20 minute read
A Case of Sudden-Onset Dysphagia During Lunch Unresolved by PPIs
TABLE 2. Components of the CIWA-Ar11,18
Nausea and vomiting (0-7) Tactile disturbances (0-7)
Tremor (0-7) Auditory disturbances (0-7)
Paroxysmal sweats (0-7) Visual disturbances (0-7)
Anxiety (0-7) Headache (0-7)
Agitation (0-7) Orientation and clouding of sensorium (0-4)
Scorea: <8: Very mild withdrawal; 8-14: Mild withdrawal; 15-20: Modest withdrawal; ≥20 Severe withdrawal
a Interpretation of cutoff scores for mild, modest, and severe vary by source.
Other scales that can be used to assess for the risk for severe alcohol withdrawal include8: • Luebeck Alcohol-Withdrawal Risk Scale (LARS) • Prediction of Alcohol Withdrawal Severity Scale (PAWSS)
Although data collected from these assessments are extremely helpful in detection of alcohol withdrawal symptoms, the screening tools should be used as supportive measures in combination with the clinical picture as provided by a detailed history and thorough physical examination. Additionally, laboratory investigations such as urine drug screening, liver functions tests, blood alcohol levels, electrolyte levels, and a complete blood count are mainstays for establishing a diagnosis.17
Treatment Setting
The treatment setting is primarily determined by the severity of the withdrawal symptoms present.11 In patients presenting with mild to moderate withdrawal, outpatient detoxification is considered safe and effective.11,17 Although outpatient followup recommendations include seeing the patient daily until symptoms subside, treatment in this environment is cost effective, less burdensome on acute care hospitals, and minimizes interruptions on the patient’s personal life.11,17 An inpatient setting is warranted for patients who experience seizures or DTs or have severe withdrawal symptoms, abnormal laboratory results, or chronic medical or psychiatric conditions.8,17
Management of Alcohol Withdrawal Syndrome
Patients at risk of developing alcohol withdrawal syndrome (AWS) may be provided with preventative pharmacotherapy with benzodiazepines when attempting to reduce or stop alcohol intake, according to the 2020 ASAM guidelines on AWS. Benzodiazepines are first-line treatment for AWS prophylaxis because of their effectiveness in reducing the signs and symptoms of withdrawal, such as the incidence of seizure and delirium.8
Mild Symptoms For patients experiencing mild withdrawal symptoms (eg, CIWA-Ar score <8) who are at minimal risk of developing severe symptoms or complications of alcohol withdrawal, the ASAM recommends treatment with pharmacotherapy or supportive care alone. Carbamazepine or gabapentin are appropriate pharmacologic treatments for mild symptoms. For patients with mild symptoms who are at risk of developing new or worsening withdrawal while away from the treatment setting, the ASAM recommends use of benzodiazepines, carbamazepine, or gabapentin.8
Moderate Symptoms Patients with moderate symptoms (eg, CIWA-Ar scores 8-20) should be treated with pharmacotherapy with benzodiazepines being the first-line treatment; carbamazepine or gabapentin are appropriate alternative therapies. Benzodiazepine may be used in combination with carbamazepine, gabapentin, or valproic acid (in patients without liver disease or childbearing potential).8
Severe Symptoms Patients with severe, but not complicated, withdrawal symptoms (eg, CIWA-Ar ≥20) should be treated with benzodiazepines or, as an alternative, phenobarbital (only use if the clinician is experienced with its use). Other options for patients with contraindications to benzodiazepine use include carbamazepine or gabapentin. Adjunctive agents may be used (eg, carbamazepine, gabapentin, and valproic acid).8
Risk for prolonged benzodiazepine use and misuse include memory impairment, psychomotor retardation, depression, and emotional anesthesia in addition to physiologic dependence.17 Because of the high addiction risk, alternative agents such as carbamazepine and gabapentin have less abuse potential, less toxicity, less sedation, and have demonstrated efficacy in the treatment of alcohol withdrawal syndrome.8
For ongoing management of AUD, the Department of Veterans Affairs and the Department of Defense recommends use of acamprosate, disulfiram, naltrexone (extended release), and/or topiramate (off-label) for the initial management of AUD.19 The American Psychiatric Association recommends first-line treatment of AUD with acamprosate and naltrexone, and use of disulfiram, gabapentin (off-label), and topiramate as second-line options.20
Gabapentin is beneficial for treating withdrawal symptoms in patients who will benefit from ongoing gabapentin use for treatment of AUD, according to the ASAM. Gabapentin (an
analog of GABA) is not thought to modulate GABA receptors. Rather it is believed to enhance GABA activity or convert to GABA itself. 21 Gabapentin is believed to normalize stressinduced GABA activation in the brain that is associated with alcohol dependence.22
Adjunctive therapies with supplemental thiamine, folate, and IV fluids are useful in correcting nutritional and electrolyte abnormalities associated with alcohol withdrawal syndrome symptoms. Folic acid 1 mg daily is recommended and thiamine 100 mg daily is shown to lower the risk of Wernicke encephalopathy.
