Malabsorption of vitamins

Several factors contribute to development of bone disease in CF (1) malabsorption of vitamins D and K and calcium (2) poor... 

Myopathy and neuropathy Colchicine myoneuropathy appears to be a common cause of weakness in patients on standard therapy who have elevated plasma levels caused by altered renal function. It is often unrecognized and misdiagnosed as polymyositis or uremic neuropathy. Proximal weakness and elevated serum creatine kinase are generally present, and resolve in 3 to 4 weeks following drug withdrawal. Maiabsorption of vitamin B-f2- Colchicine induces reversible malabsorption of vitamin B-12, apparently by altering the function of ileal mucosa. 

Indicationsand Dosages Alert Oral dosing is preferred. Administer the drugIM only in patients with GI, hepatic, or biliary disease associated with malabsorption of vitamin D. 

Bi2 are only about 2 meg, it would take about 5 years for all of the stored vitamin B12 to be exhausted and for megaloblastic anemia to develop if Bi2 absorption were stopped. Vitamin B12 in physiologic amounts is absorbed only after it complexes with intrinsic factor, a glycoprotein secreted by the parietal cells of the gastric mucosa. Intrinsic factor combines with the vitamin Bi2 that is liberated from dietary sources in the stomach and duodenum, and the intrinsic factor-vitamin Bi2 complex is subsequently absorbed in the distal ileum by a highly selective receptor-mediated transport system. Vitamin Bi2 deficiency in humans most often results from malabsorption of vitamin B12 due either to lack of intrinsic factor or to loss or malfunction of the specific absorptive mechanism in the distal ileum. Nutritional deficiency is rare but may be seen in strict vegetarians after many years without meat, eggs, or dairy products. 

In patients who have preexisting bowel disease or cholestasis, steatorrhea may occur. Malabsorption of vitamin occurs rarely, leading to hypoprothrombinemia. Prothrombin time should be measured frequently in patients who are taking resins and anticoagulants. Malabsorption of folic acid has been reported rarely. Increased formation of gallstones, particularly in obese persons, was an anticipated adverse effect but has rarely occurred in practice. 

Osteitis fibrosa does not occur, as in renal osteodystrophy. The common features that appear to be important in this group of diseases are malabsorption of calcium and malabsorption of vitamin D. Liver disease may, in addition, reduce the production of 25(OH)D from vitamin D, although its importance in all but patients with terminal liver failure remains in dispute. The malabsorption of vitamin D is probably not limited to exogenous vitamin D. The liver secretes into bile a substantial number of vitamin D metabolites and conjugates that are reabsorbed in (presumably) the distal jejunum and ileum. Interference with this process could deplete the body of endogenous vitamin D metabolites as well as limit absorption of dietary vitamin D. 

A 63-year-old man with type 2 diabetes, who had taken metformin for at least 5 years, had a low serum vitamin Bi2 concentration (110 pg/ml reference range 200-230) and a normal serum folate (90). There were no autoantibodies. A Schilling test showed malabsorption of vitamin Bi2. Metformin was withdrawn and 2 months later a Schilling test showed no malabsorption. 

In a review of 60 publications on metformin and pregnancy malabsorption of vitamin B12, which occurs in nonpregnant women, was thought to be a potential problem (116). The data did not suggest an increased risk of teratogenesis. 

Adams JF, Clark JS, Ireland JT, Kesson CM, Watson WS. Malabsorption of vitamin BI2 and intrinsic factor secretion during biguanide therapy. Diabetologia 1983 24(l) 16-8. 

The Immerslund-Najman-Grasbeck syndrome is a term used to describe a congenital malabsorption of vitamin B12. It is perhaps the most common of the familial vitamin B12 absorption disorders and more than 100 cases have been described (C21). Although the majority of patients present during the first 2 years of life, a few have been seen much later. The disorder is charac-... 

J2. Jounela, A. J., Pirttiaho, H., and Palva, P, Drug induced malabsorption of vitamin B12. 

VI. Malabsorption of vitamin B12 (luring treatment with phenformin. Acta Med. Scand. 196, 267-269 (1974). 

Gueant JL, Champigneulle B, Gaucher B and Nicolas JP (1990) Malabsorption of vitamin Bi2 in pancreatic insufficiency of the adult and of the child. Pancreas 5,559-67. 

Malabsorption of vitamin B12 was observed in 14 of 46 diabetics taking metformin or phenformin (Callaghan et al., 1980 Adams et al., 1983) metformin was more often to blame. Withdrawal of the drug resulted in normal absorption in only 7 of the 14 (Adams et al., 1983). 

Intestinal malabsorption of vitamin B12 may be caused by gastrectomy or ileal resection, with an inverse relationship between the length of ileum resected and the absorption of vitamin B12. Other causes of malabsorption are tropical sprue, inflammatory disease of the small intestine, intestinal stasis with overgrowth of colonic bacteria, which consume the vitamin 6,2 ingested by the host, and HIV infection. Another cause of vitamin B malabsorption is failure to extract cobalamin from food. Some patients fail to absorb cobalamin bound to food, whereas absorption of nonfood-bound cobalamin in the Schilling test is unimpaired. This is particularly a problem in patients with compromised gastric status or early in the course of development of pernicious anemia. 

