Denamarin was a “me too” veterinary preparation of Milk Thistle sold as a ‘proprietary’ answer to the far-more-effective “Urso” which is ‘ursodehydrocholic acid’ and had been working WELL for liver disease, cirrhotic, fibrotic, infectious….But Veterinarians didn’t ‘control’ the drug and there was a generic.
Milk Thistle contains minuscule amounts of UDCA and so it was a “me too” but didn’t work as well. So I stuck with Urso.
Denamarin contains SILYBIN as well, which is a ‘not-inconvenient’ delivery system for flavonoids. Those are ‘oils’ that can come from various thinks like Palmarosa oil, etc. Except Silybin contains SEVERAL Flavonoids.
So, I went out and found a decent study that performed to HUMAN-level stakes of research quality and reviews of thousands of pieces of literature. Thank god I didn’t have to do it LOLOLOL
Here’s the publication, in it’s entirety and not to decrease the economic value of the original document nor use it in a commercial measure. Fair use.
The following is excerpted from one of my fave sites, (Vetfolio) for my notes category. (For future reference but linked for bibliographical accuracy.)
Limbal (Epibulbar)
Limbal melanomas are the most common ocular melanomas in dogs, accounting for 20% to 50% of these tumors,17-19 and are less common in cats.7 In both species, this tumor is typically a smooth, black or heavily pigmented, subconjunctival mass ( FIGURE 3 ) that is noted incidentally by an owner or a veterinarian.20,21 These tumors usually involve the adjacent cornea and/or conjunctiva and, much less commonly, may extend intraocularly.20,21 Differentiating a tumor of limbal origin from extension of an intraocular uveal tumor into the sclera may be difficult with advanced disease. Most canine limbal melanomas are located along the superior half of the limbus, and German shepherds appear to be affected more frequently than other breeds.17,19,22
These tumors are generally considered to be benign, and no cases of confirmed metastasis have been reported in dogs.17,19,21 However, subpopulations of cells within the tumor may display more malignant characteristics.21 The tumors tend to grow more rapidly in younger dogs and more slowly in older dogs and most affected cats.20,21 Limbal melanomas in cats are similar to those in dogs in appearance, treatment, and prognosis, although distant metastasis has been reported.7,20,23The recommended treatment of a limbal melanoma depends on the rate of tumor enlargement, extent of the tumor at presentation, and expertise of the surgeon or the possibility of referral to a specialist. Because of the benign nature of most of these tumors, small, slowly growing masses may be monitored for progression, particularly in older patients.1,21 For rapidly growing tumors, surgical resection (partial- or full-thickness sclerectomy/keratectomy) is potentially curative and may maintain a functional and cosmetic globe.19,24 Techniques for removing the mass and repairing the resultant corneoscleral defect are described elsewhere.25Additional treatment modalities have also been evaluated. Cautious application of strontium irradiation26 or Nd:YAG,17 diode, or carbon dioxide laser27 energy treatment alone or in addition to surgical debulking can be effective. Cryotherapy has also been reported as an effective component of the treatment of limbal melanomas.1,10,20 The relative success of cryosurgery in treating limbal melanomas has not been thoroughly evaluated. Enucleation can be curative but is recommended only in eyes in which the melanoma has invaded the anterior chamber, filtration angle, or uveal tract and painful intraocular disease (e.g., glaucoma, uveitis) has resulted. Determining the full extent of the tumor before surgery may require diagnostics (e.g., gonioscopy, high-resolution ultrasonography) typically performed by a specialist.
This is up here mainly for me. Or in case I have a colleague who wants to see a few things I put together to help me formulate a halfway decent chemotherapy protocol.
Certain medicines are hard to get, including Chlorambucil and Cyclophosphamide. Those would run into the thousands over 2 months.
However, Doxorubicin and Vincrisine plus Prednisone are cheap, at least relatively.
So, for example if I wanted to try the CHOP protocol or the HOP-L protocol, I could except in either protocol there’s a VERY expensive piece.
I am not the author or copyright holder on any of the above. It’s stored here without adulteration and is not being sold, or used for gain. Attribution is evident in the page headers and completeness of the publications.
