Glucagonoma differential diagnosis: Difference between revisions
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* Past medical history of the patient may include [[viral]] or [[bacterial]] infection, [[Diabetes mellitus|diabetes]], [[hypertension]], [[chronic kidney disease]] and/or [[obesity]] due to an association of psoriasis with these conditions.<sup>[[Psoriasis history and symptoms#cite note-pmid24790463-3|[3]]]</sup> | * Past medical history of the patient may include [[viral]] or [[bacterial]] infection, [[Diabetes mellitus|diabetes]], [[hypertension]], [[chronic kidney disease]] and/or [[obesity]] due to an association of psoriasis with these conditions.<sup>[[Psoriasis history and symptoms#cite note-pmid24790463-3|[3]]]</sup> | ||
* A social history of the patient may indicate smoking, excessive alcohol consumption and/or a recent stressful event if life associated with an acute exacerbation of psoriasis.<sup>[[Psoriasis history and symptoms#cite note-pmid13901632-4|[4]]]</sup> | * A social history of the patient may indicate smoking, excessive alcohol consumption and/or a recent stressful event if life associated with an acute exacerbation of psoriasis.<sup>[[Psoriasis history and symptoms#cite note-pmid13901632-4|[4]]]</sup> | ||
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|[[Liver cirrhosis|End-stage liver disease]] | |||
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|[[Pemphigus foliaceus]] | |||
|It is an autoimmune blistering disease of the skin with characteristic lesions that are scaly, crusted erosions, often on an erythematous base.<sup>[[Pemphigus foliaceus#cite note-Fitz2-1|[1]]]</sup> | |||
Mucosal involvement is absent even with widespread disease.<sup>[[Pemphigus foliaceus#cite note-Bolognia-2|[2]]]</sup> | |||
The pathway is most likely either of three mechanisms: | |||
* Steric hindrance of the desmoglein 1: The antibody caps off the site for intracellular binding to another keratinocyte. | |||
* Activation of an endocytic pathway: The antibody activates a pathway which causes an internalization of desmoglein 1, which in turn causes a loss of adhesion. | |||
* Disruption of function: In this case, the antibody blocks the desmoglein 1 from being formed into a desmosome. This, in turn, causes a loss of adhesion with acantholysis as a result. | |||
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* Pemphigus foliaceus is a superficial variant of pemphigus that presents with cutaneous lesions. | |||
* Pemphigus foliaceus usually develops in a seborrheic distribution. | |||
<ref name="pmid15993235">{{cite journal| author=Bystryn JC, Rudolph JL| title=Pemphigus. | journal=Lancet | year= 2005 | volume= 366 | issue= 9479 | pages= 61-73 | pmid=15993235 | doi=10.1016/S0140-6736(05)66829-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15993235 }}</ref> | |||
* The scalp, face, and trunk are common sites of involvement. The skin lesions usually consist of small, scattered superficial blisters that rapidly evolve into scaly, crusted erosions | |||
* The skin lesions may remain localized or may coalesce to cover large areas of skin. Occasionally, pemphigus foliaceus progresses to involve the entire skin surface as an exfoliative erythroderma.<ref name="pmid159414332">{{cite journal| author=Chams-Davatchi C, Valikhani M, Daneshpazhooh M, Esmaili N, Balighi K, Hallaji Z et al.| title=Pemphigus: analysis of 1209 cases. | journal=Int J Dermatol | year= 2005 | volume= 44 | issue= 6 | pages= 470-6 | pmid=15941433 | doi=10.1111/j.1365-4632.2004.02501.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15941433 }}</ref> | |||
* Pain or burning sensations frequently accompany the cutaneous lesions. Systemic symptoms are usually absent. | |||
|Positive Nikolsky sign.<ref name="pmid21353333">{{cite journal| author=Martin LK, Werth VP, Villaneuva EV, Murrell DF| title=A systematic review of randomized controlled trials for pemphigus vulgaris and pemphigus foliaceus. | journal=J Am Acad Dermatol | year= 2011 | volume= 64 | issue= 5 | pages= 903-8 | pmid=21353333 | doi=10.1016/j.jaad.2010.04.039 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21353333 }}</ref> | |||
|Autoimmune [[IgG]] build up in the [[Epidermis (skin)|epidermis]], then nearly almost all of the antibodies are aimed against [[desmoglein 1]] | |||
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|[[Psoriasis|Pustular psoriasis]] | |||
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* Patients with early disease onset often have a positive family history of psoriasis, frequent association with [[histocompatibility]] [[antigen]] (HLA)- Cw6, and more severe disease. Those with onset after the age of 40 usually have a negative family history and a normal frequency of the HLA- Cw6 allele.<sup>[[Psoriasis history and symptoms#cite note-pmid1390163-2|[2]]]</sup> | |||
* A typical patient of psoriasis will present with a history of a long-term [[erythematous]] scaly area with [[ocular]] and [[joint]] involvement depending upon the clinical subtype and chronicity of the disease. There may be multiple relapses and remissions. | |||
* Past medical history of the patient may include [[viral]] or [[bacterial]] infection, [[Diabetes mellitus|diabetes]], [[hypertension]], [[chronic kidney disease]] and/or [[obesity]] due to an association of psoriasis with these conditions.<sup>[[Psoriasis history and symptoms#cite note-pmid24790463-3|[3]]]</sup> | |||
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* A long-term history of [[erythematous]] scaly area, which may involve multiple areas of the body | * A long-term history of [[erythematous]] scaly area, which may involve multiple areas of the body | ||
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Leukocytosis | Leukocytosis | ||
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|[[Acrodermatitis enteropathica]] | |[[Acrodermatitis enteropathica]] | ||