Monitoring
The approach to monitoring during treatment should be individualized to each patient and influenced by symptom severity. Most patients are evaluated daily until symptoms begin to decrease and medication dose is reduced.11 The method or tool used to initially evaluate symptoms and their severity should be consistently used throughout follow-up.
Although each patient’s road to recovery is different, symptoms should begin to resolve within a week. Upon completion of treatment, a patient may need to be referred to a long-term outpatient facility, addiction specialist, or inpatient treatment facility for AUD.
Conclusion
The ASAM recommends use of pharmacologic agents for patients at risk of developing severe or complicated withdrawal symptoms as well as those with at least moderate alcohol withdrawal. Patient education on the benefits and risks of each therapy is essential to providing informed consent and shared decision-making. ■
Christian Lyle, PA-C, graduated from August University physician assistant program in 2020 and is working in gastroenterology in her hometown of Savannah, Georgia.
References
1. Excessive alcohol use. Centers for Disease Control and Prevention. Updated September 21, 2020. Accessed April 27, 2021. https://www.cdc.gov/chronicdisease/resources/publications/factsheets/ alcohol.htm 2. Mason BJ, Quello S, Shadan F. Gabapentin for the treatment of alcohol use disorder. Expert Opin Investig Drugs. 2018;27(1):113-124. 3. SAMHSA, Center for Behavioral Health Statistics and Quality. 2019 National Survey on Drug Use and Health. Table 5.4B – alcohol use disorder in past year among persons aged 12 or older, by age group and demographic characteristics: percentages, 2018 and 2019. Accessed April 27, 2021. https://www.samhsa.gov/data/sites/default/files/reports/rpt29394/ NSDUHDetailedTabs2019/NSDUHDetTabsSect5pe2019.htm#tab5-4b 4. US Department of Health and Human Services, National Institute on Alcohol Abuse and Alcoholism. (2016). Alcohol Use Disorder: Comparison Between DSM-IV and DSM-5 (NIH Publication No. 13-7999). Retrieved from https://www.niaaa.nih.gov/sites/default/files/publications/DSMfact.pdf 5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Association; 2013. 6. Rahman A, Paul M. Delirium tremens (DT). In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Updated November 18, 2018. Accessed April 29, 2021. https://www.ncbi.nlm.nih.gov/books/NBK482134/ 7. Martin CS, Vergés A, Langenbucher JW, et al. Algorithm analysis of the DSM-5 alcohol withdrawal symptom. Alcohol Clin Exp Res. 2018;42(6):1073-1083. 8. American Society of Addiction Medicine. Clinical practice guideline on alcohol withdrawal management. January 23, 2020. https://www.asam.org/ docs/default-source/quality-science/the_asam_clinical_practice_guideline_on_ alcohol-1.pdf?sfvrsn=ba255c2_2 9. Zorumski CF, Isenberg KE. Insights into the structure and function of GABA-benzodiazepine receptors: ion channels and psychiatry. Am J Psychiatry. 1991;148(2):162-173. 10. Sigel E, Steinmann ME. Structure, function, and modulation of GABA(A) receptors. J Biol Chem. 2012;287(48):40224-40231. 