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==Overview==
==Overview==

Revision as of 12:40, 20 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: "sandbox:SN"

Template:Pernicious Anemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief:

Overview

Pernicious anemia (also called Addison's anemia) is a type of red blood cell disorder caused by impaired vitamin B12 metabolism. Vitamin B12 is primarily absorbed by the small intestine, after being bound to intrinsic factor secreted by parietal cells of gastric mucosa. When this process is disrupted by conditions like atrophic gastritis, celiac disease, small bowel resection etc, B12 deficiency ensues.

Historical perspective

  • Pernicious anemia was first discovered by Thomas Addison, hence it is also known as addison's anemia.
  • Loss of life from large volume blood loss in the people fighting in the first world war inspired George Whipple to investigate blood forming components such as arsenic, iron pills etc, but found liver to be the most effective. He bled dogs until they had clinical anemia and fed them cooked liver which showed an improvement in symptoms and hematopoeisis. [1]
  • In 1948, Smith, Rickles et al., isolated the anti-pernicious factor from liver extract and named it Vitamin B12. They showed that even small amounts of this factor can be used to treat and to prevent pernicious anemia. [2]

Pathophysiology

Vitamin B12 is an essential vitamin for humans and animals because we cannot synthesise it on our own. B12 is a cofactor in DNA synthesis and other important biochemical reactions. Vitamin B12 deficiency manifests as anemia because hematopoetic stem cells in the bone marrow which are rapidly dividing need B12 for division and DNA production. This process is impaired leading to ineffective hematopoeisis. Vitamin B12 is also necessary for production of myelin which is an important component in the covering sheath of nerves. Deficiency results in improper nerve conduction due to nerve destabilisation. [3]

Physiology

  • Vitamin B12 is also called cobalamin because it contains cobalt at the core of its structure. Dietary sources of vitamin B12 include meat, fish and eggs.[4]
  • When consumed through its dietary source, B12 is bound to protein till it enters the stomach.
  • In the stomach, B12 is uncoupled from its carrier protein due to the presence of gastric acid, which is why vitamin B12 deficiency is so commonly seen among those on chronic antacid medication. [5]
  • Once in the stomach, it is then bound to gastric R binder, a glycoprotein secreted by the salivary glands till it reaches the duodenum.[6]
  • In the duodenum and jejunum, the pancreatic enzymes digest the gastric R binder and cobalamin is bound to intrinsic factor (IF).
  • Intrinsic factor is secreted by the gastric parietal cells. Once bound to IF, vitamin B12 travels up to the ileum where IF is removed and B12 binds with carrier proteins called transcobalamins and this complex is taken up by the liver and bone marrow, among other tissues.
  • Inside the cells, the transcobalamin-B12 complex is dissolved and cobalamin is reduced to methylcobalamin which serves as a cofactor and coenzyme in many important biochemical reactions[7].

The two major reactions involving B12 in the human body are:

  • Vitamin B12 in the from of cyanocobalamin is required in the synthesis of methionine. Methionine is produced from homocysteine and is catalysed by the enzyme methionine synthase. This enzyme utilises cyanocobalamin as a cofactor. Deficiency of vitamin B12 causes a decreased production of methionine and buildup of homocysteine. Hyperhomocysteinemia is implicated as a risk factor in cardiovascular disease.[8]
  • The Kreb's cycle utilises vitamin B12 in the reaction converting methylmalonyl-CoA to succinyl-CoA. Thus vitamin B12 deficiency causes a buildup of methylmalonic acid, the substrate for the enzyme methylmalonyl coenzyme A mutase. Methylmalonic acid levels are elevated in the urine of people affected with pernicious anemia and other forms of B12 deficiency.

Storage

The human body can store anywhere from 2-5mg of vitamin B12. Most of this is stored in the liver and is recycled via enterohepatic circulation.

Pathogenesis

Pernicious anemia is a type of megaloblastic anemia caused due to improper vitamin B12 absorption by the body. Impaired absorption occurs because of deficiency of intrinsic factor which is produced by the parietal cells of the stomach. The etiology of pernicious anemia can be due to autoimmune causes or genetic disease. In autoimmune disease, the antibodies attack most of the gastric mucosa, but the antrum is spared.

Autoimmune causes of pernicious anemia

This is the most common cause of pernicious anemia. In autoimmune pernicious anemia, the body produces antibodies against parietal cells or intrinsic factor.

