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We describe an interesting case of a man with recurrent cutaneous and hematologic manifestations of vitamin B12 deficiency. In this deficiency, the skin, central nervous system, blood, and blood-forming tissues are commonly involved. We describe an overview of vitamin B12 deficiency and the successful treatment of a patient's ongoing cutaneous hyperpigmentation.
A case of distal falangeal hyperpigmentation in a 2-month female newborn, who did not show any other cutaneous disease at the time of our observation, is presented. The aim of our study is to focus attention on this condition, actually considered a benign, asymptomatic, transitory manifestation, rarely reported in literature. On the basis of the clinical features, it has been proposed to add this pigmentation to the transient benign dermatoses of newborns.
The authors describe a 16-month-old infant presenting with neurologic developmental regression, severe pancytopenia, excessive skin pigmentation, and tremor resulting from nutritional vitamin B12 deficiency. She had been exclusively breast-fed and had refused to take any other food. Laboratory studies showed severe pancytopenia, a decrease in serum B12 levels, and an increase in urinary methylmalonic acid levels. Bone marrow aspiration was compatible with megaloblastic changes. Schilling test was normal. The serum B12 level of the mother was also low. Megaloblastic anemia resulting from inadequate B12 intake was diagnosed. Parenteral B12 therapy was initiated. The neurologic picture did not completely resolve, but pancytopenia, tremor, and hyperpigmentation of the extremities recovered completely.
Decorative henna skin painting can provoke severe reactions in the skin. We report 3 cases of unusual and persistent hyperpigmentation following nonpermanent henna tattoo, which alerted us to identify an additional side effect.
Striking hyperpigmentation developed on the arms of a 66-year-old man following protracted oral ingestion of quinine. Although this phenomenon is well described in conjunction with other similar drugs, including quinidine, it has not been well documented following exposure to quinine. This adverse event is cosmetic in nature and is not associated with functional impairment.
Hyperpigmentation-melasma was treated in a 31-year-old female with the application of aminolevulinic acid HCL 20%-single use Levulan Kerastick followed by exposure to 10 J/cm2 of nonlaser blue light. The results have been excellent and long-lasting.
Postinflammatory hyperpigmentation (PIH) is a common acquired excess of pigment in the epidermal and/or dermal layers of the skin. Lesions persist for extended periods if untreated, thus therapy is warranted. Topical monotherapies include the standard bleaching agent hydroquinone (HQ) as well as retinoids. Recently, several fixed-dose combination products were introduced to the armamentarium: HQ 4%-retinol 0.15% in a microsponge formulation; HQ 4%-retinol 0.3%; mequinol 2%-tretinoin (RA) 0.01%; and fluocinolone acetonide (FA) 0.01%, HQ 4%, and RA 0.05%. Recent findings have suggested that mequinol 2%-RA 0.01% solution is a promising alternative for the treatment of PIH.
A 36-year-old man was treated with dapsone, rifampicin and clofazimine for borderline lepromatous leprosy. After 9 months, his leprosy plaques became progressively more red and after 23 months, the clofazimine was stopped and he was given minocycline instead. Six weeks later, he developed blue-black pigmentation in his leprosy lesions. The histology was consistent with minocycline-induced hyperpigmentation. This is the first report of minocycline-induced pigmentation in leprosy. We suggest it is important to consider this side-effect before the administration of minocycline in leprosy, particularly if it is prescribed in place of clofazimine.
We present a new case of Whipple's disease. The patient have a clinical history of steatorrhea and diarrhea of various years of evolution with hyperpigmentation of skin and mucosae and migratory polyarthralgias with inflammatory sings. The biochemicals analysis for rheumatoid and endocrinological diseases were negatives. A endoscopically yeyunal biopsy was performed and the diagnosis of Whipple's disease was made. We comment this clinical presentation of Whipple's disease with a seronegative inflammatory rheumatological disease. The differential diagnosis with seronegative arthritis was emphasized.
Hyperpigmentation of the fingernails can occur during therapy with doxorubicin (Adriamycin). Two patterns are common: diffuse, and transversely banded. The pigment is believed to be melanin, and both patterns disappeared with discontinuation of therapy and subsequent nail growth.