11. DeSimone E, Tilleman J, Powell T. Treatment of alcohol withdrawal syndrome. US Pharm. 2014;39(11):38-41. 12. Mihic SJ, Ye Q, Wick MJ, et al. Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors. Nature. 1997;389(6649):385-389. 13. Hoffman P, Grant K, Snell L, et. al. NMDA receptors: role in ethanol withdrawal seizures. Ann N Y Acad Sci. 1992;654:52-60. 14. Tsai G, Gastfriend DR, Coyle JT. The glutamatergic basis of human alcoholism. Am J Psychiatry. 1995;152(3):332-340. 15. Feuerlein W, Ringer C, Küfner H, Antons K. Diagnosis of alcoholism: the Munich Alcoholism Test (MALT). Curr Alcohol. 1979;7:137-147. 16. US Department of Agriculture and US Department of Health and Human Services. Dietary Guidelines for Americans, 2020-2025. 9th ed. December 2020. 17. Muncie HL Jr, Yasinian Y, Oge’ L. Outpatient management of alcohol withdrawal syndrome. Am Fam Physician. 2013;88(9):589-595. 18. Sullivan JT, Sykora K, Schneiderman J, Naranjo CA, Sellers EM. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br J Addict. 1989;84(11):1353-1357. 19. Department of Veteran Affairs. Va/DoD Clinical Practice Guideline for the Management of Substance Use Disorders. Department of Veteran Affairs; December 2015. Accessed April 29, 2021. https://www.healthquality.va.gov/ guidelines/MH/sud/VADoDSUDCPGRevised22216.pdf 20. American Psychiatric Association. American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. American Psychiatric Association; 2018. Accessed April 29, 2021. https://psychiatryonline.org/doi/book/10.1176/appi.books.9781615371969 21. Rey, JA. Anxiolytic and hypnotic drugs. In: Lippincotts illustrated reviews: Pharmacology, 6th ed. Wolters Kluwer; 2015:121-123. 22. Mason BJ, Quello S, Goodell V, Shadan F, Kyle M, Begovic A. Gabapentin treatment for alcohol dependence: a randomized clinical trial. JAMA Intern Med. 2014;174(1):70-77.
Dermatology Clinic
CASE #1
Circular Lesions on Hands and Arms
TEJAS JOSHI, BS; TARA L. BRAUN, MD; CHRISTOPHER RIZK, MD
A 61-year-old man presents with a 7-month history of lesions on his hands and arms. His medical history includes depression, hypertension, and hyperlipidemia. He has no personal or family history of skin problems. His skin lesions are not painful or itchy, and he is not bothered by their appearance. He has not tried any treatments for the lesions. Physical examination reveals a number of pink, annular plaques with smooth raised borders on the patient’s dorsal forearms and hands. On close inspection, small discrete papules are seen within the plaques.
What is your diagnosis? Turn to page 38
CASE #2
Red Lesions on Arms and Flank
TIFFANEY TRAN, BS; TARA BRAUN, MD; MUNEEZA MUHAMMAD, MD; CHRISTOPHER RIZK, MD
A 33-year-old Black man presents to a dermatology clinic with a 5-month history of asymptomatic lesions on his arms and trunk. He is otherwise healthy with no personal or family history of skin disease. He has no history of fevers, cough, shortness of breath, or joint pain. The patient has not tried any treatments for these lesions. On examination, there are several smooth, well-demarcated hypopigmented plaques on his upper arms and left flank. He has no similar lesions elsewhere on his body.
