Guest guest Posted February 28, 2008 Report Share Posted February 28, 2008 Listmates, Since my daughter's vitamin D level is so low (15) and some people link vitamin D deficiency to fibro, how many of you have had vitamin D measured, and if you did, and started supplementing high dose vitamin D (my daughter's doctor gave her 50,000 iu's a week), did the vitamin help or did it make you feel worse? The Marshall Protocol people make it sound like a bad idea, but in thinking about WHEN in the calendar my daughter does well, it is when she spends hours in the sun. Just wondering.... At 03:03 PM 2/28/2008, you wrote: >One of the things that prompted me to get my daughter diagnosed was >reading about pediatric FM in the FM Aware magazine. Prior to that, I >didn't know that children could be diagnosed with it. I remember it said >that they often do not have all the tender points as children, but >diagnosing was different for children. I was not in the room with the >doctor as they examined my daughter, so I can't tell you for sure what >criteria they used. I think they did do some checking of tender points, >because of what Allie said later about the exam. >Jeanne in WI > >i did read that this is a diagnosis by those docs familiar with fibro. >there is also some early form of fibro where not everyone has all the >tender points, just some of them. i did have a traumatic injury to my leg >around age 5, and my mom likes to tell me her funny story about my dad >carrying me(when i was an infant)and a pack of toilet paper up the wooden >flight of stairs, he dropped us both but caught the toilet paper. not >surprisingly, i am not fond of my mother, sorry to say. so both injuries >probably did some suppression to my hypothalmus and >started all my fibro because i complained to my mom at age 11 that i was >always tired and sleep never refreshed me, never and still never does. so >after i read one book on how this expert ties all these things together, >my horrible fibro life makes sense, at least, eventho i have >and continue to sleep it all away. >take care, >marg > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 28, 2008 Report Share Posted February 28, 2008 , I don't know how low my level was after my last bloodwork, it was below normal, but I was told by my doctor to make sure I was getting at least 2000 iu each day. Jeanne in WI Listmates, Since my daughter's vitamin D level is so low (15) and some people link vitamin D deficiency to fibro, how many of you have had vitamin D measured, and if you did, and started supplementing high dose vitamin D (my daughter's doctor gave her 50,000 iu's a week), did the vitamin help or did it make you feel worse? The Marshall Protocol people make it sound like a bad idea, but in thinking about WHEN in the calendar my daughter does well, it is when she spends hours in the sun. Just wondering.... Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 29, 2008 Report Share Posted February 29, 2008 asked: > > Since my daughter's vitamin D level is so low (15) and some > people link vitamin D deficiency to fibro, how many of you have had > vitamin D measured, > and if you did, and started supplementing high dose vitamin D (my > daughter's doctor gave her 50,000 iu's a week), did the vitamin > help or did it make you feel worse? The Marshall Protocol people > make it sound like a bad idea, but in thinking about WHEN in the > calendar my daughter does well, it is when she spends hours in the > sun. I don't know what the Marshall Protocol is, but as a weight loss surgery patient (I had a duodenal switch), my supplement needs are different from the normal population. I take 15,000 iu of dry Vitamin D per day. Dry is because with a DS, I don't absorb fats normally. High doses of Vitamin D should be done under a doc's care and according to labs. I don't really notice a difference, but then my level has never gone super-low, and I maintain constant levels of supplementation with yearly labs. But I've noticed that I do like to sit in my sunroom during sunny days, and (since my new knees) I like to be outside on sunny days, working in my yard. Z Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 1, 2008 Report Share Posted March 1, 2008 , You said: >I don't know what the Marshall Protocol is, but as a weight loss >surgery patient (I had a duodenal switch), my supplement needs are >different from the normal population. I take 15,000 iu of dry >Vitamin D per day. Dry is because with a DS, I don't absorb fats >normally. Have you been on that protocol since the beginning, or did they detect a problem