  • Antibodies against parietal cells of the gastric mucosa work to inhibit the H+/K(+)-ATPase which is the proton pump present in the parietal cells. The proton pump serves as an auto antigen and activates the cytotoxic CD4+ T cells which proceed to destroy gastric mucosal cells.[9][10]
  • Intrinsic factor antibodies are present in fewer cases of pernicious anaemia but are highly specific. There are 2 types of IF antibodies. They prevent the binding and absorption of cobalamin in the ileum via its receptor.[11]

Clinical features

  • The symptoms of pernicious anemia take months, and often years to manifest. Patients most commonly present with symptoms of anemia like lightheadedness, dizziness, shortness of breath etc. The population affected with pernicious anemia is usually the elderly (>60 years) owing to its insidious onset.
  • Pernicious anemia has hematological, gastrointestinal and neurological manifestations.
  • Hematological signs are the earliest manifestation of the disease while neurological signs are seen much later.
  • Patients with pernicious anemia usually have very low levels of hydrochloric acid in the stomach (achlorhydria) and high levels on gastrin (hypergastrinemia).

Differentiating pernicious anemia from other diseases

Pernicious anemia shares many similarities with other forms of megaloblastic anemia like B12 and folate deficiency.

  • Vitamin B12 deficiency due to insufficient intake (eg veganism) has all the features of pernicious anemia like megaloblasts, hypersegmented neutrophils, neuropsychiatric manifestations. But atrophic gastritis is absent, so achlorhydria, parietal cell antibodies or IF antibodies are absent. Intrinsic factor levels are also normal.[6]
  • Folic acid deficiency also results in megaloblastic anemia and similar hematological changes as pernicious anemia, but urinary excretion of methylmalonic acid is absent, so are features of pernicious anemia like achlorhydria, antibodies and normal IF levels.
  • Ileal resection causes B12 deficiency due to decreased absorption.
  • Certain drugs such as methotrexate, azathioprine cause folate deficiency and result in megaloblastic anemia. This is usually seen in patients taking chemotherapy or other chronic conditions such as rheumatoid arthritis. [12]
  • Chronic proton pump inhibitor therapy also results in B12 deficiency as vitamin B12 cannot dissociate from its carrier protein in the absence of an acidic environment.[13]
  • Long term use of metformin, such as in diabetics, is linked to vitamin B12 deficiency and symptoms similar to pernicious anemia, but this can be differentiated from pernicious anemia as it is seen in diabetics on chronic therapy.[14]

Associated Conditions

People affected with pernicious anemia might have other coexisting autoimmune conditions such as autoimmune thyroiditis, autoimmune diabetes, vitiligo etc. Autoimmune thyroiditis is most commonly seen in patients with pernicious anemia, particularly females. HLA DR3 has been implicated in the development of autoimmune diseases such as pernicious anemia[15].

Epidemiology and demographics

  • Pernicious anemia is a disease of the elderly. The mean age of patients who are symptomatic is >60.[16]
  • An exception is the genetic form of the disease which is a congenital deficiency of intrinsic factor and is seen in children <10 years of age.
  • Men and women are equally affected
  • Prevalence of pernicious anemia is estimated at 0.1% of the population.[17]

Genetics

  • Some forms of pernicious anemia are congenital and a genetic link has been postulated because of a higher incidence in certain populations.
  • Affected people have a complete or near total absence of intrinsic factor and the presence of antibodies against intrinsic factor.
  • The genetic variant is transmitted through an autosomal recessive pattern.[18]

Risk factors

  • People who have autoimmune conditions like diabetes mellitus, autoimmune thyroiditis are at higher risk of developing pernicious anemia.

Natural History, Complications and Prognosis

  • In most cases, patients affected with pernicious anemia remain asymptomatic for many years.
  • Early manifestations include fatigue, shortness of breath, pallor and weakness.
  • Long standing untreated pernicious anemia results in irreversible neurological damage such as subacute combined degeneration of the spinal cord.
  • Neurological changes are irreversible once they set in and do not resolve with cobalamin supplementation.

Diagnosis

A diagnosis of pernicious anemia is made by a history and physical examination, along with hematological and neurological examination.

Diagnostic criteria

  • The only specific criteria to diagnose pernicious anemia is an intrinsic factor output of less than 200U/h after pentagastrin stimulation, where normal levels would be >2000U/h. [19]

Symptoms

Symptoms of pernicious anemia are summarised below

Hematological symptoms Gastrointestinal symptoms Neurological symptoms
Fatigue Loss of appetite Parasthesias
Weakness Weight loss


Depression
Shortness of breath Nausea Gait problems
Dizziness Burning sensation on tongue Weakness
Tachycardia Diarrhea Loss of balance
Lightheadedness Vomiting Confusion

Physical examination findings

Most important physical examination findings are the neurological findings of long standing B12 deficiency which leads to subacute combined degeneration of the spinal cord.

  • Hematological signs include pallor and icterus.[20]
  • Neurological signs: Vitamin B12 deficiency causes nerve demyelination. B12 deficiency also causes a buildup of methylmalonic acid which is toxic to neuronal cells and causes apoptosis.[21].

