Diffuse Hyperpigmentation Research Articles

English

AIM OF THE STUDY: To study the different clinical patterns of cutaneous lesions in chronic renal failure patients undergoing haemodialysis. To study the distribution of lesions seen more often in both the skin and nails. To study the epidemiology of patients with cutaneous manifestations with CRF on haemodialysis in relation to age, sex and predisposing factors. PATIENTS AND METHODS: The study was conducted at Kempegowda Institute Of Medical Sciences, Bangalore between November 2009 and April 2011 for a period of 18 months. This prospective and Descriptive study included 100 patients with CRF who were undergoing dialysis. Of the 100 patients , 61 were Males and 39 were Females and the age ranged from 16 years to 70 years, with the majority of them in the age group of 41 to 60 years. The predominant cause of CRF was Diabetic Nephropathy (50%) followed by Chronic Glomerulonephritis (24%) and Chronic Interstitial Nephritis (19%). RESULTS: The predominant cutaneous manifestations included Xerosis (50%), Pruritis (38%), Cutaneous Pigmentation (36%), Nail Changes (42%), and Mucosal Changes (20%) Pallor (23%), Cutaneous Infections (27%) and Perforating Dermatoses (6%). The most common Nail Change was Leukonychia, observed in 22 patients and the most common cutaneous infection was fungal infection observed in 16 patients. The Nail Changes documented in the study included Leukonychia (22%), Dystrophic Nails (6%), Onychomycosis (8%), Half & Half Nails (5%), Clubbing (2%), Paronychia (2%), Beau's Lines (1%) and Mee's Lines (1%). The cutaneous findings specific to CRF including Perforating Dermatoses (6%), Calcinoses Cutis (2%), Beau's Lines (1%), Mee's Lines (4%) and Gynecomastia (1%) were also documented in the study. The incidence of Pruritus, Xerosis and Diffuse Hyperpigmentation increased as the severity of CRF increased. The incidence of xerosis, diffuse hyperpigmentation and nail Changes was significantly more in patients undergoing more than 100 dialysis. CONCLUSION: The incidence of pruritus decreased significantly as the total number of dialysis is increased to more than 100, as compared to those with less than 50 dialysis. The incidence of pruritus, xerosis and diffuse hyperpigmentation increased as the severity of CRF increased.

Autoimmune Polyendocrine Syndrome: A Case-Based Review

You are seeing a 14-year-old white male athlete with atopy who complains of a 6-month history of progressive proximal muscle weakness, which significantly impacts his ability to run short distances and swing his baseball bat. His mother states he has presented to multiple emergency departments (ED) for continued weakness and that most diagnosed him with dehydration and educated the family on how to maintain fluid balance. At his last ED visit, a creatine kinase (CK) level was drawn and found to be elevated at 1,247 U/L (normal range 9-185 U/L). A referral to a neurologist was made. The neurologist noted worsening fatigue, dizziness, and a documented 17-pound weight loss at the patient’s initial visit. A possible infectious versus progressive inflammatory myositis was suspected. The neurologist recommended an electromyography (EMG) to evaluate the patient’s proximal muscle weakness. Prior to completion of this EMG, the teen presents to your clinic now complaining of pre-syncopal events. On further review of symptoms, you note the patient has persistent polydipsia, headaches, nausea/vomiting, intermittent abdominal pain, and hyperpigmentation. Family history is negative for myopathies or dystrophies, but positive for hypothyroidism (mother), pineal gland tumor s/p resection (father), and rheumatoid arthritis (maternal grandmother). PHYSICAL EXAMINATION Initial physical examination reveals an afebrile, thin, adolescent male with orthostatic blood pressure changes of 113/59 mm Hg at rest and 89/44 mm Hg while standing; a pulse of 87 beats/ min; and a respiratory rate of 16 breaths/ min. His HEENT exam reveals equally reactive pupils with moist mucous membranes and no thyromegaly. His neurologic exam including cranial nerves, mental status, speech, gait, and coordination is unremarkable; there is no tremor noted. His muscle strength is noted to be 4/5 in the quadriceps bilaterally but 5/5 throughout the rest of his muscle groups. His muscle bulk and tone are mildly decreased. His cardiovascular, pulmonary, and abdominal exams are all benign. He has physiologic pubertal gynecomastia with mild tenderness. His genitourinary examination reveals normal appearing Tanner 3 male genitalia. His skin exam is remarkable for diffuse hyperpigmentation, which extends into his intertriginous areas and most notably the palms and creases of his hands. Flexor surfaces on his arms and diffuse areas on his face show ecAutoimmune Polyendocrine Syndrome: A Case-Based Review