What is your diagnosis? Turn to page 39
Dermatology Clinic
CASE #1 Localized Granuloma Annulare
Localized granuloma annulare (GA) is a common granulomatous skin condition that presents as skin-colored to erythematous papules and plaques.1 The first case of GA was described in 1895 by English dermatologist Thomas Calcott Fox as a ringed eruption, and the term granuloma annulare was coined in 1902 by Henry Radcliffe Crocker.2
GA is twice as common in women as in men, occurs most commonly in patients younger than 30 years, and displays no racial predilection.1,3 Localized GA is the most common form of GA, accounting for approximately 75% of cases.1 Generalized GA, defined by the presence of 10 or more lesions or widespread plaques, accounts for 8% to 15% of cases.1 Macular/ patch, subcutaneous, and perforating variants of GA also have been described in the literature.1
Although the etiology of GA is unknown, the inciting event is thought to be a type IV delayed hypersensitivity response to an unknown antigen. The granulomatous response is caused by type 1 helper (TH1) cells, which mediate an inflammatory reaction leading to increased levels of tumor necrosis factor-α, interferon-γ, interleukin (IL)-2, and IL-12.4 In addition, increased macrophage activity releases lysozymes that cause matrix degradation.3,4 Generalized GA may be associated with human leukocyte antigen-BW35, although no genetic etiology of localized GA has been reported.3,5
Although the majority of patients with GA are healthy,1 the condition has been linked to several systemic diseases, including thyroid disease, dyslipidemia, and hematologic and solid malignancies.1,3,4,6 Infectious agents (hepatitis B and C viruses, HIV), trauma, insect bites, and vaccinations also have been implicated as inciting factors for GA.1,3
Classically, the lesions of localized GA are arranged in an annular configuration on the dorsal hands or feet.7 Lesions are limited to the arms and dorsal hands in 60% of GA cases and to the legs and dorsal feet in 20% of cases. Involvement of both the upper and lower extremities, trunk, and other body areas is less common.3 The lesions present as papules or plaques with smooth, raised borders up to 5 cm in diameter.7 Upon closer inspection, these lesions are made up of individual small papules several millimeters in diameter.3 GA generally is asymptomatic, but mild pruritus is present in some cases.7
Histologically, GA is characterized by palisading granulomas around a focal region of collagen degradation as well as perivascular and interstitial lymphocytes and histiocytes. The presence of mucin is an important hallmark of GA.3,8
GA is diagnosed clinically and histologically; no laboratory test aids in diagnosis.3 Dermoscopic findings of GA are variable but commonly there are whitish regions, which reflect the collagen degradation and mucin deposition seen in GA, as well as yellowish-orange regions and unfocused vascular structures.9
The differential diagnosis for GA includes sarcoidosis, necrobiosis lipoidica, tinea corporis, leprosy, mycosis fungoides, and annular elastolytic giant cell granuloma (AEGCG).3,7 The presence of mucin on histologic examination will rule out sarcoidosis and necrobiosis lipoidica because mucin is absent in
these pathologies.1 Biopsy is also required to definitively rule out mycosis fungoides.3 GA lesions do not display scaling and are not accompanied by vesicles or pustules, which helps distinguish GA from tinea corporis.7 In addition, hyphae will be visualized in a potassium hydroxide preparation of a suspected tinea corporis lesion and not in a GA lesion. Leprosy can be differentiated from GA by the presence of scaling and anesthesia, which are not characteristic of GA.7 If lesions have central hypopigmentation and/or atrophy, the diagnosis of AEGCG is favored.3
Localized GA is a benign, self-limited disease with approximately 50% of cases resolving within 2 years.1 However, up to 40% of cases recur. Reassuring patients about the benign nature of the disease and monitoring them is an appropriate management strategy for many mild cases of localized GA. Patients may seek treatment if lesions are symptomatic or for cosmetic reasons.2,3 Most of the data on treatment of GA is limited to case reports, retrospective studies, and small case series. A lack of conclusive data may be due, in part, to the selflimited nature of the disease, which may make some treatments appear more efficacious than they truly are.6 High-potency topical steroids with or without occlusion are considered first-line therapy for localized disease. Lesions that do not respond to topical steroids can be treated with intralesional corticosteroids.4 Additional local treatment options include cryotherapy and topical tacrolimus.1,3 More extensive disease may be treated with phototherapy or systemic medications (eg, antimalarials, retinoids, biologics, niacinamide).1,3
Our patient was prescribed topical clobetasol, which helped the lesions fade, but he returned a year later with a recurrence.