developing after your surgery and corrected with the vitamin D? What did the supplement change for you? (I'm so anxious to know because of my daughter's prescription. Of course, if you are getting 15,000 iu daily, that is more than her 50,000 iu weekly.) I'm trying her on her second dose tonight and am praying she does OK tomorrow. This morning she was in too much pain to get out of bed to take her SAT exam, and that broke my heart, but her week had been terrible with a lot of deadlines and missed sleep. I wish I had known that would be happening when we scheduled her to take the exam! Vitamin D does increase the absorption of oxalate and so does fat malabsorption. Has your dietician mentioned a need for you to be on a reduced oxalate diet? Those with poor fat digestion are prime candidates for hyperabsorption of oxalate. Oxalate getting into the rest of your body after being absorbed in excess in the colon might be related to your pain, perhaps. I'll put some articles below about the connection between fat maldigestion and hyperabsorption of oxalate. This isn't obscure literature. There is a lot " out there " on this connection, but not much published on the pain side of the issue. However, you can find mention of pain issues at this place: http://www.vulvarpainfoundation.org/painproject.htm It really doesn't seem to matter why someone has fat maldigestion because there are articles talking about this happening in Crohn's disease, after bariatric surgery, after bowel surgery for other reasons, after taking lipase inhibitors...it doesn't matter why. IF someone has fat maldigestion, they will be absorbing an excess percentage of the oxalate in their diet which gets to be a problem if the diet is high in oxalates. The question then becomes, where is it going, and is it causing damage there. If you want to check out more about the low oxalate diet, please see www.lowoxalate.info. 1: Am J Kidney Dis. 2007 Jan;49(1):153-7. Acute oxalate nephropathy associated with orlistat, a gastrointestinal lipase inhibitor. Singh A, Sarkar SR, Gaber LW, Perazella MA. Department of Pathology, University of Tennessee Health Sciences Center, Memphis, TN, USA. Orlistat is an oral inhibitor of gastrointestinal lipase used for weight reduction in obese patients. Although most adverse drug effects manifest in the gastrointestinal tract, this is the first reported case of orlistat-induced acute kidney injury secondary to acute oxalate nephropathy in a white woman with underlying chronic kidney disease. Acute kidney injury was associated temporally with an increased dose of orlistat and the development of increased fat malabsorption (more frequent loose oily stools). Urine sediment showed abundant calcium oxalate crystals and increased 24-hour urine oxalate concentration. Kidney biopsy showed deposition of calcium oxalate crystals within tubular lumens, consistent with acute oxalate nephropathy. Orlistat therapy was discontinued, and oral fluid intake was increased. A second kidney biopsy performed 1 month later to evaluate the slow resolution of kidney failure did not show calcium oxalate crystals within tubules. A steady improvement in renal function subsequently was observed. Results of a repeated 24-hour urine oxalate collection performed 3 weeks later when kidney function had improved were within normal limits. Publication Types: Case Reports PMID: 17185156 [PubMed - indexed for MEDLINE] 2: Kidney Int. 2005 Sep;68(3):1244-9. Use of a probiotic to decrease enteric hyperoxaluria. Lieske JC, Goldfarb DS, De Simone C, Regnier C. Division of Nephrology and Hypertension, Mayo Clinic, Mayo Hyperoxaluria Center, and Mayo Complementary and Integrative Medicine Program, Rochester, Minnesota 55905, USA. Lieske.@... BACKGROUND: Patients with inflammatory bowel disease have a 10- to 100-fold increased risk of nephrolithiasis, with enteric hyperoxaluria being the major risk factor for these and other patients with fat malabsorptive states. Endogenous components of the intestinal microflora can potentially limit dietary oxalate absorption. METHODS: Ten patients were studied with chronic fat malabsorption, calcium oxalate stones, and hyperoxaluria thought to be caused by jejunoileal bypass (1) and Roux-en-Y gastric bypass surgery for obesity (4), dumping syndrome secondary to gastrectomy (2), celiac sprue (1), chronic pancreatitis (1), and ulcerative colitis in remission (1). For 3 months, patients received increasing doses of a lactic acid bacteria mixture (Oxadrop), VSL Pharmaceuticals), followed by a washout month. Twenty-four-hour urine collections were