Capsule Endoscopy in Whipple's Disease

A 70 year-old man with a history of seronegative rheumatoid arthritis and iron deficiency anemia was admitted to our hospital with severe diarrhea and weight loss. The diarrhea had been intermittent for two years and had started when he was treated with infliximab for arthritis. It had progressively increased in severity to 12-20 bowel movements per day on presentation despite loperamide and atropine/diphenoxylate. The patient had been admitted to the hospital several times previously for dehydration. His prior workup had included upper endoscopy, colonoscopy with biopsies, serum testing for celiac disease, stool studies for infection and malabsorption, and serum testing for carcinoid, HIV, and thyroid disorders, none of which explained his diarrhea. Computed tomography had shown enlarged mesenteric lymph nodes that were not suggestive of malignancy on positron emission tomography. He had been placed on iron supplementation with minimal improvement of anemia. On admission to the hospital, the physical examination showed dry mucous membranes, poor skin turgor, and diffuse skin hyperpigmentation. Laboratory data were significant for a non-anion gap metabolic acidosis and a positive stool lactoferrin; the remainder of stool studies were within normal limits. Because of persistent iron deficiency anemia and an otherwise negative workup, a small bowel capsule endoscopy was performed that showed diffuse erythema, edema, erosions, and whitish plaques throughout the small bowel (Figure A). An enteroscopy performed using a pediatric colonoscope demonstrated similar mucosal characteristics (Figure B). Biopsies of the duodenum and jejunum showed villous atrophy and many periodic acid-Schiff positive foamy macrophages in the lamina propria (Figure C) consistent with Whipple’s disease. The patient was treated with 2 weeks of intravenous ceftriaxone and will be continued on oral trimethoprim/sulfamethoxazole for at least one year. His diarrhea resolved within one month of initiation of antibiotics. Figure Whipple’s disease is an infectious process caused by the bacteria Tropheryma whipplei and, in its late-onset form, is extremely rare; only around 30 cases are reported per year1. Clinical presentation can include arthralgias, weight loss, abdominal pain, and diarrhea. Mucosal changes in Whipple’s disease are most often present within the small bowel, which makes obtaining endoscopic images more difficult2. Typical mucosal findings include edema, whitish-yellow plaques, erythematous mucosa, and subepithelial hemorrhage3. However, mucosal findings can be subtle or discontinuous4, which can lead to a delay in diagnosis. We present images from both capsule endoscopy and enteroscopy demonstrating marked mucosal changes in addition to an image demonstrating the classic pathologic appearance of the disease. Our patient’s presentation fits many of the classic descriptions of Whipple’s disease, including arthritis, skin hyperpigmentation, chronic diarrhea, and weight loss. Although it is rare, this diagnosis should always be considered in the workup of chronic diarrhea, especially if there is a history of immunomodulator use or immunosuppresion.

Letter to the Editor Adrenal function and MC1R gene analysis in a prepubertal girl with generalized hyperpigmentation:

Letter to the Editor Adrenal function and MC1R gene analysis in a prepubertal girl with generalized hyperpigmentation:

Skin lesions in histoplasmosis

Histoplasmosis is a granulomatous infection caused by Histoplasma capsulatum, a dimorphic fungus. It is distributed worldwide and prevalent in certain regions of North and Central America. Pulmonary involvement is the most common clinical presentation. Cutaneous manifestations are reported to occur in 10% to 25% of AIDS patients with disseminated histoplasmosis. The skin lesions are polymorphic papules, plaques with or without crusts, pustules, nodules, mucosal ulcers, erosions, punched out ulcers, lesions resembling molluscum contagiosum, acneiform eruptions, erythematosus papules and keratotic plaques, purpuric lesions, and localized and generalized vegetant forms of dermatitis, sometimes an eruption similar to rosacea, keratotic papules with transepidermal elimination, polymorphous erythema, erythroderma syndromes, pyoderma gangrenosum, panniculitis, diffuse hyperpigmentation, abscesses, and cellulitis.

