Pemphigus-like Eruption From Captopril

Katz, Ronald A.; Hood, Antoinette F.; Anhalt, Grant J.

doi:10.1001/archderm.1987.01660250024004

Cited by 22 publications

(6 citation statements)

References 7 publications

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“…Appearance of a pemphigus-like eruption secondary to captopril therapy was reported · in a 72-year-old man who had been receiving the drug in doses of 100 mg/day for treatment of essential hypertension (Katz et al 1987), and histologically Drug Safety 7 (I) 1992…”

Section: Pemphigoid Reactionmentioning

confidence: 99%

Adverse Effects of Angiotensin Converting Enzyme (ACE) Inhibitors

Parish

Miller

1992

Drug Safety

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The angiotensin converting enzyme (ACE) inhibitors are a group of effective drugs with a unique mechanism of action. These drugs have proven to be useful for hypertension and congestive heart failure. Early clinical trials of captopril used doses that are now known to be inappropriately high, and dose-related adverse effects were observed frequently. The recognition that lower doses are effective has reduced the incidence of adverse reactions and resulted in improved patient tolerance. When patients are properly selected and correctable risk factors are removed, serious side effects are uncommon. Unfortunately, the early reputation of nephrotoxicity persists, as does the belief that significant blood dyscrasias, endocrine effects and rash are serious risks for the average patient. After wide use of captopril, enalapril and lisinopril, and investigational trials of nearly a dozen newer agents, a sufficiency of clinical observation, experimental evidence and accurate postmarketing recording of events is accumulating to allow insight into the major toxicities with regard to more intelligent patient selection, more rational dosing and proper identification of risk factors. The most common adverse reactions are cough and skin rash. It appears that the agents are generally not cross-reactive with regard to skin rash, although it is not clear whether this effect is drug-specific or class-specific with regard to cough. Statistically but not clinically significant lowering of haemoglobin and hematocrit is common; these effects are inconsequential in most patients. Neutropenia, once thought to be prevalent, now appears to be so only in patients with autoimmune or collagen-vascular disease; the majority of patients outside these groups are at low risk. Hyperkalaemia is a frequent occurrence. This should not be surprising in view of the effect of the ACE inhibitors on plasma aldosterone. When dietary potassium intake is regulated and sources of altered potassium excretion are identified, hyperkalaemia is seldom a serious problem. Identification of sodium and water deficits allows correction before the drugs are started, and the frequency of hypotension and hyperkalaemia caused by the drugs is quite low if these factors are properly managed. An unexpected finding emerging in recent years is the dry cough associated with ACE inhibitor therapy. Its mechanism is not definitely known. Nonsteroidal anti-inflammatory drugs may control this symptom in some patients. The frequent observation of proteinuria in patients taking ACE inhibitors has gained notice and sometimes caused undue alarm. It is difficult to separate disease effects in diabetes and hypertension from true drug effects.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Pemphigoid Reactionmentioning

confidence: 99%

Adverse Effects of Angiotensin Converting Enzyme (ACE) Inhibitors

Parish

Miller

1992

Drug Safety

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“…Pemphigus vulgaris (PV) is a well‐established, autoimmune, intraepidermal, blistering disorder of the skin and mucous membranes characterized by circulating autoantibodies directed against the 130‐ and 85‐kDa antigens on the keratinocyte cell surface. Several reports of its coexistence with other autoimmune diseases, such as rheumatoid arthritis, Sjogren's syndrome, systemic lupus erythematosus (SLE), and scleroderma, neoplasms, such as thymomas, lymphoreticular malignancies, etc., and therapeutic agents, such as penicillamine, captopril, progesterone, or vaccines, have been documented in the literature 1–5 . In vivo and in vitro studies performed in these cases have suggested various etiologic mechanisms, including the dysregulation of the immune response by the drug or disease, with an increased tendency to antibody formation in genetically predisposed individuals 6,7 …”

Section: Discussionmentioning

confidence: 99%

An unusual association of pemphigus vulgaris with hyperprolactinemia

Khandpur¹,

Reddy²

2002

Int J Dermatology

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A 21‐year‐old unmarried woman presented with oral ulcerations and generalized, itchy, fluid‐filled, skin lesions of 10 days’ duration. The lesions ruptured spontaneously, resulting in extensive denuded areas covered by crusts. One month prior to this, she experienced pain and enlargement of both breasts with galactorrhea. Her menstrual cycles were normal initially, but later she developed menstrual irregularities. No past history suggestive of any other systemic or skin disease, including atopy or drug allergies, could be obtained. Her family history was not contributory. Dermatologic examination revealed multiple, flaccid bullae and extensive denuded areas of skin covered with crusts over the scalp, face, trunk, and upper and lower limbs (Fig. 1). Bulla spread sign and Nikolsky's sign were positive. The oral mucosa, including the lips, buccal surface, tongue, and palate, showed multiple erosions covered with necrotic slough. The rest of the mucocutaneous and systemic examination was within normal limits. 1 Extensive erosions and flaccid bullae over the trunk with breast enlargement The patient's diagnostic work‐up revealed: hemoglobin, 11.2 g%; total leukocyte count, 7400/mm3; differential leukocyte count, P62L34E2M2; erythrocyte sedimentation rate, 34 mm/h. A peripheral blood smear examination, urinalysis, blood sugar, and renal and liver function tests were normal. Venereal Disease Research Laboratory (VDRL) test and enzyme‐linked immunoabsorbent assay (ELISA) for human immunodeficiency virus (HIV) were nonreactive. Antinuclear antibody, lupus erythematosus (LE) cell, rheumatoid factor, and anti‐dsDNA levels were normal. Serum protein electrophoresis demonstrated increased levels of immunoglobulin G (IgG) antibody. The serum prolactin level was significantly raised to 139.49 ng/mL (normal, 3.6–18.9 ng/mL). The sex hormone levels, however, including follicle‐stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and progesterone, were within normal limits. The thyroid hormone profile was also unaltered. Chest X‐ray was normal. Ultrasound of the abdomen and pelvis revealed no visceral abnormality and computerized tomography (CT) scan of the pituitary sella showed no adenoma. Mammography was negative for breast malignancy. A Tzanck smear prepared from the base of the erosion showed multiple acantholytic cells and lymphocytes. Histologic examination from an intact vesicle was suggestive of pemphigus vulgaris (PV), showing a suprabasal cleft with acantholytic cells and the basal layer demonstrating a “row of tombstones” appearance (Fig. 2). Direct immunofluorescence (DIF) revealed the intercellular deposition of IgG and C3 throughout the epidermis in a “fishnet pattern.” Indirect immunofluorescence (IIF) test performed on rat esophagus for circulating IgG antibody was positive in a titer of 1 : 120. 2 Photomicrograph showing suprabasal cleft with “row of tombstones” appearance, suggestive of pemphigus vulgaris (hematoxylin and eosin, × 40) Based on the clinical and immunohistological features, a diag...