performed at baseline and after each month. RESULTS: Mean urinary oxalate excretion fell by 19% after 1 month (1 dose per day, P < 0.05), and oxalate excretion remained reduced by 24% during the second month (2 doses per day, P < 0.05). During the third month on 3 doses per day oxalate excretion increased slightly, so that the mean was close to the baseline established off treatment. Urinary oxalate again fell 20% from baseline during the washout period. Calcium oxalate supersaturation was reduced while on Oxadrop, largely due to the decrease in oxalate excretion, although mean changes did not reach statistical significance. CONCLUSION: Manipulation of gastrointestinal (GI) flora can influence urinary oxalate excretion to reduce urinary supersaturation levels. These changes could have a salutary effect on stone formation rates. Further studies will be needed to establish the optimal dosing regimen. Publication Types: Clinical Trial Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. PMID: 16105057 [PubMed - indexed for MEDLINE] 3: Kidney Int. 2004 Aug;66(2):676-82. Erratum in: Kidney Int. 2004 Sep;66(3):1304. Heiberg, Ita Pfeferman [corrected to Heilberg, Ita Pfeferman]. Fat malabsorption induced by gastrointestinal lipase inhibitor leads to an increase in urinary oxalate excretion. Ferraz RR, Tiselius HG, Heilberg IP. Nephrology Division, Universidade Federal de São o, UNIFESP, São o, Brazil. BACKGROUND: Unabsorbed fat and bile acids may react with calcium in the intestinal lumen, limiting the amount of free calcium binding with oxalate and thereby raising intestinal oxalate absorption leading to hyperoxaluria. The aim of the present study was to determine whether orlistat (Xenical), a gastrointestinal lipase inhibitor, might increase urinary oxalate in an experimental rat model. METHODS: Thirty-nine male adult Wistar rats were fed a standard diet alone (controls) or supplemented with either 2% sodium oxalate (NaOx) or 3.2 mL of soy oil, or with both (NaOx + soy oil) for 4 weeks (diet period). Orlistat (16 mg/day) was added to the diet from the 5th to the 8th week (diet + orlistat period). Urinary oxalate (uOx), calcium (uCa), magnesium (uMg), and citrate (uCit) were determined and the ion-activity product of calcium oxalate [AP (CaOx) index(rat)] was estimated. RESULTS: Compared to baseline uOx significantly increased after diet + orlistat in controls (0.64 +/- 0.1 mg/24 hours vs. 0.56 +/-0.1 mg/24 hours), soy oil (0.80 +/- 0.3 mg/24 hours vs. 0.49 +/-0.2 mg/24 hours), and NaOx (2.48 +/- 0.8 mg/24 hours vs. 0.57 +/- 0.2 mg/24 hours), but the most marked increase occurred in NaOx + soy oil (3.87 +/- 0.7 mg/24 hours vs. 0.47 +/- 0.1 mg/24 hours). All groups except controls presented a significant reduction in uCa and uMg. Orlistat induced a significant increase in AP (CaOx) index(rat) compared, respectively, to baseline and to the diet period in NaOx (4.52 +/- 2.34 mg/24 hours vs. 0.94 +/- 0.86 and 1.53 +/- 0.93 mg/24 hours) and NaOx + soy oil (6.49 +/- 4.03 mg/24 hours vs. 0.54 +/- 0.17 and 1.76 +/- 1.32 mg/24 hours). CONCLUSION: These data suggest that the use of lipase inhibitors, especially under a diet rich in oxalate alone or associated with fat, leads to a significant and marked increase in urinary oxalate and a slight reduction in uCa and uMg that, taken together, resulted in an increase in AP (CaOx) index(rat), elevating the risk of stone formation. Publication Types: Research Support, Non-U.S. Gov't PMID: 15253722 [PubMed - indexed for MEDLINE] 4: Am J Kidney Dis. 2003 Jan;41(1):230-7. Conjugated bile acid replacement therapy reduces urinary oxalate excretion in short bowel syndrome. Emmett M, Guirl MJ, Santa Ana CA, Porter JL, Neimark S, Hofmann AF, Fordtran JS. Department of Internal Medicine, Baylor University Medical Center, Dallas, TX 75246, USA. m.emmett@... BACKGROUND: Patients with short bowel syndrome (SBS) have steatorrhea, in part because of bile acid malabsorption that causes decreased bile acid secretion into the duodenum and consequent fat maldigestion. In SBS patients with colon in continuity, luminal calcium forms calcium fatty acid soaps rather than precipitating as insoluble calcium oxalate. Soluble oxalate is hyperabsorbed by the colon leading to hyperoxaluria and an increased risk for renal calcium oxalate stones and deposits. The authors hypothesized that oral ingestion of conjugated bile acids would increase fat absorption and thereby decrease calcium fatty acid soap formation and oxalate hyperabsorption. METHODS: The effect of conjugated bile acid replacement therapy (9 g/d) on fecal