BACKGROUND: Pigmented banding of the nails and hyperpigmentation of hands and feet may occur during cyclophosphamide therapy. Ifosfamide, an analogue of cyclophosphamide, might be expected to cause similar pigmentary changes, but, to the knowledge of the authors, there are no reports of this. METHODS: The authors describe skin pigment changes in a 5-year-old patient receiving ifosfamide, MESNA, and etoposide for the treatment of relapsed Wilms tumor. RESULTS: A review of the literature concerning cyclophosphamide-induced pigmentary changes is presented, along with a discussion of the possible correlation of renal dysfunction with pigmentary changes. CONCLUSIONS: This case should alert health care providers to this uncommon adverse effect of ifosfamide.
The tyrosinase promoter has been used to target expression of the mutated human T24 Ha-ras oncogene in pigment-producing cells of transgenic mice. Two independent founder mice carrying the transgene survived and showed the same distinct phenotype of mutated coat color, deeply pigmented skin with multiple nevi, and twirling behavior. The offspring of one of these founders were developed into a line that stably expressed the same phenotype. Histopathological analysis of the tissues revealed hyperpigmentation and/or melanocytic hyperplasia in the skin, eyes, inner ear, and meningeal membranes in the brain. Reverse transcriptase-polymerase chain reaction analysis revealed expression of the transgene in skin, brain, and spleen. We propose that these transgenic mice will be a model for studying the process of multistage melanoma carcinogenesis and a system for evaluating potential chemopreventive agents.
We describe a patient with plexiform neurofibroma and contralateral circumscribed hyperpigmentation along the lines of Blaschko. Such findings represent a form of segmental neurofibromatosis. The origin and classification of segmental neurofibromatosis and its relationship to NFI (von Recklinghausen disease) are discussed.
Hyperpigmentation, pulmonary infiltration, and erythema nodosum occurred in a patient receiving long-term minocycline therapy. Bronchoalveolar lavage revealed both a neutrophilic and an eosinophilic alveolitis. The pulmonary and systemic symptoms promptly resolved after discontinuation of minocycline.
This case is interesting in several respects. Although diffuse oral hyperpigmentation is suggestive of Addison's disease and should prompt the latter to be a prominent potential diagnosis in any setting, diagnosis was delayed by lack of constitutional and systemic symptoms, normal preliminary hematologic and electrolytic laboratory data, and the strong opinion of the pathologist that the oral mucosal biopsy specimen represented a fixed drug eruption. A subsequent orthopedic complaint and the resultant cooperative efforts of staff persons from several disciplines led to the proper diagnosis.
Following the earlier studies on the identification of injuries in unbroken cranial bones, the described method was adapted for the examination of the long bones in fatal casualties of traffic accidents. Two types of bumper injuries might occur: the bumper was found to cause fracturing of limbs [1], and femoral muscle contusions and microtraumas within compact and spongiose parts in the femoral with subsequent maculate hyperpigmentation [2]. The authors show that the correlation of above mentioned traces of the trauma, facilitates the reconstruction of the accident and also the identification of the vehicle.
Several categories of chemical and pharmacologic agents can cause alterations in cutaneous pigmentation, although the mechanisms differ and in several instances may be unknown. Fixed drug eruptions appear to have alteration of the basement membrane zone with incontinence of epidermal pigment as the mechanism of hyperpigmentation. Heavy metals produce increased pigmentation in part from deposition of metal particles and in part from an increase in epidermal melanin production. The antimalarials may bind to melanin. The phenothiazines and minocycline produce pigmentation from deposition of the drug. The mechanism, site, and nature of the pigment occurring with antineoplastic agents is not well understood, but the location is most likely predominantly epidermal. Clofazimine (Lamprene) alteration in pigmentation appears to result from deposition of the drug in subcutaneous fat.
Two kindreds manifesting an unusual form of pachyonychia congenita are described. Clinical involvement consists of nail dystrophy, which tends to improve with age, and moderate palmoplantar hyperkeratosis. In addition, all affected members show a characteristic pattern of cutaneous hyperpigmentation, which resembles macular amyloidosis around the neck and waist, but which confers a dappled appearance to the axillae, popliteal fossae, thighs, buttocks, and lower aspect of the abdomen. With advancing age the pigmentation fades. Histologic and ultrastructural examination of the hyperpigmented skin has revealed pigmentary incontinence and deposition of amyloid within the papillary dermis. These features appear to constitute a distinct variant of pachyonychia congenita.