Diffuse skin hyperpigmentation in CD30+ lymphoproliferation

CD30+ T-cell lymphoproliferative disorders (LD) comprise two main groups of diseases: CD30+ LD of the skin and systemic anaplastic large cell lymphoma (ALCL). The main feature of these disorders is the expression of CD30. We present a patient with an unusual clinical presentation of CD30+ lymphoproliferative disease in a 54-year old Caucasian male who presented with generalized lymphadenopathy and pronounced skin hyperpigmentation. In the lymph nodes and skin, CD30+ lymphoproliferation (ALCL) was diagnosed. The Prussian blue staining identified that the pigment responsible for the skin color was hemosiderin. Chemotherapy was started but the patient’s condition progressively worsened and he died a week after the first cycle. The complete color transformation of the entire skin due to hemosiderin accumulation is, to the best of our knowledge, the first reported observation in a CD30+ lymphoproliferation/ALCL patient. We speculate that hemosiderin-loaded macrophages resulted from the paraneoplastic process by some still unknown mechanism.

Whipple's disease: A case report

Whipple's disease is a chronic, multisystem, infectious disease caused by Tropheryma whipplei. It most commonly affects Caucasian males, middle-aged. Morbus Whipple is primarily gastrointestinal disease, manifested as malabsorption syndrome, and diagnosed by endoscopy and intestinal biopsy. Extraintestinal manifestations are not rare. A 48-year-old male was admitted due to diarrhea, weight loss and weakness in the extremities. Physical examination findings pointed out diffuse hyperpigmentation, pleural effusion and leg edema. Anemia, inflammatory syndrome and malabsorption signs were discovered through laboratory tests. The diagnosis was confirmed by intestinal biopsy. The patient was treated with antibiotic and symptomatic therapy. After 9 months, the patient had no symptoms, and clinical and laboratory findings were regular. Whipple's disease is a rare disease. A high degree of clinical suspicion for the disease (malabsorption, arthritis, fever, neurological symptoms) is the most important for diagnosis. Timely diagnosis and appropriate therapy prevent the disease progression and fatal outcome.

Salt-and-pepper appearance: A cutaneous clue for the diagnosis of systemic sclerosis

Sir, Systemic sclerosis is a multisystem disorder characterized by skin induration and thickening, fibrosis and chronic inflammatory infiltration of internal organs, microvascular damage and dysfunction, and immune dysfunction.[1] Systemic involvement may occur in the form of pulmonary vasculopathy, interstitial fibrosis, myocardiopathy, arrhythmia, conduction abnormality, acute renal crisis, lower esophageal incompetence, etc. [1] At times, the diagnosis of systemic sclerosis may be delayed, leading to increased morbidity and mortality. In these situations, a few clues may help in the early diagnosis of the disease. Systemic sclerosis is known to have cutaneous manifestations also; these include, especially, dyspigmentation in the form of a salt-and-pepper appearance; diffuse hyperpigmentation, with accentuation in sun-exposed areas (addisonian pigmentation); and hyper- and hypopigmentation in areas of sclerosis.[2] The salt-and-pepper appearance is characterized by the presence of vitiligo-like depigmentation with perifollicular pigmentary retention.[2] The rich capillary network surrounding the hair follicle preserves melanogenesis, and hence the retained perifollicular pigmentation in systemic sclerosis.[2] We have observed this salt-pepper appearance of the skin as one of the earliest features in systemic sclerosis in a few of our patients. With the aid of this finding early diagnosis was possible in these patients. Occasionally, this salt-and-pepper appearance may be the sole skin manifestation, i.e., without sclerosis of the skin (scleroderma sine scleroderma). In such situations an erroneous diagnosis of vitiligo may be made and the etiology of the underlying systemic problem, e.g., pulmonary fibrosis or hypertension, myocarditis or pericardial effusion, arthritis, etc., as the case may be, is missed. The patient may be dismissed with just symptomatic treatment. From June 2007 up to March 2011, we diagnosed systemic sclerosis in 16 patients. All patients fulfilled the American Rheumatism Association (ARA) diagnostic criteria for systemic sclerosis. Among the 16 patients, 15 had salt-and-pepper appearance of their skin and for 3 of these patients this was the presenting complaint. Commonly involved sites were the retroauricular area, scalp, forehead, neck, and the dorsa of the finger tips. In a study done in Nigeria among 14 patients, salt-and-pepper appearance of the skin emerged as the most common presentation.[3] In another study done at All India Institute of Medical Sciences, New Delhi, 51% of the patients had the salt-and-pepper appearance.[4] Not many studies are available on the prevalence of the salt-and-pepper appearance in patients with systemic sclerosis in Western countries. We feel that the light-colored skin in Caucasians may lead to poor contrast between depigmented and normal skin and poor appreciation of the salt-and-pepper sign in these regions, which is probably responsible for few cases being reported from the West. The salt-and-pepper appearance of the skin is presently considered as just one of many changes observed in the skin of patients with systemic sclerosis. However, we personally feel that the salt-and-pepper appearance of the skin, when seen along with sclerosis of the skin (one has to specifically look for the sclerosis), is a strong clue for the diagnosis of systemic sclerosis in people with types IV, V, and VI of skin (according to the Fitzpatrick classification scale). Recognition of this sign may help in the early diagnosis of systemic sclerosis.

