kg and Manuka honey 10 g/kg body weight significantly reduced the colonic inflammation. The present study indicates that Manuka honey is efficacious in the TNBS-induced rat colitis model, but these results require further confirmation in human studies.
PMID: 18688794 [PubMed - indexed for MEDLINE]
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Assuming he's had an abdominal x-ray? Don't want to scare you silly, but Joseph's blockage experience manifested itself with diarrhea + vomiting.
Not yet, but I think that will be in the near future. We'll see how he does today/tonight without any food in his tummy.
The vet is 100% convinced it is IBD and Doolin's scratched trachea was actually acid reflux. I wish the vet that saw him the night he had the incident was still there, he was the one that saw the scratches down his throat and saw what was happening.
I found this information on the Crohn’s & Colitis Foundation of America website:
The diagnosis of IBD is based on a combination of exams: endoscopic (different types of scopes), radiologic (x-rays) and histologic (blood and tissue) tests. If you do have IBD, you may need additional tests from time to time to monitor the disease, or diagnose possible complications or the side effects of medication.
I really do not understand how your vet could have diagnosed IBD without an x-ray at the minimum. I would also think she would be pushing for an x-ray to rule out blockage based on the initial belief of a scratched trachea.
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I know you're working with your vets and trust them, so perhaps the additional feedback is not wanted at this point, but Giselle's signs remind me so much of my girl Willow that I can't stop thinking about her. Does she still have edema/joint pain/active inflammation now? I am a conventional 'Western' vet, but I also feel that there are cases where conventional medicine does not have all the answers and alternative or holistic approaches can help.
I wouldn't abandon mainstream medicine but would consider alternative therapies in conjunction. In Willow's case, we still used antibiotics and steroids, but I truly believe that the acupuncture and Chinese herbs also contributed to her recovery. Each case is different, and especially since neither Willow nor Giselle have a definite diagnosis, and Giselle's problem is much more chronic, I have no idea if any of these things would help. But it might be worth looking into and probably won't hurt at this point.
Your the kind of vet I would want for my dogs.
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IIRC she was feeding the Canidae for a month or so before symptoms appeared. So it could be either food or any of the meds.
Didn't she stop the Canidae for a day or two and still get the reaction? I thought she did but I could be mistaken about that.
If she's still getting the reaction on beef, it likely isn't the food. If she isn't getting the reaction on beef, it is one of the foods and given the nature of the reaction I would be cautious about adding commercial foods back in.
I had to go back and check the other threads that had been started on this. The problem started 1 month into feeding Canidae and 9 months into the meds. The 1 month time could have been the time it took for the allergen level to build to cause reaction. She posted the problem on the 18th and gave him a new food on the 19th at which point the dog had another reaction, so there was no break. The reaction she is getting from the beef is different than the original reaction. With the original reactions he was turning beat red all over which lasted several hours.
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Batmon & Mcsheltie, I'm not trying to confuse things here, but I really don't understand the need here for a full elimination diet. I could see the need if she had only been feeding the TOTW. The problem started occurring when she added the canned foods. Wouldn't it have been more logical to just eliminate the canned and see what results you get. If the problem persisted then a full elimination diet would be warranted. To me throwing out both foods at the same time when one hasn't given you a problem is like throwing the baby out with the dirty bath water.
Once you rule out the TOTW as not being part of the problem you can look at the ingredients which are common to those 2 canned foods fed. Feed those ingredients one at a time and test for reaction. Wouldn't that have been a lot simpler and taken a lot less time.
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Looking at the ingredients of TOTW Wetlands and the Canidae Platinum - I didn't see where sunflower oil was a common ingredient in the two - so I am thinking perhaps it was sunflower oil from one food source and maybe potato from the other? I have also stopped the gabapentin, and he doesn't seem to be in pain (been 48 hours off that med).
You didn't have problems until you started feeding him the canned Canidae platinum. You then switched to another brand of canned which also caused problems. You need to compare the common ingredients in those foods, which by the way sunflower products are common to both these foods.
I know that in an elimination diet you should as McSheltie is instructing you start with a single ingredient and see how the dog does and then slowly add other ingredients one at a time and test for reaction. I however would have approached it more simply by eliminating everything but the TOTW you had been feeding, which hadn't been giving you any problems, to rule out any reaction to that food. If there were none then I would have compared the common ingredients in the 2 canned products which were being fed when the reactions started and one at a time added that ingredient and tested for reaction.