The main neurological manifestation of pernicious anemia and vitamin B12 deficiency is subacute combined degeneration. The posterior and lateral columns of the spinal cord are affected. Lateral column demyelination manifests as hyperreflexia and spasticity, while posterior column defects are loss of proprioception and vibration sense. Ataxia and loss of tandem gait are also manifestations of posterior column demyelination. Recreational or accidental inhalation of nitrous oxide gas (laughing gas) can precipitate subacute combined degeneration in people with low levels of vitamin B12.[22]

  • Gastrointestinal signs: Upto 25% of people affected with pernicious anemia develop glossitis. The tongue appears red, "beefy" and smooth due to atrophy and blunting of the lingual papillae.[23]

Subacute combined degeneration


Laboratory findings

  • The first step in diagnosis is a blood vitamin B12 level. Blood levels less than 200 pg/ml are seen in pernicious anemia.
  • Intrinsic factor antibodies and Parietal cell antibodies.
  • Low intrinsic factor level.[24]
  • Gastric mucosal sampling shows parietal cell atrophy with antral sparing.[25]
  • Increased level of gastrin.
  • Increased levels of homocysteine and methylmalonyl-CoA.
  • Decreased folate levels are seen due to "folate trapping" in the form of methyltetrahydrofolate.

Shilling Test

The Shilling test is no longer done to detect an IF deficiency but has historical importance. After a vitamin B12 deficiency is noted, the patient is given radioactively tagged cobalamin to take orally. Soon after this step, the patient is injected with unlabelled cobalamin intramuscularly. Urine is checked for radioactive cobalamin for the next 24 hours. In pernicious anemia, there is an intrinsic factor deficiency, therefore the orally consumed radioactive cobalamin will not be absorbed and can be detected in the urine. In the next step, the patient is given radioactive cobalamin along with intrinsic factor and their urine is checked for traces of radioactive cobalamin. Absence of radioactive cobalamin in the urine points to the deficiency of intrinsic factor in the patients stomach which is the cause of vitamin B12 deficiency[26]. If the cobalamin absorption does not increase even with intrinsic factor supplementation, patient can be given a course of antibiotics as bacterial overgrowth may hinder absorption.

Peripheral smear findings

  1. The most obvious peripheral smear finding is megaloblasts and macrocytes.

Megaloblastic anemia results due to the lagging behind of nuclear development when compared to cytoplasmic development. This is known as nuclear-cytoplasmic asynchrony. Such defective cells are destroyed in the bone marrow (intramedullary hemolysis).

  1. Decreased number of RBCs (erythopenia)
  2. Macrocytosis- the RBCs in pernicious anemia are very large. Macrocytosis is defined as cells that have an MCV >100 femtolitres (normal :80-100fL)
  3. Hypersegmented neutrophils : Neutrophils containing ≥ 6 lobes. [27]
  4. Poikilocytosis and anisocytosis
  5. Low reticulocyte count (reticulopenia)
  6. Howell-Jolly bodies
  • Atrophic gastritis

    Atrophic gastritis

  • Hypersegmented neutrophil

    Hypersegmented neutrophil


Treatment

  • Standard treatment for pernicious anemia is replacement of cobalamin via intramuscular injection. [28]
  • 1000 mcg IM everyday for one week, followed by weekly injections the next month and then monthly once injections.
  • Response to treatment is measured by an increase in reticulocyte count within 5 days of starting therapy.
  • Patient also experience a sense of wellbeing shortly after beginning therapy.
  • If reticulocytosis is not observed within the first week of therapy, other factors such as hypothyroidism, folate deficiency should be considered.
  • Intramuscular therapy can be replaced by high dose oral therapy.[17]
  • Neurological disease always warrants parenteral treatment.
  • Within the first 3-4 weeks of treatment, marrow changes revert and there is resolution in macrocytosis.
  • Most patients require lifelong monthly therapy.
  • Routine follow up should be done with a CBC every few months.
  • A small percentage of patients develop gastric carcinoma, particularly in the elderly. Regular surveillance helps in early detection and treatment. [29]

Prevention

  • There is no primary preventive measure for pernicious anemia.
  • Once sucessfully diagnosed and treated, patients with pernicious anemia are followed up every year for development of stomach cancer[30], or symptoms of anemia.

References

Overview

Primary hyperhidrosis is the condition characterized by abnormally increased perspiration, in excess of that required for regulation of body temperature. There is controversy regarding the definition of hyperhidrosis, because any sweat that drips off of the body is in excess of that required for thermoregulation. Almost all people will drip sweat off of the body during heavy exercise.

