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Diltiazem Induces Severe Photodistributed Hyperpigmentation:  Case Series, Histoimmunopathology, Management, and Review of the Literature FREE

Rao N. Saladi, MD; Steven R. Cohen, MD; Robert G. Phelps, MD; Andrea N. Persaud, MD; Donald Rudikoff, MD
[+] Author Affiliations

Author Affiliations: Departments of Dermatology (Drs Saladi, Cohen, Phelps, Persaud, and Rudikoff) and Dermatopathology (Drs Saladi and Phelps), Mount Sinai School of Medicine, New York, NY.


Arch Dermatol. 2006;142(2):206-210. doi:10.1001/archderm.142.2.206.
Text Size: A A A
Published online

ABSTRACT

Background  Diltiazem hydrochloride is a commonly prescribed benzothiazepine calcium channel blocker for the treatment of cardiovascular disease. Recently, 8 cases of diltiazem-induced photodistributed hyperpigmentation occurring predominantly in elderly African American women were reported. Here, we report occurrence for the first time in a light-skinned African American woman and a Hispanic woman. We also report this finding in an African American man. Biopsy specimens of hyperpigmented areas were obtained for histopathologic evaluation and marker studies. Photospectrometry analysis for diltiazem was performed to analyze the photoabsorption properties of this drug.

Observations  Routine laboratory examination results were normal in all patients. Serologic test results for antinuclear antibodies, including Sjögren antibodies anti-Ro (SS-A) and anti-La (SS-B), were negative. Histopathologic analysis of the skin biopsy specimens revealed a sparse lichenoid infiltrate, prominent pigmentary incontinence, and numerous melanophages in the dermis. There was no increase in dermal mucin suggestive of lupus. The mononuclear cells in the specimens were strongly positive for CD3, weakly positive for CD68, and either weakly positive or negative for CD79a. All specimens were negative for Alcian blue staining. Photospectrometry analysis of diltiazem showed an absorption range within the UV-B spectrum.

Conclusions  Photospectrometry analysis revealed diltiazem could demonstrate a photosensitizing effect within the UV-B range. Discontinuation of therapy with diltiazem is the most effective modality in resolving hyperpigmentation. Avoidance of sun exposure and consistent use of sunscreens and sun-protective clothing are indicated for patients undergoing diltiazem therapy.

Figures in this Article

The US Food and Drug Ad ministration approved 3 new calcium channel blockers (nifedipine, verapamil hydrochloride, and diltiazem hydrochloride) in the 1970s and 1980s for treating cardiovascular diseases. Diltiazem, a benzothiazepine, is a widely prescribed agent used in treating hypertension and angina. Adverse effects of the drug include rare cutaneous eruptions such as maculopapular rashes, urticaria, and pruritus.13 Even rarer severe adverse effects include subacute cutaneous lupus erythematosus, Stevens-Johnson syndrome,4 toxic epidermal necrolysis,1 and vasculitis.5 Photosensitivity reactions of the skin associated with diltiazem rarely have been reported.1,2,68 Diltiazem-induced photodistributed hyperpigmentation has been reported, until now, in 8 cases occurring mostly in African American women.912 We report occurrence for the first time in a light-skinned African American woman and a Hispanic woman. We also report this finding in an African American man.

REPORT OF CASES

All 4 patients were seen at dermatology clinics affiliated with the Mount Sinai School of Medicine in New York, with a chief complaint of increased pigmentation on the face. The demographic characteristics of the individual patients are described in Table 1. Duration of pigmentation ranged from 6 to 24 months. There were no associated local or systemic symptoms. The patients' medical histories were remarkable for hypertension treated with diltiazem but no use of other medications that could be implicated as a cause for hyperpigmentation. Physical examination in all patients revealed diffuse slate-gray to gray-blue pigmented macules and patches on the face, neck, and forearms (Figure 1). Perifollicular accentuation was noted clinically in several patients (Figure 1). A sharply demarcated hyperpigmented patch demonstrating a V shape was noted in 3 of 4 patients on the upper chest or neck (Figure 1). No periorbital edema or erythema and no periungual erythema or telangiectasia were present. After query, patients revealed a mild to moderate history of exposure to sunlight during diltiazem therapy.