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Does she limp only on hard surfaces when she walks or also when she is in the yard? If she is limping on hard surfaces it could likely be a corn on the foot, which can cause a lot of pain.
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Just got a call back from the vet. She says it's likely the ketoconazole causing his appetite change.
The good news: We can take him off of it. The tests came back negative for blastomycosis.
The bad news: The tests came back negative for blastomycosis. He has osteo.
I was so afraid of this, I'm sorry that it wasn't blasto.
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It's good that Doolin got a diagnosis...now time to heal up Doolin! I dunno about letting him eat poo though
The reason for allowing him to eat it is because it always heals him. The next day after eating it he has no stomach issues and normal, solid poop. The vet explained that horses pass a large amount of good gut bacteria. I read up that foals will eat their mother's manure because it builds up a good stomach (don't know if it's true or not - it's just what I read) All the horses are healthy and are dewormed regularly so it won't do any harm
Hey maybe you need to bag that stuff up and sell it as a proprietory blend at an outrageous price.
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I didn't see if you posted what your grey weighs, but I don't think your feeding enough. I based the following calculations on a 65 to 70 lb greyhound and feeding 3% of body weight since you want to put on weight. What I come up with is approx 2 lbs or 4 cups of ground beef to be fed daily.
If you can post your grey's weight I do have have a book at home that outlines amounts of meat and rice (grain) each required based on the weight of the dog that I would be happy to share with you later.
ETA: I just saw you've got the weight in the title.
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Sorry, I did not know that Carol was a Doctor. I would have never bothered her with the question about rattlesnakes.
I'm not Dr. Carol. I found this on another group I am on and shared it here since permission was granted to cross post. If I was Dr. Carol I would be more than happy to answer any questions you had, unfortunately I'm not.
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I have said several times that food allergies can play a role in incontinence or the inablility to hold urine. I wasn't sure if it was caused by damage to the bladder or kidneys. I had nothing to base it on other than my own experience with Nadir and a a short one sentence blurb I found in a holistic dog care book which I feel most disregarded both as unfounded. Because I felt that this is something that people should take seriously when investigating possible causes of pee accidents, or incontinence if you will, I kept searching and came across the following article from Nutramed.com on food antigens role in kidney disease with supporting documentation. These are human studies, but I see no reason why this information cannot also be applied to dogs.
http://www.nutramed.com/kidney/kidneydisease.htm
Nephritis
The kidneys present a large filtering surface to blood contents and are vulnerable to damage by circulating immune complexes (CIC). These complexes may increase when the digestive tract leaks large food molecules (mostly proteins) into the blood. Whatever comes in must go out. Our urinary system has the job of excreting unwanted, hazardous materials. If problems arise in this system, why should we not attempt to trace the problems back to body input?
The food-source of circulating immune complexes (CICs) has been neglected in clinical medicine. Doctors will often think of the most complicated, rare, outrageous things before they will think of the simple, obvious, daily intake of antigenic problems in the food supply! Transient kidney pain in the flanks signals the presence of CICs and often imitates an attack of kidney infection or renal colic. Mild, brief versions of this pain are common in people with delayed-pattern food allergy. In the worst case, patients with food allergy may have fever with flank pain and frequency of urination and are often thought to have kidney infection.
Glomerulonephritis is a serious form of kidney inflammation which may sometimes be triggered by CICs containing food protein antigens. Kidney inflammation may lead to hypertension and eventual kidney damage. The recurring triad of transient flank pain, blood or protein in the urine, and the presence of symptoms in other systems should suggest "food allergy" until proven otherwise.
Careful diet revision may show benefit in controlling kidney inflammation; A food holiday on Alpha ENF is especially useful in the beginning since all antigenic material is excluded. Patients with existing kidney disease benefit from a low protein diet and will also experience the least demand on diminishing kidney function with an ENF. Close professional supervision is always necessary with serious disease.
Nephrotic Syndrome
The nephrotic syndrome involves increased glomerular excretion of protein - Gabordi et al reported a 6 year old girl with gluten allergy expressed as celiac disease and dermatitis herpetiformis who developed nephrotic syndrome. Elimination of gluten grains resolved all three major manifestations of gluten allergy. Sandberg et al reported on 6 patients who experienced remission of nephrotic syndrome when milk was eliminated from their diet and exacerbation when it was reintroduced. Six patients in a study of 17 children with steroid resistant nephrotic syndrome responded to milk exclusion with remission of proteinuria in 3-8 days. Four of the six improved patients had other manifestations of food allergy including recurrent bronchitis, atopic dermatitis, and gastrointestinal disturbances.