Classification

  • Primary hyperhidrosis must be distinguished from secondary hyperhidrosis, which can start at any point in life. For some, it can seem to come on unexpectedly. The latter form may be due to a disorder of the thyroid or pituitary gland, diabetes mellitus, tumors, gout, menopause, certain drugs, or mercury poisoning[31]. Such secondary forms may have more serious consequences than just hyperhidrosis, making medical consultation advisable.
  • Hyperhidrosis can also be classified as focal or generalised.
  • Focal hyperhidrosis is most commonly seen during emotional outbursts like sweating of palms, axillae, face etc. Generalised hyperhidrosis affects the entire body and can be triggered by emotion or exertion/heat for thermoregulation.

Pathophysiology

  • Primary hyperhidrosis affects about 0.6-0.1% of the general population.
  • Onset of symptoms occurs during puberty, seen as excess sweating of face, palms, soles and axillae, and symptoms usually resolve with age. [32]

Physiology

  • Sweat is a hypotonic solution produced by eccrine glands and apocrine glands which are distributed all over the body.
  • Most of the body's sweat is produced by the eccrine glands. Eccrine glands have the highest concentration in the axillae. These glands play an important role in thermoregulation. [33]
  • Apocrine sweat glands are seen in the axillae and urogenital region. [34]
  • Sweating is caused by two broad impulses- thermoregulation and emotion. The thermoregulatory centre of sweating is located in the hypothalamus and is triggered by increased body temperature (eg., fever) and the emotion centre of sweating is located in the limbic system and is triggered by extreme emotional states like anxiety, fear etc.[35]

Pathology

  • It is not known what causes primary hyperhidrosis. One theory is that hyperhidrosis results from an overactive sympathetic nervous system, but this hyperactivity may in turn be caused by abnormal brain function. [36]
  • Some patients afflicted with the condition experience a certain degree of reduction in their quality of life, depending on how severe their condition is. [37]
  • Sufferers feel at a loss of control because perspiration takes place independent of temperature and emotional state. However, anxiety can exacerbate the situation for many sufferers. A common complaint of patients is that they get nervous because they sweat, then sweat more because they are nervous.
  • Other factors can play a role; certain foods & drinks, nicotine[38], caffeine, and smells can trigger a response (see also diaphoresis).
  • Primary focal hyperhidrosis is the most common type and is seen during puberty in the axillae and face. [39]
  • Secondary focal hyperhidrosis is a disorder of defective thermoregulation and is seen in neuropathy affecting peripheral nerves like diabetic neuropathy[40], spinal cord disease[41] etc.
  • Generalised primary and secondary hyperhidrosis involve the whole body. Secondary general hyperhidrosis is seen in disorders of thermoregulation like fever, hyperthyroidism etc. [42]
  • Some forms of primary Hyperhidrosis are genetically transmitted in either autosomal dominant or recessive pattern.[43]

Causes

Primary focal hyperhidrosis Secondary focal hyperhidrosis Secondary general hyperhidrosis
Puberty Neuropathy Thyrotoxicosis
Social stress Complex regional pain syndrome[47]

Diagnosis

History and Symptoms

  • Hyperhidrosis can either be generalized or localized to specific parts of the body.
  • Hands, feet, axillae, and the groin area are among the most active regions of perspiration due to the relatively high concentration of sweat glands; however, any part of the body may be affected.
  • Patients often feel embarrassed in social situations because situations like shaking hands is difficult for people with sweaty palms.
  • Patients also reports a degree of disability in writing or holding objects.

The following are diagnostic tools used to diagnose hyperhidrosis.

  • Iodine starch test is the most common initial diagnostic tool used to diagnose hyperhidrosis. To perform the test, iodine is applied to the affected skin and starch powder is applied over it. If there is sweat on the skin, the starch and iodine react and a violet colour is seen. This test is helpful to identify focal hyperhidrosis. [48]
  • The amount of sweat can be quantified by using quantitative sudometry. This test stimulates sweat production with acetylcholine electrophoresis. The sweat produced is detected by passing dehumidified nitrogen gas over the required area of skin enclosed in a chamber. The humidity and perspiration is then plotted on a chart and compared.[49]
  • Gravimetry is another method to diagnose hyperhidrosis. Filter paper is applied over affected areas (palms, soles, axillae) and after a defined period of time weight of filter paper before and after is measured[50]. Hyperhidrosis is diagnosed as axillary sweating of >136 mg/min/m2, palmar sweating sweating of >50 mg/min/m2.

Differential diagnosis

  • Diabetic hypoglycaemia
  • Thyrotoxicosis
  • Hyperpyrexia
  • Pheochromocytoma
  • Hot flushes in menopause [51]
  • Cholinergic medication[52]
  • Tricyclic antidepressant use
  • Eccrine angiomatous hamartoma [53]
  • Frey syndrome[54]

Treatment

  • Hyperhidrosis can usually be very effectively controlled, but there is no known permanent cure because little is known about the cause behind excessive sweating.
  • Treatment for hyperhidrosis consists of local therapies, surgical options and pharmacological therapy.

