white unknown spots, do you have an idea?

Question

I have 4 regions that are white and won't tan if they're exposed to sun. They're round shaped, one is on one of my breasts, two are on my back and one is somewhere on my belly. There were flat brown typed moles and later the moles disappered with a white are around them (I was about 16 yo, now 24 yo) If I don't tan they're just a bit paler than my skin, because I'm fair skinned, but anyway they are whiter and if I expose to sun or solarium, they become pink, they start to itch as well. I don't think they are vitiligo, but I don't know what they are either. Do you know something? Before I go to dermatologist, I want to have some idea and is there a way to get rid of them? :(

Answer 1

My bet is exactly what Kads has written above, a type of fungal infection.

I would suggest that you go and see a naturopath/herbalist who will look at your diet and also give you herbal medicine such as golden seal, gotu kola, pau d'arco and thyme to stop the fungus and help with skin healing and also act as an immune tonic.

You can't expect miracles quickly, but the spots will clear and then stay gone. If your body was in a state that allowed the fungus to flourish, a conventional drug that kills it will only stop that particular 'crop'. Since your body is in the same weakened state, it will still present the perfect conditions for the fungus to grow back.

In the meantime, take a good quality vitamin C (1000mg)and zinc (30mg) supplement.

You can rub a tablespoon of cold-pressed coconut oil (with 3 drops of lemon essential oil and 3 drops tea tree essential oil mixed in) into the affected areas twice daily after showering/cleansing the areas.

Answer 2

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Answer 3

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RE:
white unknown spots, do you have an idea?
I have 4 regions that are white and won't tan if they're exposed to sun. They're round shaped, one is on one of my breasts, two are on my back and one is somewhere on my belly. There were flat brown typed moles and later the moles disappered with a white are around them (I was about 16...

Answer 4

Moles should not change color. You definately need to see a doctor.

On a side note... did you ever have chicken pox? That sounds like my pox scars.

Answer 5

Tinea Versicolor - Fungal Infection

Synonyms and related keywords: pityriasis versicolor, chromophytosis, dermatomycosis furfuracea, tinea flava, aeromia parasitica, Kleinenflechte, Hodi-Potsy, cutaneous fungal infection, hypopigmented macules, hyperpigmented macules, Malassezia furfur, M furfur, Pityrosporon orbiculare, Pityrosporon ovale, Malassezia ovalis, scaly macules, scaly papules, Cushing disease

Background: Tinea versicolor is a common, benign, superficial cutaneous fungal infection usually characterized by hypopigmented or hyperpigmented macules and patches on the chest and the back. In patients with a predisposition, the condition may chronically recur. The fungal infection is localized to the stratum corneum.


Pathophysiology: Tinea versicolor is caused by the dimorphic, lipophilic organism, Malassezia furfur, which is cultured only in media enriched with C12- to C14-sized fatty acids. M furfur is now the accepted name for the organism. Pityrosporon orbiculare, Pityrosporon ovale, and Malassezia ovalis are synonyms for M furfur. M furfur is a member of normal human cutaneous flora, and it is found in 18% of infants and 90-100% of adults.

Eleven species of M furfur have been described, with Malassezia globosa being the usual form isolated in persons with tinea versicolor. The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic, mycelial morphologic form include a genetic predisposition; warm, humid environments; immunosuppression; malnutrition; and Cushing disease. Human peptide cathelicidin LL-37 plays a role in skin defense against this organism.

Even though M furfur is a component of the normal flora, it can also be an opportunistic pathogen. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, and some forms of atopic dermatitis.


Frequency:


In the US: Tinea versicolor occurs more frequently in areas with higher temperatures and higher relative humidities. The national prevalence of this condition is 2-8% of the population. The exact incidence in the United States is difficult to assess because many individuals who are affected may not seek medical attention.
Internationally: Tinea versicolor occurs worldwide, with prevalences reported to be as high as 50% in the humid, hot environment of Western Samoa and as low as 1.1% in the colder temperatures of Sweden.
Mortality/Morbidity:

Tinea versicolor is a benign skin disease that causes scaly macules or papules on the skin. As the name implies (versi means several), the condition can lead to discoloration of the skin, with colors ranging from white to red to brown. The condition is not considered to be contagious because the causative fungal pathogen is a normal inhabitant of the skin.
The skin of an individual who is affected may be either hypopigmented or hyperpigmented. In the case of hypopigmentation, tyrosinase inhibitors (resulting from the inhibitory action of tyrosinase of dicarboxylic acids formed through the oxidation of some unsaturated fatty acids of skin surface lipids) competitively inhibit a necessary enzyme of melanocyte pigment formation. In hyperpigmented macules in tinea versicolor, the organism induces an enlargement of melanosomes made by melanocytes at the basal layer of the epidermis.
Race: Although the alteration in skin pigmentation is more apparent in darker-skinned individuals, the incidence of tinea versicolor appears to be the same in all races.