This is only in my Vets Notes and Libraries section because it’s pretty much veterinarian notes on appetite, appetite stimulation, rule outs for failing appetite and medications that may help. There’s a discussion of ‘recently’ discovered hormones Leptin and gRhelin that mitigate appetite in dogs and pretty much every other mammal.
“My Dog Won’t Eat.” A Book on Appetite Science
I don’t own, and wrote barely ANY of the following.
So, I put together 39 pages of information on Cushing’s Disease, which is overactive Adrenal Glands. The body produces way too much Cortisol and the impact is insulin antagonism, and hunger and thirst, weight gain, thinning skin, premature aging. And increased vulnerability to infections.
There are two other resources on DrJohnson.com for HyperAdrenoCorticism
Actually, a lot of the same symptoms (besides thirst and elevated liver enzymes) of Hypo-Thyroidism.
And, so that I don’t look totally stupid when I walk into the exam room with my Cushing’s Cases, I put together THIS DOCUMENTto leaf through over my lunch.
There’s the diagnostic algorithm, and the numbers you want to see, and then treatments are discussed and my favorite (because it hedges itself against Addisonian Crisis) is the Utrecht Method of medicine.
Medical Treatment
Metronidazole may be recommended along with dietary modification as the first medical therapy. Metronidazole has antibiotic, anti-inflammatory, and antiprotozoal properties, and is usually fairly well tolerated, although some cats may lose their appetite when given this drug.
If dietary modification or metronidazole are not effective, corticosteroids, which are potent anti-inflammatory and immune-suppressing agents, may be recommended, either alone or in combination with metronidazole. Cats should be monitored closely while they are on corticosteroids, as diabetes and immune suppression are among their potential side effects. Nonetheless, cats tend to tolerate these drugs well as long as they receive them at an appropriate dose.
Inflammatory Bowel Disease ( IBD ) – Feline
Cats usually take corticosteroids orally, starting with a higher dose that is gradually reduced over several weeks. In cats that won’t take medication orally, or in cases in which vomiting is severe, your veterinarian may give the medications as an injection.
If none of these medications successfully controls the symptoms of IBD, more potent immunosuppressive drugs, such as chlorambucil or azathioprine, may be necessary. These drugs can suppress production of white blood cells, red blood cells, and, less commonly, platelets, in the bone marrow. A veterinarian must carefully monitor cats taking these drugs.
Inflammatory Bowel Disease ( IBD ) – Feline
As GI bacteria may play a role in the development of IBD, newer therapies include prebiotics, which are substances that promote certain bacterial populations, and probiotics, which are bacterial strains that promote GI health. The addition of soluble fiber, such as psyllium, to the diets of cats with inflammatory colitis may be helpful, and supplementation with folate or vitamin B12 should be provided if an affected cat is deficient in these B vitamins.
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I’ve always liked Sulfasalazine for IBD in the past, wondered about its use in cats: Found this quality literature.
You have to scroll past the cut and paste Bull that the online pharmacies trot out as “fact” – which is often paraphrased by non-English speakers.
Sulfasalazine is considered by many veterinarians to be the preferred drug in dogs for treatment of colitis. The recommended oral dosage in dogs is 12.5 mg/kg q8h up to a maximum of one gram q8h in refractory dogs or those having severe IBD. It is important to continue initial therapy with sulfasalazine for a minimum of four weeks before modifying drug dosage. With resolution of signs, sulfasalazine dosage is gradually decreased by 25 percent at two-week intervals and eventually discontinued while maintaining the dietary management. Caution is advised in using sulfasalazine in cats because of their sensitivity to salicylates. Other oral medications of potential use in dogs include olsalazine and mesa-lamine. Olsalazine (Dipentum) consists of two molecules of mesalamine linked by an azo bond. The enteric-coated products of mesalamine (Pentasa and Asacol) release the active drug in the distal small intestine and colon, respectively. The use of olsalazine or mesalamine for treatment of IBD in dogs and cats has not been critically evaluated, but there are substantial anecdotal reports of their efficacy. The proposed dosage is about one-half that of sulfasalazine.