Medical Therapy

Local therapy options

  • Over the counter antiperspirants containing aluminium chloride. [55]
  • Botulinum injections. Botulinum toxin type A has been shown to be effective in treating plantar hyperhidrosis. [56]
  • Microwave ablation has been shown to have longer lasting antiperspirant effect in axillary focal hyperhidrosis. [57]
  • Tap water iontophersis is used for palmar and plantar hyperhidrosis.[58]
  • Gustatory hyperhidrosis is treated with glycopyrrolate.[59]

Pharmacological therapy options

Surgical therapy

References

  1. ↑ Sinclair L (2008). "Recognizing, treating and understanding pernicious anaemia". J R Soc Med. 101 (5): 262–4. doi:10.1258/jrsm.2008.081006. PMC 2376267. PMID 18463283.
  2. ↑ SMITH EL (1948). "Purification of anti-pernicious anaemia factors from liver". Nature. 161 (4095): 638. doi:10.1038/161638a0. PMID 18856623.
  3. ↑ Miles LM, Allen E, Clarke R, Mills K, Uauy R, Dangour AD (2017). "Impact of baseline vitamin B12 status on the effect of vitamin B12 supplementation on neurologic function in older people: secondary analysis of data from the OPEN randomised controlled trial". Eur J Clin Nutr. 71 (10): 1166–1172. doi:10.1038/ejcn.2017.7. PMID 28225050.
  4. ↑ Watanabe F (2007). "Vitamin B12 sources and bioavailability". Exp Biol Med (Maywood). 232 (10): 1266–74. doi:10.3181/0703-MR-67. PMID 17959839.
  5. ↑ Jung SB, Nagaraja V, Kapur A, Eslick GD (2015). "Association between vitamin B12 deficiency and long-term use of acid-lowering agents: a systematic review and meta-analysis". Intern Med J. 45 (4): 409–16. doi:10.1111/imj.12697. PMID 25583062.
  6. ↑ 6.0 6.1 Del Corral A, Carmel R (1990). "Transfer of cobalamin from the cobalamin-binding protein of egg yolk to R binder of human saliva and gastric juice". Gastroenterology. 98 (6): 1460–6. doi:10.1016/0016-5085(90)91076-i. PMID 2110915.
  7. ↑ Harrington DJ (2017). "Laboratory assessment of vitamin B12 status". J Clin Pathol. 70 (2): 168–173. doi:10.1136/jclinpath-2015-203502. PMID 27169753.
  8. ↑ Tinelli C, Di Pino A, Ficulle E, Marcelli S, Feligioni M (2019). "Hyperhomocysteinemia as a Risk Factor and Potential Nutraceutical Target for Certain Pathologies". Front Nutr. 6: 49. doi:10.3389/fnut.2019.00049. PMC 6491750. PMID 31069230.
  9. ↑ Callaghan JM, Khan MA, Alderuccio F, van Driel IR, Gleeson PA, Toh BH (1993). "Alpha and beta subunits of the gastric H+/K(+)-ATPase are concordantly targeted by parietal cell autoantibodies associated with autoimmune gastritis". Autoimmunity. 16 (4): 289–95. doi:10.3109/08916939309014648. PMID 7517707.
  10. ↑ Toh BH, Sentry JW, Alderuccio F (2000). "The causative H+/K+ ATPase antigen in the pathogenesis of autoimmune gastritis". Immunol Today. 21 (7): 348–54. doi:10.1016/s0167-5699(00)01653-4. PMID 10871877.
  11. ↑ Schade SG, Abels J, Schilling RF (1967). "Studies on antibody to intrinsic factor". J Clin Invest. 46 (4): 615–20. doi:10.1172/JCI105563. PMC 442045. PMID 6021209.
  12. ↑ Green R, Datta Mitra A (2017). "Megaloblastic Anemias: Nutritional and Other Causes". Med Clin North Am. 101 (2): 297–317. doi:10.1016/j.mcna.2016.09.013. PMID 28189172.
  13. ↑ Heidelbaugh JJ (2013). "Proton pump inhibitors and risk of vitamin and mineral deficiency: evidence and clinical implications". Ther Adv Drug Saf. 4 (3): 125–33. doi:10.1177/2042098613482484. PMC 4110863. PMID 25083257.
  14. ↑ Aroda VR, Edelstein SL, Goldberg RB, Knowler WC, Marcovina SM, Orchard TJ; et al. (2016). "Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study". J Clin Endocrinol Metab. 101 (4): 1754–61. doi:10.1210/jc.2015-3754. PMC 4880159. PMID 26900641.