Place holder to copy figure label and caption
Figure 1.

Distinctive appearance of photodistributed hyperpigmentation in patients undergoing diltiazem hydrochloride therapy (A-I). Hyperpigmentation is consistent with the sun-exposed areas of the face, neck, and forearms. The pigmentation ranges from slate-gray to gray-blue and dark brown. Perifollicular accentuation was noted in some patients.

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Table Graphic Jump LocationTable 1. Demographic Characteristics of Cases of Photodistributed Hyperpigmentation After Diltiazem Therapy*

Results of routine laboratory testing in all patients, including a complete blood cell count, liver function tests, serum urea nitrogen and creatinine levels, complete metabolic profile, and thyroid function tests, were all normal. Serologic test results for antinuclear antibodies, including Sjögren antibodies anti-Ro (SS-A) and anti-La (SS-B), were negative.

Skin biopsy specimens of the hyperpigmented areas were obtained, and histopathologic evaluation and marker studies were conducted. Histopathologic findings were similar in all patients. Specimens showed a thinned epidermis with effaced rete ridges and focal interface vacuolar changes with small groups of hyaline globules in the uppermost papillary dermis. There were sparse lichenoid changes with interstitial and superficial perivascular infiltrates of inflammatory cells, predominantly composed of lymphocytes. Prominent pigmentary incontinence and numerous melanophages were seen in the dermis (Figure 2A and B). Some biopsy specimens showed perifollicular accentuation, colloid bodies, and association with apoptotic keratinocytes and hydropic changes of the follicular epidermis (Figure 2C). However, none of the biopsy specimens showed increased dermal mucin that might suggest lupus; they were negative for Alcian blue staining. The infiltrating mononuclear cells were strongly CD3 positive (Figure 2D), weakly CD68 positive, and weakly positive or negative for CD79a cells. The CD3-positive cells also showed striking perifollicular extension (Figure 2D).

Place holder to copy figure label and caption
Figure 2.

Histoimmunopathology of diltiazem hydrochloride–induced hyperpigmented sites. A and B, There is sparse perifollicular and focally lichenoid infiltrate in the dermis, with numerous melanophages. The infiltrate has a striking perifollicular distribution often associated with follicular plugging (original magnification ×10). C, Some specimens were associated with apoptotic keratinocytes (arrows) and hydropic changes of the follicular epidermis (original magnification ×20). D, The infiltrate is strongly CD3 positive and demonstrated lichenoid perivascular and perifollicular patterns (original magnification ×10). Scale bar is 50 μm.

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COMMENT

Photosensitivity reactions associated with the use of diltiazem were reported previously. These cutaneous adverse effects include erythema, pruritus, and/or lichenoid eruptions, which mostly develop soon after exposure to the sun.2,7,8 However, photodistributed hyperpigmentation associated with the use of diltiazem recently has been reported (Table 1). Analysis of all these reported cases in the literature showed that onset of pigmentary changes developed within 6 to 24 months after use of diltiazem. Patient age ranged between 49 and 77 years. Distribution of hyperpigmentation was consistent with sun-exposed areas of the face, neck, and forearms, with lesser pigmentation on the lower chest, back, and shins. Pigmentation was mild to severe with a slate-gray, gray-blue, or dark brown appearance.

To determine the photoabsorption spectrum of diltiazem, photospectrometry analysis of the drug was performed. The results showed diltiazem's absorption range to be 220 to 300 nm, within the UV-B spectrum (Figure 3). These results correlate with previous data showing no absorption in the UV-A spectrum.9 Although the UV-A range is thought to be the major contributory factor for photosensitivity reactions, several drugs (eg, tetracyclines, thiazides)13 exert photosensitivity properties in the UV-B range (5%-10% UV-B coexists in sunlight).14,15 Furthermore, the pattern of photodistributed pigmentation and history of mild to moderate sun exposure during diltiazem therapy in the patients in our study also supports diltiazem's photosensitizing effect. In efforts to elicit the causal mechanism, Scherschun et al9 demonstrated that persistent darkening of hyperpigmented patches occurred in patients exposed only to UV-A. However, electron microscopic evaluation did not reveal drug or metabolite deposits in the skin biopsy specimens; therefore, the authors thought diltiazem may exert its photosensitizing properties through other mechanisms. Several diltiazem metabolites have been identified; however, the specific metabolites involved in the adverse effects of the skin are not yet known.16

Place holder to copy figure label and caption
Figure 3.