He declined treatment for the recurrence because the lesions did not bother him.
References
1. Thornsberry LA, English JC. Etiology, diagnosis, and therapeutic management of granuloma annulare: an update. Am J Clin Dermatol. 2013;14(4):279-290. 2. Wang J, Khachemoune A. Granuloma annulare: a focused review of therapeutic options. Am J Clin Dermatol. 2018;19(3):333-344. 3. Rosenbach MA, Wanat KA, Reisenauer A, White KP, Korcheva V, White CR. Non-infectious granulomas. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:1644-1663. 4. Keimig EL. Granuloma annulare. Dermatol Clin. 2015;33(3):315-329. 5. Piette EW, Rosenbach M. Granuloma annulare: clinical and histologic variants, epidemiology, and genetics. J Am Acad Dermatol. 2016;75(3):457-465. 6. Wu W, Robinson-Bostom L, Kokkotou E, Jung HY, Kroumpouzos G. Dyslipidemia in granuloma annulare. Arch Dermatol. 2012;148(10):1131-1136. 7. Hsu S, Le EH, Khoshevis MR. Differential diagnosis of annular lesions. Am Fam Physician. 2001;64(2):289-296. 8. Umbert P, Winkelmann RK. Histologic, ultrastructural and histochemical studies of granuloma annulare. Arch Dermatol. 1977;113(12):1681-1686. 9. Errichetti E, Lallas A, Apalla Z, Di Stefani A, Stinco G. Dermoscopy of granuloma annulare: a clinical and histological correlation study. Dermatology. 2017;233(1):74-79.
CASE #2 Cutaneous Sarcoidosis
Cutaneous sarcoidosis refers to the skin manifestations of sarcoidosis, a chronic granulomatous disorder known to affect the lungs, lymph nodes, and other organs.1 Cutaneous involvement occurs in about one-quarter of patients with sarcoidosis, often as the initial presentation of systemic disease.1
The earliest observation of sarcoidosis is credited to British dermatologist Jonathan Hutchinson, who described painless purple lesions on the skin of a coal wharf worker in 1869.2 A quarter of a century later, Hutchison reported erythematous skin lesions on the face and forearms of a woman with the surname Mortimer and dubbed the skin findings Mortimer’s malady. He noted the absence of ulcerating or crusting in these lesions, which differentiated them from those of tuberculosis or lupus.2 Shortly afterward, in 1897, Norwegian dermatologist Caesar Boeck presented the pathology of nodular lesions resembling Mortimer’s skin findings. Referencing the condition’s sarcoma-like presentation, Boeck referred to the disease as multiple benign sarkoid of the skin and, therefore, the term sarcoidosis was born.2
The epidemiology of sarcoidosis varies by race, gender, and geographic location with the incidence ranging from 1.4 per 100,000 people in Spain and Japan to 64 per 100,000 in Scandinavia.3,4 In the US, Black individuals are at greater risk for sarcoidosis than White individuals; reported incidences are 35.5 per 100,000 and 10.9 per 100,000 in Black and White individuals, respectively.4 Black patients are also prone to have a more severe disease course marked by rapid progression and higher frequency of relapse.4 Compared with men, women tend to have a slightly greater risk for sarcoidosis across different races and age groups.3,4 The disorder also exhibits a bimodal age distribution, with separate peaks among patients in their 30s and 60s.4
Although extensive research has been conducted on sarcoidosis, its etiology remains elusive. A broad characterization of the disease process is that host factors and infectious and noninfectious environmental factors trigger systemic granulomatous inflammation in genetically susceptible individuals that presents as a heterogeneous group of disorders.5 Potential triggers include infectious agents, such as mycobacteria and Propionibacterium acnes. The role of exposure to various chemicals and metals in the etiology of sarcoidosis also has been debated.5 Sarcoid antigens are presented to CD4+ T cells via major histocompatibility complex class II molecules, leading to a type 1 helper (TH1) cell–predominant immune cascade and granulomatous inflammation in target organs.5
The exact cause of sarcoidosis has yet to be determined, but given the racial predilection and familial clustering of disease, risk factors for sarcoidosis include race, family history, and genetics.5.6 Genome-wide association studies have identified human leukocyte antigen (HLA) alleles associated with higher risk of developing sarcoidosis as well as HLA types linked with sarcoidosis disease course, severity, and organ involvement. For example, HLA DRB1*1501 and HLA DRB3*0101 both have been linked with increased risk for sarcoidosis in White and Black cohorts in the US.6 These genetic findings support the role of aberrant antigen processing and presentation in the pathophysiology of sarcoidosis.6