Ferri et al stated that ' dietary macromolecular antigens can be involved in the pathogenesis of IgA nephropathy (IgAN), the effect of a low-antigen-content diet was evaluated in 21 patients with immunohistochemical findings of active IgAN. The diet was followed for a 14-24-week period in all cases the effects of the treatment were evaluated by clinical and serological parameters, and in 11 patients also by repeat renal biopsy. After dietetic therapy a significant reduction of urinary proteins was recorded in particular, heavy proteinuria present in 12 cases during the 6 months preceding the treatment, was markedly reduced or disappeared in 11.
Sato et al reported: "... that food antigens participate strongly in the pathogenesis of some patients with IgA nephropathy."
McCrory et al reported "... the occurrence of immune complex glomerulonephritis in a patient with eosinophilic gastroenteritis and food hypersensitivity. Renal biopsy revealed immune complex glomerulonephritis with BSA, immunoglobulins M and G and complement deposited focally in the glomerular basement membrane. With strict dietary limitation of identified causative antigens and prednisone therapy, CIC levels decreased to 16,000 micrograms/dl and serum BSA antibody hemagglutinating titer fell 32-fold over a period of 15 months. There was prompt symptomatic relief and amelioration of signs of nephritis. The patient was able to consume a diet normal in protein and caloric content, and statural catch-up growth occurred. Recognition of food antigens to which the patient was hypersensitive provided a rationale for the relief of the gastrointestinal disturbance, growth stunting, and renal disease.
The Canadian Pediatric Kidney Disease Reference Center
has related a specific kidney disease in children to ground beef. They have suggested that the hemolytic uremic syndrome is related to infection by common bacteria, E.Coli, which is spread in undercooked ground beef. A cluster of "hamburger disease" occurred, for example in Washington State in 1993 in people who ate undercooked beef contaminated by E.Coli from a fast-food chain. The bacteria can then spread from an infected person to people who have not eaten beef. Milk and other foods can also be contaminated. A hypersensitivity mechanism is triggered by the bacteria which then damages red blood cells and then the kidneys.
Alpha ENF: Often, full recovery involves a food holiday. Alpha ENF can be used as a completely absorbed, fully nourishing food-replacement. Alpha ENF can be used to supply nutrients that may be in short supply - such as amino acids, B vitamins, vitamins D and B12 and minerals such as calcium, magnesium, potassium, zinc.
We think that proteins in general are high-risk food components in kidney disease and we are concerned about the adverse effects of hydrolyzed proteins. Gluten, the proteins in wheat, rye, barley and oats are definitively excluded but other high risk proteins are albumin from eggs and milk, globulin and casein from milk, muscle proteins from meat, and soy proteins. When you begin diet revision you avoid eating all these proteins. Their use is postponed until full recovery has been achieved.. Proteins from vegetable sources appear to be better tolerated. Meal replacement formulas made with milk, egg or soy proteins should be avoided. All body-building protein powders are avoided.
Alpha ENF avoids all the protein problems by supplying the nutrient requirement with pure amino acids. The amino acid content of Alpha ENF will supplement or replace dietary protein. Alpha ENF can be added to fruit and vegetable juices to make complete meals of simple beverages and can be added to soups, or puddings after they have been cooked to increase their nutritive value. The most definitive rest and recovery technique is to take a Food Holiday.
Abstracts Food Allergy and Nephritis
Do food antigens play a role in some cases of human glomerulonephritis?
Author van der Woude FJ; Hoedemaeker PJ; van der Giessen M; de Graeff PA; de Monchy J; The TH; van der Hem GK Source Clin Exp Immunol, 1983 Mar, 51:3, 587-94
Abstract Circulating immune complexes after a test meal were measured with three methods (PEG precipitation, Clq-ELISA and the indirect granulocyte phagocytosis test) in 10 controls, two symptomless persons with selective IgA deficiency and 14 patients with various types of glomerulonephritis, of which two patients (with idiopathic membranous glomerulopathy and local focal glomerulonephritis) also had selective IgA deficiency. The PEG and Clq-ELISA test did not show significant differences between the groups. In the two symptomless persons with selective IgA deficiency and in the patient with local focal glomerulonephritis and selective IgA deficiency the indirect granulocyte phagocytosis test (IGFT) showed a reproducible increase in IgG, IgM and complement containing immune complexes. In the last patient multiple food antigens were probably responsible for this phenomenon, a rapid amelioration of kidney function could be induced three times by giving an antigen free diet.