Familial progressive hypo- and hyperpigmentation: A variant case

Familial progressive hyper- and hypopigmentation (FPHH) is characterized by diffuse hyperpigmentation with variable intensity. Cafe'-au-lait macules and larger hypopigmented ash-leaf macules are also present. Herein, we reported a variant case of FPHH. The patient was a two-year-old Chinese girl showing diffuse hyper- and hypopigmented lesions, longitudinal melanonychia in both thumbs, and infantile seizures, without any lentigines.

Laugier-Hunziker syndrome

Laugier–Hunziker syndrome is a rare acquired disorder characterized by diffuse hyperpigmentation of the oral mucosa and longitudinal melanonychia in adults. They appear as macular lesions less than 5 mm in diameter. Laugier–Hunziker syndrome is considered to be a benign disease with no systemic manifestation or malignant potential. Therefore, it is important to rule out other mucocutaneous pigmentary disorders that do require medical management. Prompt clinical recognition also averts the need for excessive and invasive procedures and treatments. In India, the reported cases of this syndrome are very few. We provide a review of literature on Laugier–Hunziker syndrome with its differential diagnosis.

Familial glucocorticoid deficiency presenting with generalized hyperpigmentation in adolescence. Report of three siblings

Background:Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive disorder characterized by glucocorticoid deficiency, high ACTH levels and normal mineralocorticoid levels. FGD is caused due to defects in adrenocorticotropic hormone (ACTH) signaling. The defect can be caused by mutations in genes encoding the ACTH receptor (melanocortin 2 receptor) or its accessory protein.Patients:Here we report three siblings with FGD. The second in order of siblings presented at an age of 15 years with history of diffuse hyperpigmentation since childhood. Their parents were non consanguineous. The patients were hyperpigmented and taller compared with their parents. None of the siblings had ambiguous genitalia or neurological abnormalities. There was no history of tuberculosis in the family. Biochemical investigations revealed low serum cortisol (<1 μg/dl) and elevated plasma ACTH (>1250 pg/ml). Serum electrolytes, aldosterone, and plasma renin activity was normal. Based on the above mentioned data, a provisional diagnosis of FGD was made after ruling out the common causes of glucocorticoid deficiency.Conclusion:FGD is a rare autosomal recessive disorder which causes isolated glucocorticoid deficiency. Unawareness about the condition may lead to delayed diagnosis and treatment, which are associated with high rates of morbidity and mortality. Once a diagnosis is made it is easily treatable.

Extensive hyperpigmentation during pregnancy: a case report

IntroductionSkin hyperpigmentation is common during pregnancy and often is due to endocrinological changes. Usual patterns include linea nigra, darkening of areola and melasma. We report a rare diffused hyperpigmentation condition in a pregnant woman of dark colored skin.Case presentationA 19-year-old Tanzanian primigravida at 32 weeks gestation presented at our antenatal clinic concerned about an insidious but progressive onset of unusual darkening of her abdominal skin and both breasts. Her antenatal record was unremarkable except for this unusual onset of abnormal skin color. Findings from her physical examination were unremarkable, and she had a normal blood pressure of 120/70 mmHg. Her abdomen was distended with a uterine fundus of 34 weeks. Almost her entire abdominal skin had darkly colored diffuse deep hyperpigmentation extending cephalad from both iliac fossae to involve both breasts to 2-3 cm beyond the areolae circumferentially. She had a fetus in longitudinal lie and cephalic presentation, with a normal fetal heart rate of 140 beats per minute. Other examination findings were unremarkable. The impression at this stage was exaggerated pigmentation of pregnancy. No medical treatment was offered but she was counseled that she might need medical treatment after delivery. She progressed well and had spontaneous labor and normal delivery at 38 weeks gestation. She was lost to follow up.ConclusionUnusual pregnancy-related skin hyperpigmentation can occur with no adverse consequences to pregnancy, although may worry a pregnant woman. Reassurance and conservative management may be all that is required to allay a patient's concerns.