Photospectrometer graph of diltiazem hydrochloride showing the absorption range (220-300 nm) within the UV-B spectrum (290-320 nm). ABS indicates absorbance.

Graphic Jump Location

Generally, for a drug to be regarded as a photosensitizer, the absorption wavelength of the drug should be within the range of UV-B (290-320 nm), UV-A (320-400 nm), and/or visible light (>400 nm).13,15 Drugs that induce photodistributed hyperpigmentation are activated metabolically (via solar radiation) forming free radicals and reactive intermediates that covalently bind to cellular proteins and DNA. This binding is considered critical in eliciting drug immunotoxicity by producing various enzymatic reactions that trigger a cascade of events, including a release of erythrogenic and pigmentary mediators that result in phototoxic and hyperpigmentary drug reactions.13 Drugs that induce photosensitivity hyperpigmentation include antimicrobial agents (tetracyclines), diuretic agents, psychotropic drugs, antimalarial agents, nonsteroidal anti-inflammatory drugs, cardiovascular drugs, cytotoxic drugs, and other agents.13,17,18 Diltiazem-induced photodistributed hyperpigmentation may be similar to other drug-induced photodistributed hyperpigmentation. Amiodarone, chlorpromazine hydrochloride, imipramine hydrochloride, and desipramine hydrochloride also induce slate-gray macules or patches.1921 However, diltiazem-induced photodistributed hyperpigmentation can be distinguished from minocycline hydrochloride–induced hyperpigmentation and argyria.9 Minocycline hyperpigmentation appeacrs in areas of cutaneous inflammation, typically in acne scars.22 Argyria induces slate-gray pigmentation not only in sun-exposed areas but also in the lunulae of nails, mucous membranes, and sclerae.23 Patients undergoing treatment with calcium channel blockers such as diltiazem have developed drug-induced subacute cutaneous lupus erythematosus. These patients had positive serologic test results and characteristic subacute cutaneous lupus erythematosus histoimmunopathologic findings.24,25

Prevention of diltiazem-induced photodistributed hyperpigmentation can be achieved by initiating photoprotective measures, including use of broad-spectrum sunscreens containing UV-A and UV-B blockers with a sun protection factor of 15 or greater and behavioral modification by limiting sun exposure and wearing sun-protective clothing. Sunscreen use should be initiated at the beginning of diltiazem therapy. If hyperpigmentation develops during diltiazem therapy, discontinuation of diltiazem is the most effective remedy. Better resolution of hyperpigmentation gradually has been observed in patients discontinuing diltiazem912 than in those using topical bleaching agents or chemical peels while continuing therapy.12 Application of topical bleaching agents (hydroquinone cream) may be useful in reducing the hyperpigmentation across time. In the patients in our study, use of 4% hydroquinone cream caused partial resolution across time. The patient showed complete clearance of hyperpigmentation after 1 year of diltiazem discontinuation and use of hydroquinone cream. Furthermore, substitution with another calcium channel blocker such as nifedipine3,4,2628 or verapamil1 in patients with adverse cutaneous reactions to diltiazem causes no further complications.

Some conclusions can be drawn on the basis of the cases reported (Table 1 and Table 2). Diltiazem-induced photodistributed hyperpigmentation has been found in other ethnic groups and skin types, but dark-skinned individuals and women were more prone to hyperpigmentation. The association of drug-induced hyperpigmentation in darker skin has never been understood. Results of previous reports and our case series indicate that only patients with severe hyperpigmentation seek dermatological care. Family practitioners, internists, cardiologists, and dermatologists who care for patients using diltiazem should be aware of diltiazem-induced hyperpigmentation and its association with sun exposure. We recommend that these patients limit their sun exposure, wear sun-protective clothing, and use broad-spectrum sunscreen from the start of diltiazem therapy.