Food antigens, IgA-immune complexes and IgA mesangial nephropathy.
Author Fornasieri A; Sinico RA; Maldifassi P; Paterna L; Benuzzi S; Colasanti G; D'Amico G Source Nephrol Dial Transplant, 1988, 3:6, 738-43
Abstract To investigate whether patients with IgA nephropathy have an exaggerated serum IgA response to ubiquitous food antigens we measured serum IgA antibodies to gliadin, ovalbumin, bovine serum albumin (BSA), beta-lactoglobulin and casein in 120 patients and 53 normal controls, using ELISA. No significant differences were observed between patients and controls in serum IgA antibodies against each of the antigens tested. Moreover, no correlation was found between serum IgA antibodies and IgA-immune complexes (IgA CIC). However, nine patients but no controls had an association of two or more IgA antibodies to dietary antigens. Sixty-six per cent of these patients (vs 24% in the remaining population) had IgA CIC, suggesting a possible involvement of these antibodies in the constitution of IgA CIC. Analysis of sera by HPLC revealed that both monomeric and higher molecular forms of IgA antibodies were present, the latter being coincident with the peak of IgA CIC. Preincubation of sera with serial concentrations of the specific antigen decreased significantly IgA CIC, suggesting that in this subgroup of patients IgA antibodies to food antigens (mainly BSA) are involved in the formation of IgA CIC. BSA-containing IgA CIC were in fact demonstrated by ELISA using rabbit IgG anti-BSA coated plates and peroxidase-conjugated anti-human IgA. The role of these CIC in the pathogenesis of IgA nephropathy needs to be further elucidated.
Estimation of circulating immune complexes following oral challenge with cow's milk in patients with IgA nephropathy.
Author Sato M; Takayama K; Wakasa M; Koshikawa S. Source Nephron, 1987, 47:1, 43-8
Abstract We recently reported on an experimentally induced model of IgA nephropathy in mice by long-term oral immunization under the reticuloendothelial dysfunction, which was found to be effectively inhibited by the administration of the antiallergic agent sodium cromoglycate (SCG). On the basis of these findings, we investigated the participation of food antigens in patients with IgA nephropathy. We studied 24 patients with IgA nephropathy, 11 patients with primary glomerulonephritis (PGN) except IgA nephropathy and 11 healthy controls. Serum levels of immunoglobulins (IgG, IgA, IgE) and circulating immune complexes containing IgG (IgG-CIC) or IgA (IgA-CIC) were measured in the fasting state and 30, 60, 120 or 180 min after oral challenging with cow's milk (400 ml). After the oral challenge IgA-CIC levels remained within the normal range in healthy controls and in patients with PGN, while 3 out of the 24 patients with IgA nephropathy showed a transient elevation and 2 cases showed a significant rise of IgA-CIC levels. The levels of IgG, IgA, IgE and IgG-CIC remained uninfluenced by the challenge test in all subjects. In addition, we carried out the same challenge test under SCG administration. These cases indicating an oral-challenge-induced IgA-CIC elevation demonstrated an inhibition of this elevation, and in 3 out 7 patients who showed hyper-IgA-CIC-emia before and after oral challenge IgA-CIC levels returned to the normal range through SCG administration. These results suggest that food antigens participate strongly in the pathogenesis of some patients with IgA nephropathy, and that SCG is an effective agent for such patients.
Immune complexes in IgA nephropathy:
Author Sancho J; Egido J; Rivera F; Hernando L Source Clin Exp Immunol, 1983 Oct, 54:1, 194-202
Abstract
Several features suggest that IgA nephropathy is an immune complex (IC)-mediated disease. The source of antigen(s) is unknown but the predominant involvement of IgA suggest that it is associated in some way with the gut or respiratory tract. Taking into account the specific hepatobiliary transport by polymeric IgA of circulating antigens entering through the mucosal surfaces we examined the possible involvement of antibodies against food antigens in the circulating IC and the existence of a defect in their blood clearance in patients with IgA nephropathy. A rise in multimeric IgA-IC (Raji assay) occurred in three of seven control subjects with a peak at 2-4 h after food ingestion. The amount of multimeric IgA-IC present at fasting in four out of six patients, diminished 2-4 h after food challenge, reaching a new peak around 6 h. At fasting, three out of six patients had IC containing antibodies against diet antigens (e.g. ovalbumin). These IC paralleled, both in patients and controls, the levels of multimeric IgA-IC. In patients small multimeric IgA-IC predominated at fasting and 24 h after food ingestion, while larger IC were detected at 2-4 h of food challenge. The specific polymeric IgA-IC showed in controls a maximal peak with similar distribution to that of multimeric IgA-IC, but with a quicker disappearance from the circulation. By contrast, polymeric IgA-IC remained elevated 24 h after food ingestion in most patients. These results suggest that antibodies against common antigens are within circulating IC and that a defect in the hepatic clearance of circulating polymeric IgA-IC exists in patients with IgA nephropathy.