  15. ↑ Zulfiqar AA, Andres E (2017). "Association pernicious anemia and autoimmune polyendocrinopathy: a retrospective study". J Med Life. 10 (4): 250–253. PMC 5771255. PMID 29362601.
  16. ↑ Carmel R (1996). "Prevalence of undiagnosed pernicious anemia in the elderly". Arch Intern Med. 156 (10): 1097–100. PMID 8638997.
  17. ↑ 17.0 17.1 Andres E, Serraj K (2012). "Optimal management of pernicious anemia". J Blood Med. 3: 97–103. doi:10.2147/JBM.S25620. PMC 3441227. PMID 23028239.
  18. ↑ Gordon MM, Brada N, Remacha A, Badell I, del Río E, Baiget M; et al. (2004). "A genetic polymorphism in the coding region of the gastric intrinsic factor gene (GIF) is associated with congenital intrinsic factor deficiency". Hum Mutat. 23 (1): 85–91. doi:10.1002/humu.10297. PMID 14695536.
  19. ↑ Cattan D (2011). "Pernicious anemia: what are the actual diagnosis criteria?". World J Gastroenterol. 17 (4): 543–4. doi:10.3748/wjg.v17.i4.543. PMC 3027024. PMID 21274387.
  20. ↑ Seynabou F, Fatou Samba Diago N, Oulimata Diop D, Abibatou Fall S, Nafissatou D (2016). "Biermer anemia: Hematologic characteristics of 66 patients in a Clinical Hematology Unit at Senegal". Med Sante Trop. 26 (4): 402–407. doi:10.1684/mst.2016.0625. PMID 28073728.
  21. ↑ Han L, Wu S, Han F, Gu X (2015). "Insights into the molecular mechanisms of methylmalonic acidemia using microarray technology". Int J Clin Exp Med. 8 (6): 8866–79. PMC 4538064. PMID https://www.ncbi.nlm.nih.gov/pubmed/26309541 Check |pmid= value (help).
  22. ↑ Choi C, Kim T, Park KD, Lim OK, Lee JK (2019). "Subacute Combined Degeneration Caused by Nitrous Oxide Intoxication: A Report of Two Cases". Ann Rehabil Med. 43 (4): 530–534. doi:10.5535/arm.2019.43.4.530. PMC 6734019 Check |pmc= value (help). PMID 31499607.
  23. ↑ Stoopler ET, Kuperstein AS (2013). "Glossitis secondary to vitamin B12 deficiency anemia". CMAJ. 185 (12): E582. doi:10.1503/cmaj.120970. PMC 3761039. PMID 23359038.
  24. ↑ Lahner E, Annibale B (2009). "Pernicious anemia: new insights from a gastroenterological point of view". World J Gastroenterol. 15 (41): 5121–8. doi:10.3748/wjg.15.5121. PMC 2773890. PMID 19891010.
  25. ↑ Korman MG, Strickland RG, Hansky J (1972). "The functional 'G' cell mass in atrophic gastritis". Gut. 13 (5): 349–51. doi:10.1136/gut.13.5.349. PMC 1412218. PMID 5036089.
  26. ↑ "StatPearls". 2020. PMID 29939561.
  27. ↑ Farrelly SJ, O'Connor KA (2017). "Hypersegmented neutrophils and oval macrocytes in the setting of B12 deficiency and pancytopaenia". BMJ Case Rep. 2017. doi:10.1136/bcr-2016-218508. PMC 5612428. PMID 28821482.
  28. ↑ Annibale B, Lahner E, Fave GD (2011). "Diagnosis and management of pernicious anemia". Curr Gastroenterol Rep. 13 (6): 518–24. doi:10.1007/s11894-011-0225-5. PMID 21947876.
  29. ↑ Murphy G, Dawsey SM, Engels EA, Ricker W, Parsons R, Etemadi A; et al. (2015). "Cancer Risk After Pernicious Anemia in the US Elderly Population". Clin Gastroenterol Hepatol. 13 (13): 2282-9.e1-4. doi:10.1016/j.cgh.2015.05.040. PMC 4655146. PMID 26079040.
  30. ↑ Venerito M, Link A, Rokkas T, Malfertheiner P (2016). "Gastric cancer - clinical and epidemiological aspects". Helicobacter. 21 Suppl 1: 39–44. doi:10.1111/hel.12339. PMID 27531538.
  31. ↑ Schlereth T, Dieterich M, Birklein F (2009). "Hyperhidrosis--causes and treatment of enhanced sweating". Dtsch Arztebl Int. 106 (3): 32–7. doi:10.3238/arztebl.2009.0032. PMC 2695293. PMID 19564960.
  32. ↑ Vlahovic TC (2016). "Plantar Hyperhidrosis: An Overview". Clin Podiatr Med Surg. 33 (3): 441–51. doi:10.1016/j.cpm.2016.02.010. PMID 27215162.