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* Measurement of zinc in plasma, erythrocytes, neutrophils, lymphocytes, and hair. | * Measurement of zinc in plasma, erythrocytes, neutrophils, lymphocytes, and hair. | ||
* A low plasma zinc usually is defined as a value less than 60 mcg/ | * A low plasma zinc usually is defined as a value less than 60 mcg/dL. | ||
* Zinc levels in neutrophils or lymphocytes may be more sensitive than plasma zinc | * Zinc levels in neutrophils or lymphocytes may be more sensitive than plasma zinc.<ref name="pmid6696358">{{cite journal| author=Prasad AS, Cossack ZT| title=Zinc supplementation and growth in sickle cell disease. | journal=Ann Intern Med | year= 1984 | volume= 100 | issue= 3 | pages= 367-71 | pmid=6696358 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6696358 }}</ref> | ||
* The criteria for zinc deficiency are decreased zinc level in either | * The criteria for zinc deficiency are decreased zinc level in either lymphocyte.<ref name="pmid1940572">{{cite journal| author=Meftah S, Prasad AS, Lee DY, Brewer GJ| title=Ecto 5' nucleotidase (5'NT) as a sensitive indicator of human zinc deficiency. | journal=J Lab Clin Med | year= 1991 | volume= 118 | issue= 4 | pages= 309-16 | pmid=1940572 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1940572 }}</ref> | ||
* Depressed serum alkaline phosphatase levels for age provide supportive evidence for zinc deficiency | * Depressed serum alkaline phosphatase levels for age provide supportive evidence for zinc deficiency.<ref name="pmid9481631">{{cite journal| author=Kiliç I, Ozalp I, Coŝkun T, Tokatli A, Emre S, Saldamli I et al.| title=The effect of zinc-supplemented bread consumption on school children with asymptomatic zinc deficiency. | journal=J Pediatr Gastroenterol Nutr | year= 1998 | volume= 26 | issue= 2 | pages= 167-71 | pmid=9481631 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9481631 }}</ref> | ||
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|[[Pellagra]] | |[[Pellagra]] | ||
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* It is Niacin | * It is Niacin deficincy disease characterized by a photosensitive pigmented dermatitis (typically located in sun-exposed areas), diarrhea, and dementia. | ||
* Hisotry of alcoholics, bariatric surgery, anorexia nervosa, or malabsorptive disease | * Hisotry of alcoholics, bariatric surgery, anorexia nervosa, or malabsorptive disease.<ref name="pmid12777163">{{cite journal| author=Prousky JE| title=Pellagra may be a rare secondary complication of anorexia nervosa: a systematic review of the literature. | journal=Altern Med Rev | year= 2003 | volume= 8 | issue= 2 | pages= 180-5 | pmid=12777163 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12777163 }}</ref> | ||
* Dietary deficiency especially in infants | * Dietary deficiency especially in infants | ||
* Past history of Carcinoid syndrome, in which metabolism of tryptophan is to 5-OH tryptophan and serotonin rather than to nicotinic acid. This leads to the deficiency of active forms of niacin and the development of pellagra. | * Past history of Carcinoid syndrome, in which metabolism of tryptophan is to 5-OH tryptophan and serotonin rather than to nicotinic acid. This leads to the deficiency of active forms of niacin and the development of pellagra. | ||
* Prolonged use of isoniazid | * Prolonged use of isoniazid.<ref name="pmid21128910">{{cite journal| author=Wan P, Moat S, Anstey A| title=Pellagra: a review with emphasis on photosensitivity. | journal=Br J Dermatol | year= 2011 | volume= 164 | issue= 6 | pages= 1188-200 | pmid=21128910 | doi=10.1111/j.1365-2133.2010.10163.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21128910 }}</ref> | ||
* A | * A family history of Hartnup disease which is a congenital defect of a membrane transport in the intestinal and renal cells normally responsible for the absorption of tryptophan. | ||
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* [[Photosensitivity]] | * [[Photosensitivity]] | ||
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* [[Insomnia]] | * [[Insomnia]] | ||
* [[Weakness| | * [[Weakness|Weakness]] | ||
* [[Mental confusion]] | * [[Mental confusion]] | ||
|The most characteristic finding is the presence of a symmetric hyper pigmented rash, similar in color and distribution to a sunburn, which is present in the exposed areas of skin. | |The most characteristic finding is the presence of a symmetric hyper pigmented rash, similar in color and distribution to a sunburn, which is present in the exposed areas of skin. | ||
|Niacin status can be assessed by measuring urinary N-methylnicotinamide or by measuring the erythrocyte NAD/NADP (ratio). | |Niacin status can be assessed by measuring urinary N-methylnicotinamide or by measuring the erythrocyte NAD/NADP (ratio). | ||
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* High levels of antibodies in the blood signify an allergy to that substance. | * High levels of antibodies in the blood signify an allergy to that substance. | ||
* Skin biopsy which is a procedure that removes a small piece of the affected skin that is sent for microscopic examination in a pathology laboratory. | * Skin biopsy which is a procedure that removes a small piece of the affected skin that is sent for microscopic examination in a pathology laboratory. | ||
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Revision as of 16:28, 3 August 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2]
Overview
Glucagonoma must be differentiated from certain skin lesions (acrodermatitis enteropathica, psoriasis, pellagra, eczema) and other causes of hyperglucagonemia (infection, diabetes mellitus, Cushing syndrome, renal failure, acute pancreatitis, severe stress, and prolonged fasting).