25 – 50 mg every 12 hours = Cat dose up to 12-14 pounds.
Dr Yanong wrote thisdown in Florida for the fish farmers and the aquaculture people, and is keenly important to, and relevant to, the tropical and pond fish trade.
It is extremely thorough and the section on bath treatments with the doxycyclines / OTC’s against certain bacteria and in varying water quality was interesting to me. But the discussion of the new thiamphenicols, (Florfenicol) was also illuminating.
This document is authoritative for Ibuprofen toxicity in dogs. It’s in my Vets Notes library section for my future reference. I did not write this and it is produced in its entirety.
Bromethalin, a nonanticoagulant, single-dose rodenticide, is a neurotoxin available as bars (blocks), pellets, seed, and a fake worm you can give to Moles.
The net result is cerebral and spinal edema and increased CSF pressure, leading to neurologic dysfunction.
Bromethalin can cause either an acute or a subacute/chronic syndrome, depending on the dose ingested. At doses equivalent to or more than the average lethal dose, dogs may develop an acute convulsant (or high-dose) syndrome resulting in clinical signs within 4–36 hr of exposure; such signs include hyperexcitability, muscle tremors, grand mal seizures, hindlimb hyperreflexia, CNS depression, hyperthermia, and death. The paralytic (subacute or chronic) syndrome is seen at lower doses, and clinical signs may not appear for several days (up to 7 days) after exposure. Initial signs may include depression, hindlimb weakness or paresis, decreased propioception, ataxia, and possible tremors. Muscle weakness often progresses from posterior to anterior muscles. Cats typically develop paralytic syndrome irrespective of dose of bromethalin.
Based on the history of exposure, bromethalin toxicosis should be considered when there is moderate to acute onset of weakness, hindlimb paralysis, tremors, and seizures. Some other toxicologic and nontoxicologic differential diagnoses should include ethylene glycol toxicosis, marijuana ingestion, 2,4-D and other phenoxyacetic acid herbicide toxicosis, copper head snake envenomation (cats), intervertebral disc problems, spinal cord and CNS trauma, and tick paralysis.
The following can be used as a guideline to treat bromethalin exposure in dogs and cats:
At a bromethalin dosage of 0.1–0.49 mg/kg in dogs, or 0.05-0.1 mg/kg in cats, emesis alone within 4 hr of exposure may be adequate. If emesis is not successful, or if > 4 hr have elapsed since ingestion, a single dose of activated charcoal at 1–2 g/kg body wt is indicated. Whenever administering activated charcoal, the clinician must remain aware of the risk of aspiration or hypernatremia secondary to fluid shift into the gut. The clinical signs of acute hypernatremia may mimic those seen with bromethalin toxicosis.
Diazepam, barbiturates, and other anticonvulsant medications should be used to control seizures and other CNS signs. Full recovery may require days to weeks of treatment.
At a bromethalin dosage of 0.5–0.75 mg/kg in dogs, or 0.1–0.3 mg/kg in cats, an initial dose of activated charcoal at 1–2 g/kg body wt should be considered. A repeat dose at half the original dose at 8-hr intervals for a total of three doses can be administered, again being aware of and monitoring for possible hypernatremia.
At a bromethalin dosage of ≥0.75 mg/kg in dogs, or ≥0.3 mg/kg in cats, administration of six doses of activated charcoal over 48 hr (repeat every 8 hr) can be considered to reduce the body burden by interrupting enterohepatic recirculation.
Use of mannitol and corticosteroids has been suggested to treat clinical signs, because they may help manage cerebral edema due to other causes. However, this has not been shown to be very helpful, likely because of the presence of intra-myelin edema. Diazepam, barbiturates, and other anticonvulsant medications should be used to control seizures and other CNS signs. Full recovery may require days to weeks of treatment.
This doesn’t pass for what someone like Terence Hamilton knows, as he is an oncology specialist, but for ‘the basics’ out here in general practice, this has good information. Looks like it was written / compiled by an AHT – not a doctor but it’s damn good nonetheless. So I’m putting it here for my reference, hence it’s in the Vet’s Notes Library category.