Low doses of drugs able to alter intestinal mucosal permeability to food antigens (5-aminosalicylic acid and sodium cromoglycate) do not reduce proteinuria in patients with IgA nephropathy: a preliminary noncontrolled trial.
Author Bazzi C; Sinico RA; Petrini C; Rizza V; Torpia R; Arrigo G; Ragni A; D'Amico G Source Nephron, 1992, 61:2, 192-5
Abstract
In an uncontrolled trial, patients with IgA nephropathy (IgAN) were treated with drugs that can alter the intestinal mucosal permeability to food antigens. These drugs are known to ameliorate urinary abnormalities and histological lesions of IgAN associated with ulcerative colitis or Crohn's disease [5-aminosalicylic acid (5-ASA)] or to prevent, in mice, the induction of IgAN-like disease by oral immunization [disodium cromoglycate (SCG)]. Nine patients [serum creatinine (s-Cr) less than 2 mg/dl; 24-hour proteinuria higher than 1.5 g, but not nephrotic) were treated with 5-ASA (2.4 g/day for 6 months); 9 similar patients were treated with SCG (400 mg/day for 6 months); the follow-up extended to 6 months after stopping therapy. The 5-ASA group showed a slight but not significant decrease in s-Cr, 24-hour/proteinuria, IgA circulating immune complexes (IgA-CIC) and IgA rheumatoid factor (IgA-RF); serum beta 2-microglobulin and serum IgA were unchanged; 2 of 9 treated patients showed, after 6 months of therapy, a reduction in proteinuria of more than 50% that lasted for the subsequent 18 months. The SCG-treated group showed a slight but not significant increase in 24-hour proteinuria and a significant decrease in serum IgA; unchanged were s-Cr, IgA-CIC, IgA-RF, serum beta 2-microglobulin; no patient treated with SCG showed a reduction in proteinuria of more than 50%. At the dosages and for the periods used, 5-ASA and SCG did not show a significant influence on clinical and laboratory parameters of disease in IgAN; other trials with increased dosages are warranted to definitely ascertain the possible therapeutic role of these drugs in IgAN.
Circulating immune complexes following food: delayed clearance in idiopathic glomerulonephritis.
Author Cairns SA; London A; Mallick NP Source J Clin Lab Immunol, 1981 Sep, 6:2, 121-6
Abstract Following a meal containing a variety of animal and vegetable proteins circulating immune complexes (CIC) have been found in sera from eight normal subjects. Levels of CIC rose to significantly higher levels in ten patients with idiopathic immune complex glomerulonephritis and return to fasting levels was significantly delayed. The type of CIC detected bore no relation to those in renal biopsy material. The CIC which accumulated in GN were small (MW similar to or approximately 350,000), and plasma exchange did not influence the extent or duration of CIC rise following the meal. An immunological defect manifested by impaired clearance of frequently encountered antigens may exist in subjects who develop GN. The CIC detected in the serum of these patients may be markers of this state and cannot be assumed to be the pathogenic agents in the disease.
Immune complex glomerulopathy in a child with food hypersensitivity.
Author McCrory WW; Becker CG; Cunningham-Rundles C; Klein RF; Mouradian J; Reisman L
Source Kidney Int, 1986 Oct, 30:4, 592-8
Abstract
This report describes the occurrence of immune complex glomerulonephritis in a patient with eosinophilic gastroenteritis and food hypersensitivity. A coincident allergen injection may have been a contributing factor in the sudden development of the nephrotic syndrome. Markedly elevated levels of circulating immune complexes (greater than 6400 mg/dl) were found containing kappa-casein and bovine serum albumin (BSA), the latter predominating. Markedly elevated serum BSA hemagglutinating titers were also present (1:40,960). Cross-reacting precipitating antibodies to BSA, beef, and pork were demonstrated, but not to flounder or ovalbumin. Renal biopsy revealed immune complex glomerulonephritis with BSA, immunoglobulins M and G and complement deposited focally in the glomerular basement membrane. With strict dietary limitation of identified causative antigens and prednisone therapy, CIC levels decreased to 16,000 micrograms/dl and serum BSA antibody hemagglutinating titer fell 32-fold over a period of 15 months. There was prompt symptomatic relief and amelioration of signs of nephritis. The patient was able to consume a diet normal in protein and caloric content, and statural catch-up growth occurred. Recognition of food antigens to which the patient was hypersensitive provided a rationale for the relief of the gastrointestinal disturbance, growth stunting, and renal disease.