  33. ↑ Sato K, Kang WH, Saga K, Sato KT (1989). "Biology of sweat glands and their disorders. I. Normal sweat gland function". J Am Acad Dermatol. 20 (4): 537–63. doi:10.1016/s0190-9622(89)70063-3. PMID 2654204.
  34. ↑ Sato K, Leidal R, Sato F (1987). "Morphology and development of an apoeccrine sweat gland in human axillae". Am J Physiol. 252 (1 Pt 2): R166–80. doi:10.1152/ajpregu.1987.252.1.R166. PMID 3812728.
  35. ↑ Davidson JR, Foa EB, Connor KM, Churchill LE (2002). "Hyperhidrosis in social anxiety disorder". Prog Neuropsychopharmacol Biol Psychiatry. 26 (7–8): 1327–31. doi:10.1016/s0278-5846(02)00297-x. PMID 12502021.
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  38. ↑ Molin S, Ruzicka T, Herzinger T (2015). "Smoking is associated with combined allergic and irritant hand eczema, contact allergies and hyperhidrosis". J Eur Acad Dermatol Venereol. 29 (12): 2483–6. doi:10.1111/jdv.12846. PMID 25405274.
  39. ↑ <ref name="pmid15280843">Strutton DR, Kowalski JW, Glaser DA, Stang PE (2004). "US prevalence of hyperhidrosis and impact on individuals with axillary hyperhidrosis: results from a national survey". J Am Acad Dermatol. 51 (2): 241–8. doi:10.1016/j.jaad.2003.12.040. PMID 15280843.
  40. ↑ <ref name="pmid30859595">Amano M, Namiki T, Munetsugu T, Nakamura M, Hashimoto T, Fujimoto T; et al. (2019). "Dyshidrosis associated with diabetes mellitus: Hypohidrosis associated with diabetic neuropathy and compensated hyperhidrosis". J Dermatol. 46 (8): e292–e293. doi:10.1111/1346-8138.14840. PMID 30859595.
  41. ↑ <ref name="pmid19222501">Kocyigit P, Akay BN, Saral S, Akbostanci C, Bostanci S (2009). "Unilateral hyperhidrosis with accompanying contralateral anhidrosis". Clin Exp Dermatol. 34 (8): e544–6. doi:10.1111/j.1365-2230.2008.03070.x. PMID 19222501.
  42. ↑ <ref name="pmid30710604">Nawrocki S, Cha J (2019). "The etiology, diagnosis, and management of hyperhidrosis: A comprehensive review: Etiology and clinical work-up". J Am Acad Dermatol. 81 (3): 657–666. doi:10.1016/j.jaad.2018.12.071. PMID 30710604.
  43. ↑ Henning MA, Pedersen OB, Jemec GB (2019). "Genetic disposition to primary hyperhidrosis: a review of literature". Arch Dermatol Res. 311 (10): 735–740. doi:10.1007/s00403-019-01966-1. PMID 31435740.
  44. ↑ <ref name="pmid15280843">Strutton DR, Kowalski JW, Glaser DA, Stang PE (2004). "US prevalence of hyperhidrosis and impact on individuals with axillary hyperhidrosis: results from a national survey". J Am Acad Dermatol. 51 (2): 241–8. doi:10.1016/j.jaad.2003.12.040. PMID 15280843.
  45. ↑ Norcliffe-Kaufmann L, Kaufmann H (2012). "Familial dysautonomia (Riley-Day syndrome): when baroreceptor feedback fails". Auton Neurosci. 172 (1–2): 26–30. doi:10.1016/j.autneu.2012.10.012. PMID 23178195.
  46. ↑ <ref name="pmid18557586">Shargall Y, Spratt E, Zeldin RA (2008). "Hyperhidrosis: what is it and why does it occur?". Thorac Surg Clin. 18 (2): 125–32, v. doi:10.1016/j.thorsurg.2008.01.001. PMID 18557586.
  47. ↑ <ref name="pmid32174618">Alkali NH, Al-Tahan AM, Al-Majed M, Al-Tahan H (2020). "Complex regional pain syndrome: A case report and review of the literature". Ann Afr Med. 19 (1): 68–70. doi:10.4103/aam.aam_23_19. PMC 7189882 Check |pmc= value (help). PMID 32174618 Check |pmid= value (help).
  48. ↑ Hansen C, Wayment B, Klein S, Godfrey B (2018). "Iodine-Starch test for assessment of hyperhidrosis in amputees, evaluation of different methods of application". Disabil Rehabil. 40 (25): 3076–3080. doi:10.1080/09638288.2017.1367965. PMID 28826272.