Table Graphic Jump LocationTable 2. Analytical Observations and Management of Diltiazem-Induced Photodistributed Hyperpigmentation

ARTICLE INFORMATION

Correspondence: Donald Rudikoff, MD, Department of Dermatology, Mount Sinai Medical Center, 1425 Madison Ave, Campus Box 1047, New York, NY 10029 (RNAhybrid@aol.com).

Financial Disclosure: None.

Accepted for Publication: July 15, 2005.

Acknowledgment: We thank Jane B. Hilfer, MD, and Sapna R. Palep, BS, for their assistance in this project.

REFERENCES

Stern  RKhalsa  JH Cutaneous adverse reactions associated with calcium channel blockers. Arch Intern Med 1989;149829- 832
PubMed Link to Article
Seggev  JSLagstein  Z Photosensitivity skin reactions to calcium channel blockers. J Allergy Clin Immunol 1996;97852- 855
PubMed Link to Article
Wirebaugh  SRGeraets  DR Reports of erythematous macular skin eruptions associated with diltiazem therapy. DICP 1990;241046- 1049
PubMed
Taylor  JWCleary  JDAtkinson  RC Stevens-Johnson syndrome associated with diltiazem. Clin Pharm 1990;9948- 950
PubMed
Sheehan-Dare  RAGoodfield  MJ Severe cutaneous vasculitis induced by diltiazem [letter]. Br J Dermatol 1988;119134
PubMed Link to Article
Knowles  SGupta  AKShear  NH The spectrum of cutaneous reactions associated with diltiazem: three cases and a review of the literature. J Am Acad Dermatol 1998;38 ((2, pt 1)) 201- 206
PubMed Link to Article
Hashimoto  MTanaka  SHorio  T Photosensitivity due to diltiazem hydrochloride. Acta Dermatol 1979;74181- 186
Young  LShehade  SAChalmers  RJ Cutaneous reactions to diltiazem [letter]. Clin Exp Dermatol 1990;15467
PubMed Link to Article
Scherschun  LLee  MWLim  HW Diltiazem-associated photodistributed hyperpigmentation: a review of 4 cases. Arch Dermatol 2001;137179- 182
PubMed
Chawla  AGoyal  S Diltiazem-induced hyperpigmentation in an African American woman [letter]. J Am Acad Dermatol 2002;46468- 469
PubMed Link to Article
Boyer  MKatta  RMarkus  R Diltiazem-induced photodistributed hyperpigmentation. Dermatol Online J 2003;910
PubMed
Kuykendall-Ivy  TCollier  SLJohnson  SM Diltiazem-induced hyperpigmentation. Cutis 2004;73239- 240
PubMed
Moore  DE Drug-induced cutaneous photosensitivity: incidence, mechanism, prevention and management. Drug Saf 2002;25345- 372
PubMed Link to Article
Miller  SAHamilton  SLWester  UGCyr  WH An analysis of UVA emissions from sunlamps and the potential importance for melanoma. Photochem Photobiol 1998;6863- 70
PubMed Link to Article
Morison  WL Clinical practice: photosensitivity. N Engl J Med 2004;3501111- 1117
PubMed Link to Article
 Physicians' Desk Reference. 57th ed. Montvale, NJ Thomson Healthcare Inc2003;
Dereure  O Drug-induced skin pigmentation: epidemiology, diagnosis and treatment. Am J Clin Dermatol 2001;2253- 262
PubMed Link to Article
Svensson  CKCowen  EWGaspari  AA Cutaneous drug reactions. Pharmacol Rev 2001;53357- 379
PubMed
Blackshear  JLRandle  HW Reversibility of blue-gray cutaneous discoloration from amiodarone. Mayo Clin Proc 1991;66721- 726
PubMed Link to Article
Wolf  MERicher  SBerk  MAMosnaim  AD Cutaneous and ocular changes associated with the use of chlorpromazine. Int J Clin Pharmacol Ther Toxicol 1993;31365- 367
PubMed
Narurkar  VSmoller  BRHu  CHBauer  EA Desipramine-induced blue-gray photosensitive pigmentation. Arch Dermatol 1993;129474- 476
PubMed Link to Article
Pepine  MFlowers  FPRamos-Caro  FA Extensive cutaneous hyperpigmentation caused by minocycline. J Am Acad Dermatol 1993;28 ((2, pt 2)) 292- 295
PubMed Link to Article
Shelley  WBShelley  EDBurmeister  V Argyria: the intradermal “photograph,” a manifestation of passive photosensitivity. J Am Acad Dermatol 1987;16 ((1, pt 2)) 211- 217
PubMed Link to Article
Crowson  ANMagro  CM Diltiazem and subacute cutaneous lupus erythematosus-like lesions [letter]. N Engl J Med 1995;3331429
PubMed Link to Article
Crowson  ANMagro  CM Subacute cutaneous lupus erythematosus arising in the setting of calcium channel blocker therapy. Hum Pathol 1997;2867- 73
PubMed Link to Article
Hammentgen  RLutz  GKohler  UNitsch  J Maculopapular exanthema during diltiazem therapy [in German]. Dtsch Med Wochenschr 1988;1131283- 1285
PubMed Link to Article
Lambert  DGDalac  SBeer  FChavannet  PPortier  H Acute generalized exanthematous pustular dermatitis induced by diltiazem. Br J Dermatol 1988;118308- 309
PubMed Link to Article
Jones  SKReynolds  NJCrossley  JKennedy  CT Cutaneous reaction to diltiazem resulting in an exacerbation of angina. Clin Exp Dermatol 1989;14457- 458
PubMed Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

