Someone help

[Norman18]

I too, have pins and needles on scalp and arms and legs.......sooo tired and no energy and declining......blood test showed antithyroid peroxidase antibody is 24......normal <9. Gastric Parietal Cell Ab is 45.4.........normal is below 20.. My Dr. said weird symptoms.......been in hospital 4 times for vomiting....Dr. just said your immune system is attacking itself. Can anyone give me a suggestion what to do? My hemoglobin and hematicrit are high.

[JanD236]

Have you had your vitamin B12 level and intrinsic factor antibodies tested?

[Norman18 in reply to JanD236]

B12 is 380 and no intrinsic factor........2 years ago B 12 was 880.....

[JanD236 in reply to Norman18]

Your B12 is in range but has fallen dramatically and may warrant further investigation.

As would your thyroid in view of the antibodies. Have you had TSH, free T4 and free T3 tested? If so, it may be worth putting your results on the thyroid forum.

Symptoms from thyroid problems and B12 deficiency often overlap.

[Norman18 in reply to JanD236]

Thank you......no thyroid tests except TSH which is .9

[JanD236 in reply to Norman18]

Although TSH on its own is by no means a full snapshot of what’s happening with your thyroid, your TSH level appears to be in range.

So that leaves the vomiting and high haemoglobin and hematocrit. I’m sorry, I know nothing about these but I hope that your doctor is investigating if they are above range.

[martinec]

Have you been diagnosed with PA? I am guessing you also have autoimmune gastritis, if your parietal cell antibodies are so high. This would explain the vomiting. Also potentially Hashimoto's as one of the parietal cell antibodies disease cluster.

Is your iron/ferritin low? I was always very low but my haemoglobin would usually hover in range strangely.

The below prepared by functional nutritionist Lori Taylor may help you:

PART ONE: ABOUT PERNICIOUS ANEMIA AND AUTOIMMUNE GASTRITRIS

Pernicious anemia is a hematologic manifestation of chronic atrophic gastritis affecting the corpus of the stomach that denudes the gastric mucosa of gastric parietal cells. Asymptomatic autoimmune gastritis, a chronic inflammatory disease of the gastric mucosa, precedes the onset of corpus atrophy by 10–20 years. The gastritis arises from activation of pathologic Th1 CD4 T cells to gastric H/K ATPase that is normally resident on gastric mucosal secretory membranes. The onset of autoimmune gastritis is marked by circulating parietal cell antibody to gastric H/K ATPase. Gastric parietal cells produce two essential biologics: intrinsic factor and HCl acid. Pernicious anemia is a consequence of intrinsic factor loss and neutralizing intrinsic factor antibody that impairs cobalamin absorption. Acid loss leads to iron deficiency anemia that precedes cobalamin-deficient pernicious anemia by 20 years. Laboratory diagnosis rests on parietal cell antibody with or without intrinsic factor antibody, cobalamin-deficient megaloblastic anemia and elevated serum gastrin from loss of acid secretion. Autoimmune gastritis is associated with autoimmune thyroiditis and type 1 diabetes mellitus.

PREVALENCE/COMORBIDITIES

•AIG is the second most common autoimmune disease, found in 4.3% of outpatient gastroenterology patients. (Miceli, 2012).

•7.8-19.5% of the population has antibodies. (Toh, 2014).

•For reference, the prevalence of autoimmune thyroiditis is 5% and celiac disease 0.5-1%.

•AIG is an unrecognized cause of refractory iron deficiency and rarely screened for. AIG is 4-6 times more likely to cause iron deficiency than celiac. (Hershko, 2007).

•Comorbitidies: autoimmune disorders such as Hashimoto’s thyroiditis, rheumatoid arthritis, Grave's disease, celiac disease, type 1 diabetes vitiligo and psoriasis. AIG is found in up to 35% of patients with autoimmune thyroiditis. (Kulnigg-Dabsch, 2016).

•AIG is heritable and is the cause of pernicious anemia, which has a prevalence of 0.1% and 2% in age 60 or older.

MECHANISM

•AIG is characterized by atrophy of the corpal and fundal areas of the stomach.

•AIG results from an autoimmune attack against the H+/K+ ATPase of the gastric parietal cells.

•Parietal cells produce intrinsic factor for vitamin B12 absorption as well as hydrochloric acid for digestion.

•The loss of HCl and intrinsic factor lead to hypochlorhydria, iron and B12 deficiency.

PRESENTATION

First symptoms are often digestive:

•Functional dyspepsia and/or GERD

•SIBO/IBS that does not respond consistently to diet therapy

Other classic symptoms:

•Refractory iron deficiency, especially in premenopausal women

•Signs and symptoms of B12 deficiency (even if B12 and methylmalonic acid levels are normal)

•Anemia may not be present.