Amyloidosis cutis dyschromica associated with atypical Parkinsonism, spasticity and motor weakness in a Pakistani female

Amyloidosis cutis dyschromica is a rare form of cutaneous amyloidosis in which there is deposition of keratinocyte-derived amyloid with involvement of almost the entire integument, leading to diffuse dyschromia without associated systemic abnormalities. We report the case of a 40-year-old female who presented with the onset of diffuse hyperpigmentation shortly after birth, which was followed by the widespread development of numerous 2-5 mm hypopigmented macules. Biopsy of the one of these macules revealed eosinophilic globular material in the papillary dermis with Congo red birefringence which also stained positively for high-molecular weight cytokeratin. Electron microscopy confirmed the presence of 11 nm hollow fibrils, consistent with amyloid. Similar clinical changes were noted in a younger male sibling. Both patients also suffered from an unexplained neurological disorder characterized by atypical Parkinsonism, spasticity and motor weakness. This association has not been shown before and may represent a heretofore unreported contiguous gene syndrome.

Amyloidosis cutis dyschromica in two female siblings: cases report

BackgroundCutaneous amyloidosis has been classified into primary cutaneous amyloidosis (PCA, OMIM #105250), secondary cutaneous amyloidosis and systemic cutaneous amyloidosis. PCA is the deposition of amyloid in previously apparent normal skin without systemic involvement. Amyloidosis cutis dyschromica (ACD) is a rare distinct type of PCA. Here, the unique clinical and histological findings of two Chinese female siblings with ACD were described.Cases presentationsPatient 1 was a 34-year-old female, presented with mildly pruritic, diffuse mottled hyperpigmentation and hypopigmentation. The lesions involved all over the body since she was 10 years old. There were a few itchy blisters appearing on her arms, lower legs and truck, especially on the sun-exposed areas in summer. Some hypopigmented macules presented with slight atrophy. Patient 2 was 39-year-old, the elder sister of patient 1. She had similar skin lesions since the same age as the former. The atrophy and blisters on the skin of the patient with amyloidosis cutis dyschromica have not been described in previous literature. Histological examinations of the skin biopsies taken from both patients revealed amyloid deposits in the whole papillary dermis. Depending on the histological assessment, the two cases were diagnosed as amyloidosis cutis dyschromica.ConclusionThe two cases suggest that the atrophy and blisters may be the uncommon manifestations of amyloidosis cutis dyschromica. It alerts clinicians to consider the possibility of ACD when meeting patients with cutaneous dyschromia. Skin biopsy is essential and family consultation of genetic investigation is very important in such cases.

Recurrence of Hydroxyurea-induced Leg Ulcer After Discontinuation of Treatment

Hydroxyurea (HU) is a hydroxylated derivative of urea that has been recognized since 1960 as effective against cancer (1). It is an inhibitor of cellular DNA synthesis, and it promotes cell death in the S phase of the cell cycle through inhibition of the enzyme ribonucleotide reductase (2). The most common indications for HU therapy are chronic myeloid leukaemia and other myeloproliferative disorders (3, 4) such as essential thrombocythemia (5) and polycythemia vera (PV) (6). Cutaneous side-effects, such as alopecia, diffuse hyperpigmentation, scaling, lichen planus-like lesions, poikiloderma, atrophy of the skin and subcutaneous tissues, and nail changes, can occur during the treatment with HU (7–9). The occur-rence of painful leg ulcers represents another rare and incompletely characterized complication that has been described in patients with myeloproliferative diseases receiving high-dose long-term HU treatment (10). While the mode of action of HU on bone marrow elements is well established, its effects on actively proliferating epit-helial cells remain less described (11). Poor response to traditional local and systemic therapy is a typical feature of HU-induced leg ulcers, and discontinuation of the drug is often required to achieve complete wound healing (6, 8). Cessation of the drug usually improves the skin ulcer; although, in some cases, the ulcer remains and additional therapies, such as skin grafting, are needed (12). We report here the first case of a leg ulcer that recurred even after discontinuation of HU treatment. CASe rePorTThe patient was an 82-year-old Japanese male who had been diagnosed with PV 9 years before and had been treated only with phlebotomy and an anti-platelet agent for several years. Due to splenomegaly and elevated blood cell counts, HU therapy was started 3 years ago at a dosage of 1 g daily for a month, followed by 1.0 or 1.5 g daily for 28 months. A good clinical response was achieved. However, the patient developed painful ulcers on the left second toe after two years of HU treatment.He visited our outpatient clinic and was diagnosed with an HU-induced skin ulcer. HU was discontinued, topical application of sulfadiazine silver was performed, an oral antibiotic (cefdinir) was administered, and the ulcer epithelialized. However, a new ulcer appeared on the left lateral malleolar area 46 days after cessation of HU and gradually enlarged in size. The patient was admitted to our hospital for treatment of the ulcer.examination revealed a 48 × 56 mm ulcer with yellow necrotic tissue and marginal erythematous oedema (Fig. 1). Laboratory examination revealed a white blood cell count of 11.6×10