fat excretion and urine oxalate excretion was measured in an appropriate patient, utilizing the metabolic balance technique. The effects of chronic bile acid replacement therapy on oxalate excretion and nutritional status also were measured in a 3-month outpatient study. RESULTS: Natural conjugated bile acid replacement therapy reduced fecal fat excretion from 119 to 79 g/d (Delta40 g/d), and urinary oxalate excretion from 87 to 64 mg/d (966 to 710 micromol/d; Delta23 mg/d). Cholylsarcosine, a synthetic conjugated bile acid, had similar but less powerful effects. During a 3-month outpatient trial of natural conjugated bile acids (9 g/d), urine oxalate decreased to normal levels (27 mg/d) in association with weight gain, decreased hunger, and decreased hyperphagia. CONCLUSION: Conjugated bile acid replacement therapy reduced fecal fat excretion, reduced urinary oxalate excretion, and improved nutritional status in a patient with SBS with colon in continuity, hyperoxaluria, and oxalate nephrolithiasis. Copyright 2003 by the National Kidney Foundation, Inc. Publication Types: Case Reports Comparative Study Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. PMID: 12500242 [PubMed - indexed for MEDLINE] 5: J Int Med Res. 1989 Nov-Dec;17(6):526-31. Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption. Sangaletti O, Petrillo M, Bianchi Porro G. Gastro-intestinal Unit, L. Sacco Hospital, Milan, Italy. Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption. PMID: 2628129 [PubMed - indexed for MEDLINE] 6: Clin Chim Acta. 1984 Dec 29;144(2-3):155-61. Oxalate-loading tests to screen for steatorrhoea: an appraisal. PN, Will EJ, Kelleher J, Losowsky MS. We have evaluated two procedures as screening tests for steatorrhoea: firstly, a simplified, two-day, oxalate-loading test and secondly the rate of urinary oxalate excretion following a single oral dose of oxalate. Following two-day oxalate loading there was almost complete overlap of the values for 24-h urinary oxalate between 15 apparently healthy volunteers and 10 patients with steatorrhoea. The rate of oxalate excretion following a single dose of oxalate was increased in one patient with Crohn's disease and ileal resection who had normal faecal fat excretion, but three patients with steatorrhoea due to other causes had normal rates of excretion. We conclude that these oxalate-loading tests are not a useful alternative to faecal fat estimation in patients with suspected malabsorption. PMID: 6529853 [PubMed - indexed for MEDLINE] 7: Dig Dis Sci. 1982 May;27(5):401-5. Increased risk of nephrolithiasis in patients with steatorrhea. Dharmsathaphorn K, Freeman DH, Binder HJ, Dobbins JW. Patients with ileal disease have increased absorption of dietary oxalate, hyperoxaluria, and an increased incidence of nephrolithiasis. Patients with steatorrhea of varying etiologies also have hyperoxaluria. To determine whether steatorrhea per se is associated with nephrolithiasis, we reviewed the charts of all adult patients who had a 72-hr fecal fat analysis from 1968 to 1978. The 159 patients with steatorrhea were compared to 162 patients without steatorrhea. The two groups were comparable in age, sex, urine specific gravity, and serum uric acid and phosphorus; serum calcium was slightly less in the steatorrhea group (8.7 +/- 0.1 vs 9.0 +/- 0.1, P less than 0.02). Although 19 patients with steatorrhea had nephrolithiasis compared to 7 control patients (P = 0.01), 15 of these 19 patients had ileal disease and only 4 of the 118 patients with steatorrhea but without ileal disease had stones. Categorical data analysis revealed that steatorrhea, diarrhea (stool weight greater than 225 g/day), male sex, and ileal disease were significantly associated with nephrolithiasis with a relative risk of 3.0, 2.7, 3.1, and 8.0, respectively. When patients without ileal disease were analyzed separately, however, steatorrhea, diarrhea, and sex were no longer risk factors. In contrast, in patients with ileal disease the incidence of nephrolithiasis increased with the severity of steatorrhea. The relative risk of nephrolithiasis in male patients with ileal disease and fecal fat greater than 20 g/day was 26.3 (P less than 0.01). Thus, the presence of both ileal disease and steatorrhea greatly increases the risk of nephrolithiasis; however, neither steatorrhea alone nor ileal disease alone are risk factors for nephrolithiasis. Publication Types: Research Support, U.S. Gov't, P.H.S. PMID: 7075427 [PubMed - indexed for MEDLINE] 8: Urol Int. 1981;36(1):1-9. Hyperoxaluria in malabsorptive states. Andersson