•Iron deficiency symptoms often appear first.

•Megaloblastic anemia is an end-stage symptom

• Normal tissue vs. atrophic gastritis

•Consider AIG with Comorbid autoimmunity (thyroid, T1DM, celiac, RA, Graves, vitiligo)

•Gastroparesis

•Global changes in neurological and/or digestive function

•GI intolerance to gentle and appropriate iron supplementation

•Hypothyroid symptoms with normal thyroid panel and negative antibodies

•Peripheral neuropathy

•Pancreatic insufficiency

•Restless legs syndrome

•Unexplained iron deficiency or iron deficiency symptoms (hair loss, fatigue, cold intolerance)

•Vitamin B12 levels < 500 pg/ml

HYPOCHLORHYDRIA IN AIG

Increased gastric pH causes reduction in:

•Activation of pepsin from pepsinogen

•Release of iron from protein

•Release of B12 from food

Resulting in:

•Dyspepsia (50-60% of patients)

•GERD

•Delayed gastric emptying

•Early satiety

•Poor iron absorption - 43% reduction in non-heme iron absorption. (Ferric iron precipitates at pH >3)

•Bacterial overgrowth (SI and gastric)

•Elevated gastrin levels and 3x greater risk of gastric cancers (carcinoid and adenocarcinoma)

•Increased need for thyroid hormone dosage in hypothyroidism

Posited:

Food sensitivity/intolerance

Gastroparesis

Maldigestion of proteins

Neutralization of ascorbic acid (demonstrated in vitro)

Poor pancreatic response to gastric contents in duodenum

DIAGNOSIS

•Blood test for anti-parietal cell antibodies (APCA) and anti-intrinsic factor antibodies (AIFA).

•Note that AIFA can interfere with measurement of B12 levels, giving a false normal B12 in the context of AIG. (Scarpa, 2013).

•Test for Helicobacter pylori stool antigen to rule out infective cause of atrophic gastritis.

•If positive for AIG, referral to gastroenterology for confirmation by upper endoscopy (EGD) with antral and fundal biopsies to assess level of atrophy. EGD should also biopsy for stomach cancer, due to increased risk of intestinal metaplasia.

•Gastrin levels should also be measured. Gastrin levels rise in response to lack of acid and can promote stomach cancer.

•50% of patients with gastric carcinoid tumors have pernicious anemia.

•Follow-up with blood work for autoimmune thyroiditis, which occurs in up to 35% of AIG patients.

•May want to test for other autoimmune disorders.

TREATMENT AND QUESTIONS

•Replacement of vitamin B12 by 1000 mcg intramuscular injection at intervals that relieve symptoms of B12 deficiency. (3-14 days per patient reports).

•B12 does not need to be methylated. (Obeid et. al., 2015).

•Sublingual supplementation of 1000 mcg daily may be sufficient, but may not result in rapid neurological symptom resolution.

•Repletion of stomach acid by use of betaine hydrochloride (BHCl), with progressive use of capsules taken with each meal.

•650-750 mg capsules, 2 or more per meal; titrate to GI comfort/outcome

•BHCl can decrease stomach pH to <3 in an average of 6 minutes, with a rebound time of just over 1 hour. (Yago et. al., 2013).

•The addition of pepsin may not be necessary as sufficient acid will activate it from pepsinogen.

•Iron therapy may not be needed once acid is corrected. Patients are often refractory to oral supplementation.

•Proton-pump inhibitors (PPIs) are often prescribed by gastroenterologists but are entirely contraindicated as they worsen effects of hypochlorhydria.

•Deglycyrrhyzinated licorice (DGL) powder may be useful in calming gastritis if patient experiences irritation. 1/8 tsp in 1C water AC and HS

•Other demulcents (aloe vera, marshmallow, slippery elm) may also have utility,

•Diet: Acid supplementation should correct digestive and absorptive issues

•Some are helped by plant-based or lower animal protein if gastric atrophy is wide-spread.

•Preserve barrier function with autoimmune diet customized to patient. Autoimmune paleo may not be appropriate due to difficulty digesting proteins.

[Norman18 in reply to martinec]

thank you sooo much.....they did the gastric antibody and the antithyroid peroxidase antibody and that was it......been in hospital 4 times for this and everything is normal. They have offered no suggestions, but to live with this.........your reply has given me direction,if these Dr. will consent to do some investigating.......I am so desperate. Living in the central valley of California, doesnt leave many options. The only help I get is not eating or drinking any fluid......feel like I am dying inside. Thank you for this answer.

[Sita505USA in reply to martinec]

Martinec

I want to copy the above wonderful informative post. I cannot copy from the HU site, or even when I email the post to myself.

Can you somehow send me the content directly via email?

I can send you my email if you can PM me. Thanks so very much! SitaUSA