A young boy with diffuse hyperpigmentation and delayed puberty

An 18-year-old male patient had presented with diffuse hyperpigmentation after birth and with adrenal insufficiency syndrome since childhood. After puberty, no secondary sexual signs developed. Laboratory examination showed an extremely high concentration of serum triglycerides (9.14 mmol/L) and plasma adrenocorticotropic hormone (>275 pmol/L), however, a low concentration of plasma free cortisone (<25.1-67.6 nmol/L). Abdomen computed tomography detected atrophy of both adrenals glands.

Laugier-Hunziker syndrome: A case report and review of the literature

Laugier-Hunziker syndrome (LHS) is a rare acquired disorder characterized by diffuse macular hyperpigmentation of the oral mucosa and, at times, longitudinal melanonychia. Although LHS is considered a benign disease with no systemic manifestations or malignant potential, it is important to rule out other mucocutaneous pigmentary disorders that do require medical management. Prompt clinical recognition also averts the need for excessive and invasive procedures and treatments. To date, only four cases have been reported in the United States. We present a 77-year-old man who had clinical features typical of LHS and we then provide a review of the literature on LHS and its mimickers.

37 Diffuse skin hyperpigmentation in CD30+ lymphoproliferation: A case report

37 Diffuse skin hyperpigmentation in CD30+ lymphoproliferation: A case report

A case of congenital erythropoietic porphyria

An 8-year-old boy presented with recurrent cutaneous bullae and scar on exposed sites for 8 years. After birth, he suffered from severe photosensitivity and anaemia, and developed recurrent blisters,erosions, ulcers and scar on esposed sites. There was passage of red urine. Family history was negative.Physical examination revealed perioral radial furrow. brown teeth, facial diffuse hyperpigmentation with depigmentation, atrophic scar and hypertrichosis, as well as nasal erosion. Hyperpigmentation, together with blisters, ulcers and scar contracture, was observed on both dorsal hands. Laboratory examination showed the presence of fluorescing erythrocytes, urinary porphyrin, urine bilirubin and urobilinogen. B-mode ultrasonography showed the presence of cholecystolithiasis and splenomegaly. A diagnosis of congenital erythropoietic porphyria was made. The condition was controlled by treatment with oral β-carotene and photoprotective precautions, and remained stable in a 2-year follow-up. Key words: Porphyria, erythropoietic; Case reports

Hydroxychloroquine-Induced Myopathy

A 70-year-old woman with a history of undifferentiated connective tissue disease was admitted for work-up of shortness of breath and progressive weakness over the course of 1 year. She had been treated with hydroxychloroquine (HCQ) for last 5 years. Her evaluation revealed diffuse muscle weakness and hyperpigmentation of the skin consistent with HCQ deposition, although this did not entirely explain the patient's dyspnea. The patient underwent cardiac evaluation because of occasional substernal chest pain and persistent elevation in serum troponin I, but her ECG and adenosine thallium study did not show any signs of ischemic heart disease. The diagnosis of HCQ-induced myopathy was made with electromyography and muscle biopsy. HCQ was discontinued, with improvement of the patient's signs and symptoms over the course of the next 18 months.We propose that this patient was experiencing myocardial toxicity as a consequence of HCQ deposition disease with her clinical picture of skeletal muscle myopathy and HCQ deposition in the skin. A Medline search yielded several case reports as well as a case series of patients with antimalarial-induced myopathy. HCQ-induced myopathy may be less recognized because of its presentation with signs, symptoms, and laboratory results which suggest other critical diseases. Moreover, this medication is often prescribed to treat illnesses whose clinical manifestations may include myopathy.