H, Bosaeus I. During the last 10 years it has become apparent that hyperoxaluria often is present in malabsorptive states. This secondary hyperoxaluria could be explained by an increased uptake of dietary oxalate due to malabsorption of fatty acids and bile salts. Dietary prescriptions, including a low fat diet is advocated in the treatment of hyperoxaluria in Crohn's disease or after small bowel resection. Publication Types: Review PMID: 7020204 [PubMed - indexed for MEDLINE] 9: Gut. 1979 Dec;20(12):1089-94. Oxalate loading test: a screening test for steatorrhoea. Rampton DS, Kasidas GP, Rose GA, Sarner M. To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4.44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0.33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19--186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0.25 mmol/24 h, range 0.08--0.59 mmol) (normal less than 0.20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0.91 mmol/24 h, range 0.46--1.44 mmol) (normal less than 0.44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r = 0.73, P less than 0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 5.8 +/- 0.99% (+/- 1 SD) in normal subjects and 14.7 +/- 6.0% (P less than 0.002) in patients with steatorrhoea. Measurement of urinary oxalate output during oral sodium oxalate loading appears to be a reliable and convenient screening test for steatorrhoea. PMID: 527884 [PubMed - indexed for MEDLINE] 10: Scand J Gastroenterol. 1978;13(5):577-88. Enteric hyperoxaluria: dependence on small intestinal resection, colectomy, and steatorrhoea in chronic inflammatory bowel disease. Hylander E, Jarnum S, Jensen HJ, Thale M. The importance of intestinal resection, exclusion of the colon, and steatorrhoea for secondary hyperoxaluria was studied in 81 patients with Crohn's disease and 12 patients with ileostomy after colectomy for ulcerative colitis during a metabolic regime including a fixed oral supply of fat, calcium, and oxalate. Hyperoxaluria (greater than 48 mg (greater than 0.5 mmol) per 24 h) was present in 21 patients with Crohn's disease. All but one half or more of the colon preserved. Renal oxalate excretion was related to the amount of ileum resected. 14C-oxalate absorption was significantly higher in patients with ileal resection and the whole colon preserved than in patients with ileal resection plus hemicolectomy, despite the fact that the latter group had the most extensive ileal resections. Faecal fat and oxalate excretion agreed well in patients without ileostomy (r = 0.76, p less than 0.001), and renal oxalate excretion was significantly higher in patients with steatorrhea and the colon preserved than in patients without steatorrhoea. In all 93 patients 14C-oxalate absorption and renal oxalate excretion was positively correlated with a coefficient of correlation of 0.76 (p less than 0.001). No correlation was present between 47Ca- and 14C-oxalate absorption. The study confirm that a preserved colon is necessary for secondary hyperoxaluria and stresses the importance of ileal resection and steatorrhoea. Publication Types: Comparative Study PMID: 705253 [PubMed - indexed for MEDLINE] 11: Scand J Gastroenterol. 1978;13(4):423-31. Standardized ( " trifixed " ) diet in the study of chronic malabsorption syndromes. Hylander E, Jarnum S, Keldsbo IL, Thale M. 143 patients (70 patients with Crohn's disease, 11 with ulcerative colitis, 40 with an intestinal by-pass operation, 9 with non-tropical sprue, 10 with short bowel syndrome, and 3 with other gastrointestinal disease) were studied during a metabolic regime including a fixed oral supply of 70 g fat, 800 mg calcium, and 200 mg oxalate. Faecal fat, 47Ca-absorption, 14C-oxalate absorption, and renal oxalate excretion were measured, and in the majority of patients a 14C-glyco-cholic acid breath test was also performed. 14Ca-absorption was practically identical (r = 0.92), whether determined by whole-body counting or from the accumulation of absorbed 47Ca in the skeleton of the underarm. 