Specific and nonspecific skin manifestations of sarcoidosis demonstrate significant heterogeneity and may mimic other dermatologic diseases, earning cutaneous sarcoidosis its title as a great imitator.3 Common skin manifestations include papular sarcoidosis, characterized by multiple small macules and papules on the face or neck; plaque sarcoidosis, characterized by erythematous to violaceous plaques on the face, back, buttocks, or extremities; lupus pernio, characterized by indurated red to violaceous plaques on the nose, cheeks, or ears; and scar and tattoo-associated sarcoidosis, in which erythematous papules or nodules appear on scars or tattoos.1,7,8
Dermatology Clinic
Less common manifestations include psoriasiform sarcoidosis, which is characterized by erythematous scaly plaques; hypopigmented sarcoidosis, which is identified by well-demarcated light-colored macules or papules; and Darier-Roussy sarcoidosis, which is characterized by nontender subcutaneous nodules.1,7 Additional rare morphologies may involve ulcerative, erythrodermic, or ichthyosiform lesions.7
Patients also may present with nonspecific lesions such as erythema nodosum (EN), calcinosis cutis, or prurigo.1 Of these, the most common is EN, which is seen more frequently in White patients compared with Black individuals or people of Asian descent.7 EN also may occur as a component of Löfgren syndrome, which is a type of acute sarcoidosis characterized by fever, bilateral hilar lymphadenopathy, arthralgias, and EN.6,7 EN is associated with a favorable prognosis with fewer respiratory symptoms, whereas other skin lesions are associated with more extensive disease.7
The differential diagnosis for cutaneous sarcoidosis includes leprosy, fungal infection, cutaneous lupus, rosacea, psoriasis, and cutaneous malignancy.1 However, because of its highly variable presentation, the diagnosis primarily is formulated according to morphology. For instance, for maculopapular lesions, the physician may additionally consider acne, lichen planus, and benign tumors, and for papulonodular lesions on scars or tattoos, the differential diagnosis also would include hypertrophic and keloid scars.1
The diagnosis of cutaneous sarcoidosis is usually one of exclusion. Serum tests may be useful because elevated antinuclear antibody titers occur in approximately 30% of patients
and serum angiotensin-converting enzyme levels are elevated in approximately 60% of patients.9 Diascopy also can be performed on lesions. Applying pressure to the lesion causes blanching and a characteristic yellow-brown “apple jelly” color, although this is easier to appreciate in lighter pigmented skin.9 Skin biopsy can aid in diagnosis, especially in discerning lesions from those of leprosy or lupus.1 The hallmark of cutaneous sarcoidosis is the presence of noncaseating epithelioid granulomas with scant lymphocytes on histologic evaluation. Schaumann bodies or asteroid bodies may be seen.1 When appropriate, stains for acid-fast and fungal organisms should be obtained and tissue culture performed because the histologic differential diagnosis includes multiple infections. Polarization also should be performed on specimens to assess for foreign material, but the presence of foreign material does not rule out sarcoidosis.1,9
First-line therapy for cutaneous sarcoidosis consists of topical or intralesional corticosteroids for more limited disease and systemic corticosteroids for more extensive disease or disfiguring lesions.10 Additional nonsteroidal medications used in widespread disease include methotrexate, azathioprine, mycophenolate mofetil, hydroxychloroquine, minocycline, and thalidomide.1,9,10 The tumor necrosis factor inhibitors adalimumab and infliximab also have been used to treat both systemic and cutaneous sarcoidosis.9 Given that cutaneous sarcoidosis may signify systemic disease, chest radiography, pulmonary function tests, ophthalmologic examinations, electrocardiogram, and liver function tests may be warranted to assess for multiorgan involvement.3
In this case, the lesions were biopsied to confirm a diagnosis of hypopigmented cutaneous sarcoidosis. Additional workup for involvement of other organs was negative. He was treated with clobetasol ointment to affected areas twice daily. ■
Risk factors for sarcoidosis include race, family history, and genetics. Women have a slightly greater risk compared with men.