IgA-containing immune complexes after challenge with food antigens in patients with IgA nephropathy.
Author Jackson S; Moldoveanu Z; Kirk KA; Julian BA; Patterson TF; Mullins AL; Jilling T; Mestecky J; Galla JH
Source Clin Exp Immunol, 1992 Aug, 89:2, 315-20
Abstract
The possibility that patients with IgA nephropathy (IgAN) might have abnormal IgA immune responses to immunogens commonly encountered at mucosal surfaces, resulting in the formation of circulating immune complexes (CIC), was examined. Since it is generally held that such increased IgA responses are characterized by detectable aberrancies in handling of IgA-containing CIC, IgAN patients and controls were given a large volume of bovine milk (after dietary deprivation of bovine antigens) and immune complex levels were measured over a period of 12 h. An assay based on binding of CIC containing C3 to solid-phase anti-C3 and subsequent development with isotype-specific antibody revealed no differences in responses of patients and controls with respect to IgG- and IgM-containing CIC. Although IgAN patients tended to have higher levels of IgA-containing CIC, there were no differences in response patterns when IgA CIC levels after ingestion of the milk stimulus were related to baseline levels. Polymorphonuclear leucocytes (PMNC), which bear surface receptors for IgA, were isolated from some subjects at the same times as the samples for CIC levels and examined by two-colour immunofluorescence for the coincident presence of IgA and milk antigens. In contrast to the data obtained in the CIC assays, these experiments revealed the simultaneous presence of IgA and two of three milk proteins in PMNC of IgAN patients but not controls. Follow-up experiments designed to assess more quantitatively the coincidental presence of IgA and milk antigens indicated no significant differences between patients and controls. However, milk proteins seemed to be more commonly associated with IgA in PMNC of IgAN patients, suggesting the presence of non-complement-fixing IgA/antigen CIC after mucosal challenge of some IgAN patients.
Mucosal immunity in primary glomerulonephritis: II. Study of the serum IgA subclass repertoire to food and airborne antigens.
Author Rostoker G; Petit-Phar M; Delprato S; Terzidis H; Lang P; Dubert JM; Weil B; Lagrue G Source Nephron, 1991, 59:4, 561-6
Abstract IgA specific for 7 food and 6 airborne antigens were sought in the serum of 30 adult patients with IgA mesangial nephropathy (IgA GN), 23 with membranous nephropathy (MGN), 20 with idiopathic nephrotic syndrome (INS), 11 with membranoproliferative GN (MPGN) and 22 healthy controls by means of an enzyme-linked immunoassay. The IgA subclass was determined using monoclonal antibodies. Increased levels of IgA specific for gliadin, bovine serum albumin (BSA), ovalbumin, lysozyme and alpha-lactalbumin were found in IgA GN, while increased levels of IgA to BSA, ovalbumin, lysozyme and alpha-lactalbumin were observed in MGN; IgA specific for alpha-lactalbumin were increased in INS, and MPGN patients had reduced levels of IgA to BSA and increased levels of IgA to beta-lactoglobulin and alpha-lactalbumin. These specific IgA to food antigens were restricted to the IgA1 subclass. Patients with IgA GN had significantly increased levels of IgA specific for Dermatophagoides pteronyssinus (DP) and Dactil while the MGN group showed increased levels of IgA specific for DP, feathers, Dactil and mold. INS patients had increased levels of IgA specific for DP, feathers, Dactil, mold and dog hairs, while MPGN patients had increased levels of IgA specific for feathers, Dactil, dog hairs and mold. All these specific IgA to airborne antigens were restricted to the IgA1 subclass. Patients with the four types of primary glomerulonephritis had decreased IgA specific for cat hairs which were of both the IgA1 and IgA2 subclasses. We conclude that anomalies of the IgA repertoire to environmental antigens are also encountered in primary glomerulonephritis other than IgA GN.