14C-oxalate absorption and renal oxalate excretion agreed well (r = 0.85). Steatorrhoea correlated weakly with renal oxalate excretion (r = 0.63, p less than 0.001), whereas no correlation was present between faecal fat and calcium absorption or between oxalate and calcium absorption under the constant conditions prevailing during the study. It is recommended that a " trifixed " regime with absorption studies of fat, calcium, and oxalate be undertaken previous to therapy that aims at a reduction of steatorrhoea or hyperoxaluria or an improvement of calcium absorption in chronic malabsorption syndromes, not least because therapy of these categories of patients most often continues for years. PMID: 675151 [PubMed - indexed for MEDLINE] 12: Am J Dig Dis. 1977 Oct;22(10):921-8. Hyperoxaluria and intestinal disease. The role of steatorrhea and dietary calcium in regulating intestinal oxalate absorption. Stauffer JQ. Hyperoxaluria was documented in patients with pancreatic insufficiency, adult celiac disease, regional enteritis after ileectomy and partial colectomy, and jejunoileal bypass. The degree of hyperoxaluria correlated directly with the severity of the steatorrhea and inversely with the dietary calcium content. High-calcium diets suppressed oxalate excretion to normal when fecal fat excretion was approximately 30 g/day or less. In patients with more severe steatorrhea, decreasing dietary fat and oxalate content further reduced urinary oxalate excretion. These data suggest that, while steatorrhea is the most important determinant for enhanced absorption of dietary oxalate, variations in dietary calcium content modulate the amount of oxalate absorbed. Publication Types: Comparative Study Research Support, U.S. Gov't, P.H.S. PMID: 920694 [PubMed - indexed for MEDLINE] 13: Lancet. 1977 Oct 1;2(8040):677-9. Urinary oxalate on a high-oxalate diet as a clinical test of malabsorption. Andersson H, Gillberg R. 100 g of spinach a day was added to the hospital diet of fifty-four patients with suspected malabsorption. Hyperoxaluria was found in thirty-eight patients; all of them had steatorrhoea. No patient with steatorrhoea had a urinary oxalate excretion of less than 40 mg a day. Ten other patients had hyperoxaluria, but the faecal fat determinations were regarded as unreliable in almost all and malabsorption could not be confirmed. It is suggested that in clinical practice determination of urinary oxalate after an oral load of oxalate could replace faecal fat determination in most patients with suspected malabsorption. Publication Types: Comparative Study PMID: 71494 [PubMed - indexed for MEDLINE] 14: Gut. 1977 Jul;18(7):561-6. Hyperoxaluria correlates with fat malabsorption in patients with sprue. Mc GB, Earnest DL, Admirand WH. The effect of fat malabsorption on the absorption and renal excretion of dietary oxalate was studied in four patients with sprue and in two patients with dermatitis herpetiformis and sprue-like jejunal histology. Hyperoxaluria was present in all patients with sprue when fat malabsorption was severe. Urinary oxalate excretion decreased in two of the three patients with coeliac sprue when their fat malabsorption had improved after three months of dietary gluten restriction. Neither patient with dermatitis herpetiformis and sprue had steatorrhoea. In these patients, urinary oxalate excretion was always within normal limits. A significant positive linear relationship (y=28.25 +4-84x; r=0-82; P less than 0-01) was demonstrated between faecal fat and urinary oxalate excretion. The results of this study support the concept that severe malabsorption of dietary fat plays a primary causative role in enteric hyperoxaluria. Publication Types: Research Support, U.S. Gov't, P.H.S. PMID: 873337 [PubMed - indexed for MEDLINE] At 05:01 AM 2/29/2008, you wrote: > asked: > > > > > Since my daughter's vitamin D level is so low (15) and some > > people link vitamin D deficiency to fibro, how many of you have had > > vitamin D measured, > > and if you did, and started supplementing high dose vitamin D (my > > daughter's doctor gave her 50,000 iu's a week), did the vitamin > > help or did it make you feel worse? The Marshall Protocol people > > make it sound like a bad idea, but in thinking about WHEN in the > > calendar my daughter does well, it is when she spends hours in the > > sun. > >I don't know what the Marshall Protocol is, but as a weight loss >surgery patient (I had a duodenal switch), my supplement needs are >different from the normal population. I take 15,000 iu of dry >Vitamin D per day. Dry is because with a DS, I don't absorb fats >normally. > >High doses of Vitamin D should be done under a doc's care and >according to labs. > >I don't really notice a difference, but then my level has never gone >super-low, and I maintain constant levels of supplementation with >yearly labs. But I've noticed that I do like to sit in my sunroom >during sunny days, and (since my new knees) I like to be outside on >sunny days, working in my yard. > > Z > > Quote Link to comment Share on other sites More sharing options...
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