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Оглавление

Hypervitaminosis A

BASICS

DEFINITION/OVERVIEW

Hypervitaminosis A is well recognized health concern in chelonians. It can be caused by OTC supplements provided by well‐ meaning owners, parenteral overdosing by veterinarians, or diets with high animal vs. plant‐based (beta carotene) vitamin A levels.

ETIOLOGY/PATHOPHYSIOLOGY

In vertebrates, the vitamin A forms are trans‐retinyl esters, trans‐retinol, ‐retinal and ‐retinoic acid (99% of all vitamin A present in the body), while the major dietary provitamin A carotenoid is beta carotene.

The all‐trans‐vitamin A isomers are the only forms used physiologically.

The liver absorbs and stores preformed vitamin A; at a certain point, storage capacity is reached and toxicity occurs. Other storage sites include adipose tissue, lung, and kidney.

In humans, the retinoid delivery pathway to tissues involves primarily retinol bound to retinol‐binding protein; chylomicrons, very low density lipoprotein, low density lipoprotein, and albumin also provide transport.

Adverse effects in humans include increased bone turnover by suppressing osteoblast activity and stimulating osteoclast formation. This can lead to hypercalcemia, osteoporosis, pathologic fractures, altered skeletal development in children, and skeletal pain.

Vitamin A is fat soluble and high levels can affect metabolism of other fat‐soluble vitamins (D, E, K); with the effects on vitamin D contributing to the aforementioned bone pathology, although stimulation of bone resorption by vitamin A is reported independent of effects on vitamin D.

Vitamin A can have a toxic effect on mitochondrial function and is reported to cause hypothyroidism in mice.

SIGNALMENT/HISTORY

First time owner of reptiles/species and young animals.

Owner using OTC vitamin A drops, OTC multivitamin with vitamin A in formulation other than beta carotene, using cod liver oil or feeding liver to a carnivorous/omnivorous animal.

Occasional issues with extruded diets with inadvertent toxic levels of non‐beta carotene vitamin A.

CLINICAL PRESENTATION

Patients present with vague signs such as anorexia, dehydration, lethargy.

Usually has a dermatological component including: dysecdysis, epidermal flakiness, ulceration, and sloughing.

Bilateral epiphora and periorbital edema may be noted.

Ulcerative stomatitis can be seen.

Secondary bacterial and fungal infections can occur.

Based on pathophysiology, suspect that metabolic bone disease may have interplay with hypervitaminosis A.

RISK FACTORS

Juvenile animal

Reproductively active female

Liver disease

Husbandry

N/A

Others

Iatrogenic dietary or parenteral over supplementation of non‐beta carotene vitamin A.

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Hypovitaminosis A

Infection

Hepatic or renal disease

UVB or thermal burns

Poor overall husbandry or diet

Improper conspecific arrangement

Metabolic bone disease

DIAGNOSTICS

Liver biopsy for histopathology and testing vitamin A levels (need normal values for the species).

Presumptive diagnosis based upon history and clinical presentation.

PATHOLOGICAL FINDINGS

Hepatic fibrosis

Osteoporosis

Decreased or abnormal bony growth in juvenile animals.

Epidermal ulceration

TREATMENT

APPROPRIATE HEALTH CARE

N/A

NUTRITIONAL SUPPORT

Often need assisted feeding

Esophageal feeding tube is often recommended, especially in chelonians with skin sloughing, which makes it difficult to manipulate the head and neck.

CLIENT EDUCATION/HUSBANDRY RECOMMENDATIONS

Proper education about the correct diet and formulation of vitamin A for the species.

Education about differences between water soluble and fat‐soluble vitamins.

MEDICATIONS

DRUG(S) OF CHOICE

Discontinuing supplementation of non‐ beta carotene vitamin A.

Other treatment focuses on supportive therapy and managing secondary infections.

Systemic fluid therapy may be needed but with the goal of transitioning to oral fluids or passive soaking.

Pain management can be important.

Judicious topical use of silver sulfadiazine cream for epidermal ulcers can help.

Vitamins E and K and taurine administration have all been shown to help mitigate hypervitaminosis A in rat studies, but no studies are available in reptiles.

PRECAUTIONS/INTERACTIONS

Oversupplementation of vitamin A can have negative interactions with other fat‐soluble vitamins (D, E, K) leading to either decreased absorption or excess accumulation.

FOLLOW‐UP

PATIENT MONITORING

Reassessment of clinical manifestation

Review of current diet plan

Repeat liver biopsy if feasible

EXPECTED COURSE AND PROGNOSIS

In the acute form, hypervitaminosis A generally resolves quickly and clinical manifestation is uncommon (except in very high overdosing).

The chronic form is most common. Clinical resolution can take many months, with most dermatological manifestations resolving, although skeletal and hepatic damage may be permanent.

MISCELLANEOUS

COMMENTS

N/A

ZOONOTIC POTENTIAL

N/A

SYNONYMS

N/A

ABBREVIATIONS

OTC = over the counter

UVB = ultraviolet B