  49. ↑ Low PA, Caskey PE, Tuck RR, Fealey RD, Dyck PJ (1983). "Quantitative sudomotor axon reflex test in normal and neuropathic subjects". Ann Neurol. 14 (5): 573–80. doi:10.1002/ana.410140513. PMID 6316835.
  50. ↑ Stefaniak TJ, Proczko M (2013). "Gravimetry in sweating assessment in primary hyperhidrosis and healthy individuals". Clin Auton Res. 23 (4): 197–200. doi:10.1007/s10286-013-0201-2. PMC 3735961. PMID 23761115.
  51. ↑ Huguet I, Grossman A (2017). "MANAGEMENT OF ENDOCRINE DISEASE: Flushing: current concepts". Eur J Endocrinol. 177 (5): R219–R229. doi:10.1530/EJE-17-0295. PMID 28982960.
  52. ↑ Yamada S, Ito Y, Nishijima S, Kadekawa K, Sugaya K (2018). "Basic and clinical aspects of antimuscarinic agents used to treat overactive bladder". Pharmacol Ther. 189: 130–148. doi:10.1016/j.pharmthera.2018.04.010. PMID 29709423.
  53. ↑ Shin J, Jang YH, Kim SC, Kim YC (2013). "Eccrine angiomatous hamartoma: a review of ten cases". Ann Dermatol. 25 (2): 208–12. doi:10.5021/ad.2013.25.2.208. PMC 3662915. PMID 23717013.
  54. ↑ Motz KM, Kim YJ (2016). "Auriculotemporal Syndrome (Frey Syndrome)". Otolaryngol Clin North Am. 49 (2): 501–9. doi:10.1016/j.otc.2015.10.010. PMC 5457802. PMID 26902982.
  55. ↑ Swaile DF, Elstun LT, Benzing KW (2012). "Clinical studies of sweat rate reduction by an over-the-counter soft-solid antiperspirant and comparison with a prescription antiperspirant product in male panelists". Br J Dermatol. 166 Suppl 1: 22–6. doi:10.1111/j.1365-2133.2011.10786.x. PMID 22385032.
  56. ↑ Bernhard MK, Krause M, Syrbe S (2018). "Sweaty feet in adolescents-Early use of botulinum type A toxin in juvenile plantar hyperhidrosis". Pediatr Dermatol. 35 (6): 784–786. doi:10.1111/pde.13628. PMID 30178509.
  57. ↑ Nasr MW, Jabbour SF, Haber RN, Kechichian EG, El Hachem L (2017). "Comparison of microwave ablation, botulinum toxin injection, and liposuction-curettage in the treatment of axillary hyperhidrosis: A systematic review". J Cosmet Laser Ther. 19 (1): 36–42. doi:10.1080/14764172.2016.1248438. PMID 27782761.
  58. ↑ Dagash H, McCaffrey S, Mellor K, Roycroft A, Helbling I (2017). "Tap water iontophoresis in the treatment of pediatric hyperhidrosis". J Pediatr Surg. 52 (2): 309–312. doi:10.1016/j.jpedsurg.2016.11.026. PMID 27912978.
  59. ↑ Kim WO, Kil HK, Yoon DM, Cho MJ (2003). "Treatment of compensatory gustatory hyperhidrosis with topical glycopyrrolate". Yonsei Med J. 44 (4): 579–82. doi:10.3349/ymj.2003.44.4.579. PMID 12950111.
  60. ↑ Delort S, Marchi E, Corrêa MA (2017). "Oxybutynin as an alternative treatment for hyperhidrosis". An Bras Dermatol. 92 (2): 217–220. doi:10.1590/abd1806-4841.201755126. PMC 5429108. PMID 28538882.
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  62. ↑ Cheshire WP, Fealey RD (2008). "Drug-induced hyperhidrosis and hypohidrosis: incidence, prevention and management". Drug Saf. 31 (2): 109–26. doi:10.2165/00002018-200831020-00002. PMID 18217788.
  63. ↑ Lee D, Cho SH, Kim YC, Park JH, Lee SS, Park SW (2006). "Tumescent liposuction with dermal curettage for treatment of axillary osmidrosis and hyperhidrosis". Dermatol Surg. 32 (4): 505–11, discussion 511. doi:10.1111/j.1524-4725.2006.32103.x. PMID 16681657.
  64. ↑ Yuncu G, Turk F, Ozturk G, Atinkaya C (2013). "Comparison of only T3 and T3-T4 sympathectomy for axillary hyperhidrosis regarding treatment effect and compensatory sweating". Interact Cardiovasc Thorac Surg. 17 (2): 263–7. doi:10.1093/icvts/ivt160. PMC 3715172. PMID 23644731.


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