Distinctive appearance of photodistributed hyperpigmentation in patients undergoing diltiazem hydrochloride therapy (A-I). Hyperpigmentation is consistent with the sun-exposed areas of the face, neck, and forearms. The pigmentation ranges from slate-gray to gray-blue and dark brown. Perifollicular accentuation was noted in some patients.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Histoimmunopathology of diltiazem hydrochloride–induced hyperpigmented sites. A and B, There is sparse perifollicular and focally lichenoid infiltrate in the dermis, with numerous melanophages. The infiltrate has a striking perifollicular distribution often associated with follicular plugging (original magnification ×10). C, Some specimens were associated with apoptotic keratinocytes (arrows) and hydropic changes of the follicular epidermis (original magnification ×20). D, The infiltrate is strongly CD3 positive and demonstrated lichenoid perivascular and perifollicular patterns (original magnification ×10). Scale bar is 50 μm.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Photospectrometer graph of diltiazem hydrochloride showing the absorption range (220-300 nm) within the UV-B spectrum (290-320 nm). ABS indicates absorbance.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Demographic Characteristics of Cases of Photodistributed Hyperpigmentation After Diltiazem Therapy*
Table Graphic Jump LocationTable 2. Analytical Observations and Management of Diltiazem-Induced Photodistributed Hyperpigmentation