Differentiating Glucagonoma from other Disease
Glucagonoma must be differentiated from certain skin lesions in which necrolytic migratory erythema can be found and other causes of hyperglucagonemia:[1][2]
Disease | Clinical Picture | Investigations | Pictures | ||
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History | Symptoms | Signs | |||
Glucagonoma |
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End-stage liver disease | |||||
Pemphigus foliaceus | It is an autoimmune blistering disease of the skin with characteristic lesions that are scaly, crusted erosions, often on an erythematous base.[1]
Mucosal involvement is absent even with widespread disease.[2] The pathway is most likely either of three mechanisms:
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Positive Nikolsky sign.[5] | Autoimmune IgG build up in the epidermis, then nearly almost all of the antibodies are aimed against desmoglein 1 | |
Pustular psoriasis |
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Skin biopsy
Perivascular and dermal inflammatory cell infiltration Vascular dilation Absent granular layer Parakeratosis Spongiform pustules of Kogoj (pathognomic of psoriasis) Munro's micro abscesses (pathognomic of psoriasis) In psoriasis, skin biopsy of the affected area of skin shows that the epidermal/supra-papillary thickness ratio is increased Basal cell layer is expanded Leukocytosis | |
Acrodermatitis enteropathica |
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Pellagra |
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The most characteristic finding is the presence of a symmetric hyper pigmented rash, similar in color and distribution to a sunburn, which is present in the exposed areas of skin. | Niacin status can be assessed by measuring urinary N-methylnicotinamide or by measuring the erythrocyte NAD/NADP (ratio). | |
Chronic eczema (atopic dermatitis) |
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References
- ↑ Glucagonoma. Wikipedia. https://en.wikipedia.org/wiki/Glucagonoma. accessed on October 10, 2015
- ↑ Fang S, Li S, Cai T (2014). "Glucagonoma syndrome: a case report with focus on skin disorders". Onco Targets Ther. 7: 1449–53. doi:10.2147/OTT.S66285. PMC 4140234. PMID 25152626.
- ↑ Bystryn JC, Rudolph JL (2005). "Pemphigus". Lancet. 366 (9479): 61–73. doi:10.1016/S0140-6736(05)66829-8. PMID 15993235.
- ↑ Chams-Davatchi C, Valikhani M, Daneshpazhooh M, Esmaili N, Balighi K, Hallaji Z; et al. (2005). "Pemphigus: analysis of 1209 cases". Int J Dermatol. 44 (6): 470–6. doi:10.1111/j.1365-4632.2004.02501.x. PMID 15941433.
- ↑ Martin LK, Werth VP, Villaneuva EV, Murrell DF (2011). "A systematic review of randomized controlled trials for pemphigus vulgaris and pemphigus foliaceus". J Am Acad Dermatol. 64 (5): 903–8. doi:10.1016/j.jaad.2010.04.039. PMID 21353333.
- ↑ Prasad AS, Cossack ZT (1984). "Zinc supplementation and growth in sickle cell disease". Ann Intern Med. 100 (3): 367–71. PMID 6696358.
- ↑ Meftah S, Prasad AS, Lee DY, Brewer GJ (1991). "Ecto 5' nucleotidase (5'NT) as a sensitive indicator of human zinc deficiency". J Lab Clin Med. 118 (4): 309–16. PMID 1940572.
- ↑ Kiliç I, Ozalp I, Coŝkun T, Tokatli A, Emre S, Saldamli I; et al. (1998). "The effect of zinc-supplemented bread consumption on school children with asymptomatic zinc deficiency". J Pediatr Gastroenterol Nutr. 26 (2): 167–71. PMID 9481631.
- ↑ Prousky JE (2003). "Pellagra may be a rare secondary complication of anorexia nervosa: a systematic review of the literature". Altern Med Rev. 8 (2): 180–5. PMID 12777163.
- ↑ Wan P, Moat S, Anstey A (2011). "Pellagra: a review with emphasis on photosensitivity". Br J Dermatol. 164 (6): 1188–200. doi:10.1111/j.1365-2133.2010.10163.x. PMID 21128910.