IgA antibodies to dietary antigens and lectin-binding IgA in sera from Italian, Australian, and Japanese IgA nephropathy patients.
Author Coppo R; Amore A; Roccatello D; Gianoglio B; Molino A; Piccoli G; Clarkson AR; Woodroffe AJ; Sakai H; Tomino Y. Source Am J Kidney Dis, 1991 Apr, 17:4, 480-7
Abstract We studied serum IgA as antibodies to dietary antigens (Ag), as lectin-binding molecules, and as conglutinin-binding immune complexes (IgAIC) in people from geographical areas in which IgA nephropathy (IgAGN) is particularly frequent. Sera from 63 Italian, 21 Australian, and 25 Japanese patients affected by IgAGN and 24 Italian, 20 Australian, and 40 Japanese healthy controls were studied. Increased values of IgAIC were detected in 42.8% of Italian patients, while only in 23.8% and 8% of Australian and Japanese patients, respectively. Mean values were significantly increased only in Italian patients (P less than 0.0001). Positive values of IgA antibodies against dietary Ag had variable prevalences, but again Italian patients showed the highest frequency, from 19% to 28.5% versus 0 to 38% in Australians and 0 to 16% in Japanese. Mean values of these antibodies were not significantly increased in any patient groups in comparison to the corresponding healthy populations. However, patients with elevated values of IgAIC had significantly higher serum concentrations of antibodies to alimentary components and a linear correlation was found between IgAIC and some IgA antibodies to food components. The relationship between these two series of data was particularly evident for Italian and Australian IgAGN patients. Moreover, the patients with positive data tended to have a cluster of increased levels of IgA antibodies against several alimentary Ag at the same time. A linear correlation was evident between values of IgA antibodies to gluten fractions and to heterologous albumins. None of these correlations was evident among healthy controls.
Low-antigen-content diet in the treatment of patients with IgA nephropathy.
Author Ferri C; Puccini R; Longombardo G; Paleologo G; Migliorini P; Moriconi L; Pasero G; Cioni L Source Nephrol Dial Transplant, 1993, 8:11, 1193-8
Abstract Since dietary macromolecular antigens can be involved in the pathogenesis of IgA nephropathy (IgAN), the effect of a low-antigen-content diet was evaluated in 21 patients (10 women, 11 men, mean age 27.7 +/- 10 years) with immunohistochemical findings of active IgAN. The diet was followed for a 14-24-week period (mean 18.8 +/- 6); in all cases the effects of the treatment were evaluated by clinical and serological parameters, and in 11 patients also by repeat renal biopsy. After dietetic therapy a significant reduction of urinary proteins was recorded present in 12 cases during the 6 months preceding the treatment, was markedly reduced or disappeared in 11. At post-treatment control biopsy mesangial and parietal deposits of immunoglobulins, complement C5 fraction and fibrinogen were significantly reduced. The improvement of the objective parameters such as heavy proteinuria, a strong predictor of a poor prognosis, and of immunohistochemical alterations indicate that a low-antigen diet can positively affect patients with IgAN. These results could be ascribed to a reduction of nephritogenic food antigen input and to a putative functional restoration of the mononuclear phagocytic system.
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Permission to cross-post granted from Dr Carol of Grassmere Clinic in Nashville,
TN.
"For any adopters whose greyhounds (or other dogs) received the Pfizer dental
vaccine, you should know that it is being discontinued for lack of proof of
efficacy. It was originally granted conditional approval, pending proof of
efficacy, but that was not forthcoming.
Response from Pfizer Animal Health:
The USDA licensed the Porphyromonas Denticanis-Gulae-Salivosa Bacterin as a
conditionally licensed vaccine. Conditional vaccine licenses must be renewed by
the USDA Center for Veterinary Biologicals each year with disclosure of any new
efficacy and potency data and progress to a full license must be demonstrated.
Periodontal disease due to its complex, chronic, and progressive nature is a
challenging disease to study. Pfizer Anima l Health conducted an unprecedented
48 month field efficacy study intended to support the full licensure of this
product. Unfortunately the study did not demonstrate a vaccine effect in
vaccinates (as compared to controls) for either of the key efficacy variables
assessed (attachment loss and gingival bleeding index). The current conditional
license for this vaccine will lapse on April 6th 2011 (except in the state of
Minnesota where it lapses on April 2, 2011) and given that these results do not
support efficacy the only available course of action was to discontinue the
vaccine.