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“…As mentioned it has been theorized that the free sulfhydryl group in captopril contributes to causing skin disorders (Parfrey et al, 1980). Since that time increasing evidence suggested a relationship between onset of pemphigus and treatment with ACE-I or angiotensin receptor blockers (enalapril, lisinopril, benazepril hydrochloride, fosinopril sodium, quinapril hydrochloride, and ramipril) (Brenner & Goldberg, 2011, Ruocco & Sacerdoti, 1991, Ruocco et al, 1993,Gavras & Gavras, 1983 , Shelton, 1991, Arnoux, Guiguen, & Verdier, 1987, Katz, Hood, & Anhalt, 1987, Ricci et al, 1986, Saraceno, Citarella, Spallone, & Chimenti, 2008. Recently, it has been reported a case of mucosal-dominant pemphigus vulgaris in a woman taking captopril during arterial hypertension (Gornowicz-Porowska, Dmochowski, .…”

Section: Other Non-thiol Non-amide Non-phenolic Drugsmentioning

confidence: 99%

“…Each compound has a highly reactive negatively charged sulfhydryl group in a stable stereochemical relationship to a similarly negatively charged carbonyl group. Since that time increasing evidence suggested a relationship between onset of pemphigus and treatment with ACE-I or angiotensin receptor blockers (enalapril, lisinopril, benazepril hydrochloride, fosinopril sodium, quinapril hydrochloride, and ramipril) (Brenner & Goldberg, 2011, Ruocco & Sacerdoti, 1991, Ruocco et al, 1993,Gavras & Gavras, 1983 Hutton, & Muller, 1994, Bastiaens, Zwan, Verschueren, Stoof, & Nieboer, 1994, Shelton, 1991, Arnoux, Guiguen, & Verdier, 1987, Katz, Hood, & Anhalt, 1987, Ricci et al, 1986, Saraceno, Citarella, Spallone, & Chimenti, 2008 that the most frequently used culprit drugs were ramipril and enalapril . Since that time increasing evidence suggested a relationship between onset of pemphigus and treatment with ACE-I or angiotensin receptor blockers (enalapril, lisinopril, benazepril hydrochloride, fosinopril sodium, quinapril hydrochloride, and ramipril) (Brenner & Goldberg, 2011, Ruocco & Sacerdoti, 1991, Ruocco et al, 1993,Gavras & Gavras, 1983 Hutton, & Muller, 1994, Bastiaens, Zwan, Verschueren, Stoof, & Nieboer, 1994, Shelton, 1991, Arnoux, Guiguen, & Verdier, 1987, Katz, Hood, & Anhalt, 1987, Ricci et al, 1986, Saraceno, Citarella, Spallone, & Chimenti, 2008 that the most frequently used culprit drugs were ramipril and enalapril .…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers induced pemphigus: A case series and literature review

Palleria

Bennardo

Dastoli

et al. 2018

Dermatologic Therapy

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Pemphigus is a group of autoimmune diseases characterized by the formation of erosions and/or flaccid bullae of the skin and/or mucosae. The definition "drug-induced pemphigus" has been coined to indicate cases of pemphigus with clinical, histological and immunopathologic features similar to those of the idiopathic disease but induced by systemic ingestion or local use of some drugs. The present authors analyzed a case series of three case reports with clinical and pharmacological features compatible with the diagnosis of angiotensin converting enzyme inhibitors or angiotensin II receptor blocker drug-induced pemphigus. The patients were visited by the dermatological Unit of Magna Graecia University in Catanzaro. All suspected drug induced pemphigus were treated by suspending the suspected drug and by starting a treatment with systemic corticosteroid drugs, leading to a remission of the clinical manifestations in some months.When a drug induced bullous disease is probable, it is necessary to interrupt the suspected substance and to start a high dose treatment with corticosteroid drugs to resolve the clinical case in a short period of time.

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Pemphigus-like Eruption From Captopril

Cited by 22 publications

References 7 publications

Adverse Effects of Angiotensin Converting Enzyme (ACE) Inhibitors

Adverse Effects of Angiotensin Converting Enzyme (ACE) Inhibitors

An unusual association of pemphigus vulgaris with hyperprolactinemia

Angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers induced pemphigus: A case series and literature review

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