Sex: Several studies have addressed the frequency of tinea versicolor based on sex, and no dominance of either sex is apparent.

Age: In the United States, the disease is most common in persons aged 15-24 years, when the sebaceous glands are more active. Its occurrence before puberty or after age 65 years is uncommon. In more tropical countries, age frequency varies; most cases involve people aged 10-19 years who live in warmer, humid countries, such as Liberia and India.

History:

Most individuals with tinea versicolor complain of cosmetically disturbing, abnormal pigmentation.
The involved skin regions are usually the trunk, the back, the abdomen, and the proximal extremities. The face, the scalp, and the genitalia are less commonly involved.
The color of each lesion varies from almost white to reddish brown or fawn colored.
A fine, dustlike scale covers the lesions.
Patients often complain that the involved skin lesions fail to tan in the summer.
Occasionally, a patient also complains of mild pruritus.
Physical: Tinea versicolor can present in 3 forms.

Form 1
The most common appearance of the disease is as numerous, well-marginated, finely scaly, oval-to-round macules scattered over the trunk and/or the chest, with occasional extension to the lower part of the abdomen, the neck, and the proximal extremities.
The macules tend to coalesce, forming irregularly shaped patches of pigmentary alteration. As the name versicolor implies, the disease characteristically reveals a variance in skin hue. The involved areas can be either darker or lighter than the surrounding skin.
The condition is more noticeable during the summer months when the discrepancy in color from the normal skin becomes more apparent.
Light scraping of the involved skin with a scalpel blade characteristically yields a copious amount of keratin.
Form 2
An inverse form of tinea versicolor also exists in which the condition has an entirely different distribution, affecting the flexural regions, the face, or isolated areas of the extremities. This form of tinea versicolor is more often seen in hosts who are immunocompromised.
This form of the disease can be confused with candidiasis, seborrheic dermatitis, psoriasis, erythrasma, and dermatophyte infections.
Form 3
The third form of M furfur infections of the skin involves the hair follicle. This condition is typically localized to the back, the chest, and the extremities.
This form can be clinically difficult to differentiate from bacterial folliculitis. The presentation of Pityrosporum folliculitis is a perifollicular, erythematous papule or pustule.
Predisposing factors include diabetes, high humidity, steroid or antibiotic therapy, and immunosuppressant therapy. Additionally, several reports reveal that M furfur also plays a role in seborrheic dermatitis.
Causes: Most cases of tinea versicolor occur in healthy individuals with no immunologic deficiencies. Nevertheless, several factors predispose some people to develop this condition. These factors include genetic predisposition; warm, humid environments; immunosuppression; malnutrition; and Cushing disease.

The reason why this organism causes tinea versicolor in some individuals while remains as normal flora in others is not entirely known. Several factors, such as the organism's nutritional requirements and the host's immune response to the organism, are significant.

The organism is lipophilic, and lipids are essential for growth in vitro and in vivo. Furthermore, the mycelial stage can be induced in vitro by the addition of cholesterol and cholesterol esters to the appropriate medium. Because the organism more rapidly colonizes humans during puberty when skin lipids are increased more than that of adolescent levels and tinea versicolor is manifested in sebum-rich areas (eg, chest, back), individual variations in skin surface lipids are hypothesized to play a major role in disease pathogenesis. However, patients with tinea versicolor and control subjects do not demonstrate any quantitative or qualitative differences in skin surface lipids. Skin surface lipids are significant for the normal presence of M furfur on human skin, but they probably play little role in the pathogenesis of tinea versicolor.

Evidence has been accumulating to suggest that amino acids, rather than lipids, are critical for the appearance of the diseased state. In vitro, the amino acid asparagine stimulates the growth of the organism, while another amino acid, glycine, induces hyphal formation. In vivo, the amino acid levels have been shown to be increased in the uninvolved skin of patients with tinea versicolor in 2 separate studies.

Another significant causative factor is the patient's immune system. Although sensitization against M furfur antigens is routinely present in the general population (as proven by lymphocyte transformation studies), lymphocyte function on stimulation with the organism has been shown to be impaired in patients who are affected. This outcome is similar to the situation of sensitization with Candida albicans. In short, cell-mediated immunity plays some role in disease causation.