Quote from Liz on March 3, 2019, 12:02 am

I thought it would ve good to have a topic where we can post studies that is purely about hypervitaminosis A and its symtoms, as well. We already have a pubmed thread but it is really mixed.

This case study is very interesting. A vegetarian male who developed hepatitis and hypervitaminosis A. It is not clear how he got hepatitis in the first place though.. I have not pasted the whole study, but most of it. It is from 1982 and already back then they knew hypervitaminosis A was fairly easy to get with diet alone and as vit A was easily obtained over the counter (and still is) they suspected more toxicity cases in the future.

The study is a pdf, so have to paste the google link:

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.gastrojournal.org/article/0016-5085(82)90133-0/pdf&ved=2ahUKEwiTjuOlpOXgAhUL7KYKHSRCDjMQFjACegQIBBAB&usg=AOvVaw0uBtAk1Y757Z5JRGK19GYL

A 42-yr-old previously healthy white male presented to the Veterans Administration Medical Center complaining of 2 wk of upper respiratory symptoms, myalgias, arthralgias, nausea, anorexia, and abdominal pain. Three days earlier he developed dark urine, acholic stools, and jaundice. He drank three beers a week but denied drug abuse, exposure to hepatitis, homosexual activity, and recent travel. He was a vegetarian and ingested vitamin C daily.

Ofc people can "hide the truth regarding most things, question is, did getting hepatitis cause vit A toxicity, or did the A toxicity cause hepatitis? Either way, hepatitis loweres RBP which causes A toxicity.

He was sent home with a diagnosis of acute viral hepatitis and told not to ingest large supplements of vitamin C. Twenty days later he was brought to the hospital by friends because of increasing mental confusion and weak-ness. He described a 2-wk history of anorexia, nausea, and vomiting. For the past 2 days he had noted headache, fever, chills, and nonpruritic, scaling skin over his entire body.

Because of total body desquamation, vegetarianism, and history of ingesting vitamin C, he was closely questioned regarding other vitamin intake. He then stated that for 10 yr he had taken one 25,000 IU vitamin A capsule daily plus one additional capsule daily when “under stress” or not feeling well. In addition, he ate carrot and raisin salad daily and large amounts of green, leafy vegetables. These sources provided an estimated daily vitamin A intake of between 50,000 and 75,000 III. The recommended daily allowance is 5000 IU. He also ingested 1000 IU of vitamin D daily and unknown quantities of vitamin E, B-complex, and bone meal. In retrospect, he recalled that over the past year he had experienced cracked lips, dry skin, and excessive fatigue. He steadfastly maintained he had taken only one vitamin A capsule since the diagnosis of hepatitis 3 wk previously. That capsule caused indigestion and severe heartburn which he attributed to the oil (to dissolve vitamin A) sealed within the capsule. To avoid these symptoms, he stopped taking vitamin A supplements 3 wk before admission. Serum vitamin A, obtained almost 4 wk after his most recent vitamin supplement, was 182 pg/dl (normal, 20-80).

A liver biopsy was performed on the 16th hospital day. The hepatic vitamin A level was 3200 pg/g liver (normal <300) by the trifluoroacetic acid method (7). Light microscopy of the biopsy specimen (Figure 2) revealed changes compatible with acute viral hepatitis in its late stage [...] 

The patient continued to improve and was discharged on the 19th hospital day. After discharge he experienced transient, universal alopecia including scalp hair, body hair, and mustache. By 3 mo after the onset of jaundice, hepatitis B surface antibody (anti-HB,) appeared. Aside from persistent fatigue, he felt fit and had resumed normal activities.

The discussion is quite interesting:

Hypervitaminosis A has been frequently described, and vitamin A is a recognized hepato-toxin (2-4). The spectrum of hepatic injury resulting from chronic, excessive vitamin A ingestion ranges from mild elevations of liver enzymes (5) to hepato-splenomegaly with portal hypertension (4) to frank cirrhosis (6), depending on the dose and duration of exposure. Progressive hepatic damage occurs with continued vitamin ingestion (8). 

The present patient presented dramatically with hypervitaminosis A 20 days after the diagnosis of viral hepatitis B. Although a long-term user of supplemental vitamin A, he became intolerant to oil-containing vitamin A capsules at the onset of hepatitis. Despite the absence of recent vitamin ingestion, he returned with several features of acute hypervitaminosis A (9) including headache, skin desquamation, hypercalcemia, and confusion. He eventually experienced alopecia, a sign of more chronic toxicity (9). Liver and serum vitamin A levels confirmed the clinical diagnosis. In retrospect, the patient probably had mild, unrecognized chronic hypervitaminosis A prior to his acute illness; he had noted dry skin, cracked lips, and fatigue for the year preceding admission. The metabolism of vitamin A has been studied in viral hepatitis. Both vitamin A and retinol binding protein, its specific serum carrier, are low in acute hepatitis (10-13).

The present case is unusual because serum vitamin A was high, not low, during hepatitis.

In hypervitaminosis A the metabolic situation differs. Mallia et al. (16) showed elevated levels of lipoprotein-bound retinyl esters in rats made toxic with vitamin A, while levels of retinol remained normal (16). Retinol binding protein levels fell despite the elevation of total serum vitamin A. Smith and Goodman found a similar pattern in 3 patients with chronic hypervitaminosis A (17). They demonstrated an excess of total vitamin A relative to retinol binding protein, a difference largely accounted for by elevated levels of lipoprotein-bound retinyl esters. These findings suggest toxicity occurs when excessive amounts of vitamin A circulate that are not bound to retinol binding protein. Thus, retinol binding protein seems to prevent vitamin A toxicity in two ways, by regulating the interaction of plasma vitamin A with target cells and by controlling release of hepatic vitamin A.

We propose that two pathological processes combined to cause acute hypervitaminosis A in the present case. First, the patient had chronic vitamin A overload as suggested by his past dietary history and proven by his elevated vitamin A stores. Second, he developed acute viral hepatitis, a form of liver injury associated with low serum levels of retinol binding protein. This fall may have been even steeper than usual because albumin, another liver-derived serum protein, also fell markedly. As a result, high levels of vitamin A circulated in the presence of low levels of retinol binding protein, the pattern associated with toxicity. Massive release of vitamin A from necrotic liver probably did not contribute to the problem because vitamin A levels are usually low during hepatitis and because Ito cells are not known to be harmed by hepatitis viruses. This complication of hepatitis requires the presence of excessively large body stores of vitamin A. Such stores can result from the daily ingestion of only 35,000 IU, or 7 times the recommended daily allowance (18). An intake of this magnitude is easily achieved because capsules containing 25,000 IU are available over-the-counter. Moreover, the vitamin is used therapeutically for a variety of dermatologic conditions (9) and some workers have suggested a role for the vitamin in both cancer therapy and prevention (19). These latter developments have been reported in the lay press and will undoubtedly influence many individuals to use vitamin A supplement. 

In noting these facts, we suspect that the population with abnormally large hepatic stores of vitamin A is growing. Thus, the process described in this paper and other manifestations of hypervitaminosis A may be seen more frequently in the future.