Tejas Joshi, BS, and Tiffaney Tran, BS, are medical students at Baylor College of Medicine;Tara L. Braun, MD, and Muneeza Muhammad, MD, are residents in the Department of Dermatology at Baylor College of Medicine; and Christopher Rizk, MD, is a dermatologist affiliated with Baylor College of Medicine in Houston, Texas.
References
1. Wanat KA, Rosenbach M. Cutaneous sarcoidosis. Clin Chest Med. 2015;36(4):685-702. 2. Sharma OP. Sarcoidosis: a historical perspective. Clin Dermatol. 2007;25(3):232-241. 3. Karadag AS, Parish LC. Sarcoidosis: a great imitator. Clin Dermatol. 2019;37(3):240-254. 4. Rybicki BA, Major M, Popovich J, Maliank MJ, Iannuzzi MC. Racial differences in sarcoidosis incidence: a 5-year study in a health maintenance organization. Am J Epidemiol. 1997;145(3):234-241. 5. Ruocco E, Gambardella A, Langella GG, Lo Schiavo A, Ruocco V. Cutaneous sarcoidosis: an intriguing model of immune dysregulation. Int J Dermatol. 2015;54(1):1-12. 6. Fingerlin TE, Hamzeh N, Maier LA. Genetics of sarcoidosis. Clin Chest Med. 2015;36(4):569-584. 7. Heath CR, David J, Taylor SC. Sarcoidosis: are there differences in your skin of color patients? J Am Acad Dermatol. 2012;66(1):121.e1-121.e14. 8. Sepehri M, Carlsen KH, Serup J. Papular-nodular reactions in black tattoos as markers of sarcoidosis: study of 92 tattoo reactions from a hospital material. Dermatology. 2016;232(6):679-686. 9. Rosenbach MA, Wanat KA, Reisenauer A, White KP, Korcheva V, White CR. Non-infectious granulomas. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:1644-1663. 10. Wijsenbeek MS, Culver DA. Treatment of sarcoidosis. Clin Chest Med. 2015;36(4):751-767.
Dermatologic Look-Alikes
Pruritic Papules During Pregnancy
DINA ZAMIL, BS; TARA L. BRAUN, MD; CARLY DUNN, MD; AND CHRISTOPHER RIZK, MD
CASE #1
A 28-year-old woman presents with a 2-day history of a rash on her abdomen. She is 33 weeks pregnant with her first child. The patient has no other medical conditions, has had no recent illnesses, and her pregnancy has been uncomplicated thus far. The rash is very itchy and has been worsening. The patient has not yet tried any treatments for the rash. She denies any recent changes in body washes, lotions, detergents, and other body products. On examination, there are erythematous papules within the abdominal striae, with sparing of the umbilicus.
CASE #2
A 23-year-old Hispanic woman 28 weeks into her second pregnancy presents with a 1-day history of rash. The rash started on her abdomen and is progressing rapidly. She reports having had a blistering rash on her abdomen during her prior pregnancy; the rash was never biopsied. The lesions are extremely itchy. On examination, there are numerous erythematous plaques with small vesicles and erosions within the plaques. Lesions are located on the abdomen, including the periumbilical region, and on the chest, back, and proximal upper and lower extremities.