Serial PT measurements also can be used to differentiate between cholestasis and severe hepatocellular disease. In practice, PT should be measured again after vitamin K injection, because cholestasis wiD. cause a decrease in PT because of malabsorption of vitamin K. The patient has cholestasis if the PT corrects after vitamin K replacement (10 mg sub-cutaneously or intramuscularly, followed by PT measurement 4 hours later). With time, if the PT does not return to normal, the patient has severe hepatocellular disease. 

Pernicious anemia is a megaloblastic anemia caused by malabsorption of vitamin Bn secondary to inadequate secretion of normal IF. The word pernicious reflects the unremitting and usually fatal... 

Anemia occurs when there is significant blood loss from the GI tract. If the patient can consume oral medication, ferrous sulfate should be administered. If the patient is unable to take oral medication and the patient s hematocrit is sufficiently low, blood transfusions or intravenous iron infusions may be required. Anemia may also be related to malabsorption of vitamin B12 or fohc acid, so these may also be required. 

Secondary hyperparathyroidism arises from chronic hypocalcemia. This condition can result from renal failure leading to poor reabsorption of calcium from the urinary filtrate. It can also arise from poor nutrition or malabsorption of vitamin D by the intestine. In response, parathyroid glands increase their secretion of PTH. This condition also leads to decalcification of bone. Tertiary hyperparathyroidism is often seen after renal transplantation. In these patients, the parathyroid gland secretes the hormone independently of blood calcium levels. 

Vitamin Bj should be given prophylactically only when there is a reasonable probability that a deficiency exists or wdl exist. Dietary deficiency in the strict vegetarian, the predictable malabsorption of vitamin Bj in patients who have had a gastrectomy, and certain diseases of the small intestine constitute such indications. When GI function is normal, an oral prophylactic supplement of vitamins and minerals, including vitamin Bj, may be indicated. Otherwise, the patient should receive monthly injections of cyanocobalamin. 

It is obvious that a variety of disorders would result from a disturbance of the vitamin D endocrine system. Fat malabsorption would result in a deficiency of vitamin D giving rise ultimately to osteomalacia or rickets or secondary hyperparathyroidism. A hepatic disorder such as severe cirrhosis, or biliary atresia, may result in malabsorption of vitamin D and defective vitamin D-25-hydroxylation. Dilantin and phenobarbital cause low plasma 25-OH-D levels resulting in rickets and osteomala-cia246) Qf parathyroid glands would cause a severe hypocalcemia and tetany. 

Palva IP, Rytkonen U, Alatulkkila M, PalvaHLA. Drug-induced malabsorption of vitamin Bo. V. Intestinal pH and absorption of vitamin B12 during treatment with para-aminosalicylic acid. ScandJHaematol (1972) 9, 5-7,... 

Therapy malabsorption of vitamin B12, i.e., in pernicious or other macrocytic anemias, sprue, gastrointestinal pathology or surgery, enteropathy concomitant with folic acid deficiency, stimulation of hematopoiesis... 

The vitamin is absorbed through the intestine by a mechanism similar to that involved in the absorption of other liposoluble vitamins consequently, intestinal disorders leading to lipid malabsorption are associated with malabsorption of vitamin E. Humans with such malabsorption syndromes have reduced levels of vitamin E in their tissues. They do not show classical symptoms of muscular dystrophy, although a certain degree of muscular fatigue may be observed. 

Malabsorption of vitamin A occurs associated with diarrhea, intestinal infections, and infestations (Rosenberg et aL, 1977 Mansour et aL, 1979). Children with a recent history of diarrhea are at higher risk of developing clinical evidence of deficiency than those without (Sommer, 1982a). Sivakumar and Reddy (1972, 1978) used labeled vitamin A to demonstrate a depressed absorption of vitamin A in acute gastroenteritis and in respiratory infections. Presumably this was primarily due to excessively rapid passage more than to a defective intraluminal hydrolytic system, because providing a vitamin A supplement to children with diarrhea results in improved absorption (Sivakumar and Reddy, 1978). 

Malabsorption of vitamin A is also associated with intestinal parasitism in children (Sivakumar and Reddy, 1975 Mahalanabis et aL, 1979 Chavalit-tamrong et aL, 1980) and in adults (Mahalanabis et aL, 1976). The malabsorption that accompanies Ascaris lumbricoides infections is associated with an altered mucosal morphology that reverts to normal, concurrent with improved absorption efficiency after deworming (Tripathy et aL, 1972). The role of parasites in the epidemiology of hypovitaminosis A is discussed later in this chapter. 

Infants with severe cholestasis due to 3jff-HSDH deficiency may have hypo-calcaemia due to malabsorption of vitamin D or severely deranged clotting due to malabsorption of vitamin K. Vitamins D and K should be given either parenterally or orally in a form that is absorbed despite intestinal bile salt deficiency (e.g. la-hydroxy-cholecalciferol or 1,25-dihydroxy-chole-calciferol). Fresh frozen plasma and intravenous calcium supplement may occasionally be required. 

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