References

Stern  RKhalsa  JH Cutaneous adverse reactions associated with calcium channel blockers. Arch Intern Med 1989;149829- 832
PubMed Link to Article
Seggev  JSLagstein  Z Photosensitivity skin reactions to calcium channel blockers. J Allergy Clin Immunol 1996;97852- 855
PubMed Link to Article
Wirebaugh  SRGeraets  DR Reports of erythematous macular skin eruptions associated with diltiazem therapy. DICP 1990;241046- 1049
PubMed
Taylor  JWCleary  JDAtkinson  RC Stevens-Johnson syndrome associated with diltiazem. Clin Pharm 1990;9948- 950
PubMed
Sheehan-Dare  RAGoodfield  MJ Severe cutaneous vasculitis induced by diltiazem [letter]. Br J Dermatol 1988;119134
PubMed Link to Article
Knowles  SGupta  AKShear  NH The spectrum of cutaneous reactions associated with diltiazem: three cases and a review of the literature. J Am Acad Dermatol 1998;38 ((2, pt 1)) 201- 206
PubMed Link to Article
Hashimoto  MTanaka  SHorio  T Photosensitivity due to diltiazem hydrochloride. Acta Dermatol 1979;74181- 186
Young  LShehade  SAChalmers  RJ Cutaneous reactions to diltiazem [letter]. Clin Exp Dermatol 1990;15467
PubMed Link to Article
Scherschun  LLee  MWLim  HW Diltiazem-associated photodistributed hyperpigmentation: a review of 4 cases. Arch Dermatol 2001;137179- 182
PubMed
Chawla  AGoyal  S Diltiazem-induced hyperpigmentation in an African American woman [letter]. J Am Acad Dermatol 2002;46468- 469
PubMed Link to Article
Boyer  MKatta  RMarkus  R Diltiazem-induced photodistributed hyperpigmentation. Dermatol Online J 2003;910
PubMed
Kuykendall-Ivy  TCollier  SLJohnson  SM Diltiazem-induced hyperpigmentation. Cutis 2004;73239- 240
PubMed
Moore  DE Drug-induced cutaneous photosensitivity: incidence, mechanism, prevention and management. Drug Saf 2002;25345- 372
PubMed Link to Article
Miller  SAHamilton  SLWester  UGCyr  WH An analysis of UVA emissions from sunlamps and the potential importance for melanoma. Photochem Photobiol 1998;6863- 70
PubMed Link to Article
Morison  WL Clinical practice: photosensitivity. N Engl J Med 2004;3501111- 1117
PubMed Link to Article
 Physicians' Desk Reference. 57th ed. Montvale, NJ Thomson Healthcare Inc2003;
Dereure  O Drug-induced skin pigmentation: epidemiology, diagnosis and treatment. Am J Clin Dermatol 2001;2253- 262
PubMed Link to Article
Svensson  CKCowen  EWGaspari  AA Cutaneous drug reactions. Pharmacol Rev 2001;53357- 379
PubMed
Blackshear  JLRandle  HW Reversibility of blue-gray cutaneous discoloration from amiodarone. Mayo Clin Proc 1991;66721- 726
PubMed Link to Article
Wolf  MERicher  SBerk  MAMosnaim  AD Cutaneous and ocular changes associated with the use of chlorpromazine. Int J Clin Pharmacol Ther Toxicol 1993;31365- 367
PubMed
Narurkar  VSmoller  BRHu  CHBauer  EA Desipramine-induced blue-gray photosensitive pigmentation. Arch Dermatol 1993;129474- 476
PubMed Link to Article
Pepine  MFlowers  FPRamos-Caro  FA Extensive cutaneous hyperpigmentation caused by minocycline. J Am Acad Dermatol 1993;28 ((2, pt 2)) 292- 295
PubMed Link to Article
Shelley  WBShelley  EDBurmeister  V Argyria: the intradermal “photograph,” a manifestation of passive photosensitivity. J Am Acad Dermatol 1987;16 ((1, pt 2)) 211- 217
PubMed Link to Article
Crowson  ANMagro  CM Diltiazem and subacute cutaneous lupus erythematosus-like lesions [letter]. N Engl J Med 1995;3331429
PubMed Link to Article
Crowson  ANMagro  CM Subacute cutaneous lupus erythematosus arising in the setting of calcium channel blocker therapy. Hum Pathol 1997;2867- 73
PubMed Link to Article
Hammentgen  RLutz  GKohler  UNitsch  J Maculopapular exanthema during diltiazem therapy [in German]. Dtsch Med Wochenschr 1988;1131283- 1285
PubMed Link to Article
Lambert  DGDalac  SBeer  FChavannet  PPortier  H Acute generalized exanthematous pustular dermatitis induced by diltiazem. Br J Dermatol 1988;118308- 309
PubMed Link to Article
Jones  SKReynolds  NJCrossley  JKennedy  CT Cutaneous reaction to diltiazem resulting in an exacerbation of angina. Clin Exp Dermatol 1989;14457- 458
PubMed Link to Article

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