Anyone who has listened to me rant about vaccines has heard this before, but
I'll repeat again... please be VERY sure of the vaccine needs of your greyhounds
and DO NOT get vaccines that are unproven, unnecessary, and sometimes
potentially harmful to a breed that seems to have a delicate immune system to
begin with.
Drug companies h ave produced many different vaccines over the years, but the
fact is that the only "core" vaccines every dog needs are rabies and the
distemper/parvo vaccine.
ALL OTHER VACCINES ARE "FRINGE" VACCINES, and should only be accepted by you for
your greyhound if you are sure of their need, their efficacy, and their safety.
And, remember the distemper/parvo vaccine should only be given every 3 years,
NOT annually."
Don't be afraid to question - don't be afraid to say no.
Carol
Digger, Triple, Horseshoe, Rising, Success, Sting and Funky
And waiting... Mariah, Shiloh, Lorrie, Zoeie and Doc
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Yes sometimes I/D is necessary unfortunately for some dogs, I'm just saying try a more healthy approach first which can and most likely will resolve the problem without requiring any food changes.
ETA: My apologies tbhounds for my first post coming across like it did.
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Just a suggestions, but TOTW is a very reasonable priced food that many members on here are feeding with good success. They make 4 different formulas so you should be able to find one that will work. As far as weight loss goes remember each dog is different and may require more or less than what the packaging guidelines tell you to feed. For example, Nadir weighs 69 lbs and I have to feed him 4 cups everyday. This amount is in the midrange according to the packaging of what you would feed an 80-100lb dog, which happens to also be the same amount I feed my 100lb bulldog Bruiser. I feed the Pacific Stream version and a bag which runs about $46 with tax will last 1 month for him. I too used to feed Orijen 6 Fish and the Red, but like you it just got too expensive, especially when feeding 4. I also understand your reasons for not wanting to do raw.
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Before you do a food change and feed a bad quality overpriced food do your grey and yourself a favor and just give him a tsp of Manuka honey a few times before his meals. You will find that not only does it stop the noisy gurgles and give him his appetite back, but these occurences will happen less and less frequently.
I use either Wedderspoons Raw Manuka Active 16+ or Y.S. Organic Bee Farms Raw Manuka 15+. Both can be bought through Vitacost.com
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God, the emotions you must be feeling now. It's so hard to brace yourself for the moment when you finally must say goodbye. You don't want that moment to come, but at the same time to prepare yourself for that moment and having it postponed has got to be tough.
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Did you feed the hamburger only last night? If so, was there any reaction like those that had been occurring? Inquiring minds are eager to know.
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What I read was that risk of bleeding is increased when taken with asprin or NSAIDs. It can also like NSAIDs be irritable to the GI tract which can be a cause of bleeding. This is information I found when searching Rehmannia glutinosa.
I'm all for using natural remedies, but with due caution. In this case I would not use it unless you can find something else he can take instead of an NSAID that would work better together with less risk.
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Alicia,
I'll be thinking of you today and keeping you and your loved ones in my prayers. Sending lots of white light and healing thoughts for a successful surgery and quick recovery. Looking forward to a good post surgery update.
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I stopped feeding raw exclusively over a year ago for money reasons and for time reasons. The pups still get it a few times a week for dinner, but they are on Taste of the Wild Pacific Stream kibble too.
When feeding exclusively raw it ranged from $60-$70 per dog/month.
What I am feeding now really works and it's half the cost.
Don't get me wrong, I love raw and one day my guys will eat raw totally again, but it's cost prohibitive at times.
I had to stop feeding raw for the same reason. I was okay with the cost with 3 dogs, but then when Chase joined us and Anna stayed with us while her mom was deployed I just couldn't afford it any more. I was feeding Orijen 6 Fish or Red kibble in the morning and raw at night. When I did a comparison of then two costs, it was actually cheaper to feed Orijen at $75 a bag vs the raw for the same amount of meals. I do want to start adding some raw back into their diets though.
Congratulating myself on buying the small jar ... 
Doolin Update
in Health and Medical discussion
Posted
I'm hoping your on the way to an e-vet now. This can't waiting another minute. As far as your vet goes you need to remember, she may have graduated from Vet School it doesn't mean she wasn't at the bottom of her class. After you get Doolin hopefully straightened out at the e-vet I'd be looking for another vet. Continuing with this vet could very well cost him his life.