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Suci Widhiati
Bagian Ilmu Kesehatan Kulit dan Kelamin, Fakultas Kedokteran, Universitas Sebelas Maret Surakarta/RSUD Dr. Moewardi, Surakarta
Biochemistry, Genetics & Molecular Biology Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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Laporan Kasus Acrodermatitis Enteropathica pada Anak 5 Tahun dengan Level Zink Serum Normal Adniana Nareswari; Moerbono Mochtar; Suci Widhiati; Arie Kusumawardani; Endra Yustin Ellistasari; Indah Julianto
MEDICINUS Vol 34 No 1 (2021): MEDICINUS
Publisher : PT Dexa Medica

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (123.849 KB) | DOI: 10.56951/medicinus.v34i1.51

Abstract

Acrodermatitis enterophatica (AE) is an inherited or acquired condition associated with zinc malabsorption. Clinical symptoms of AE are periorificial and acral dermatitis, alopecia, and diarrhea. Serum zinc levels usually decrease in AE patients. A 5-year-old boy presented with crusted erosion on the face, trunks and extremities that have been appeared for one year and worsened last month. It also accompanied by hair and eyebrow loss, diarrhea, and eating disorder. Patient was also malnourished. Dermatovenereology examination showed papules, patches, multiple erythematous plaques with squama, erosions with brownish yellow crust above located on perioral, periorbital, posterior trunk, inguinal, perianal, cubital, popliteal and dorsum pedis region. The oral region showed stomatitis and cheilitis. The orbital region showed conjunctival injection and eye discharge. The scalp, eyebrows and lashes showed total alopecia. Laboratory test showed normal serum zinc levels and decreased levels of alkaline phosphatase. The patient was diagnosed with acquired form of AE. Clinical improvement was seen after zinc supplementation. The diagnosis of AE cannot be made only by low serum zinc levels. If a classical triad of AE was found, we must be able to recognize it immediately, thus prompt and appropriate therapy could be given.
Sindrom Kindler Budi Eko Prasetyorini; Suci Widhiati
MEDICINUS Vol 36 No 1 (2023): MEDICINUS
Publisher : PT Dexa Medica

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.56951/medicinus.v36i1.117

Abstract

Kindler syndrome (KS) is a very rare form of epidermolysis bullosa (EB) and is a disease with defective FERMT1 gene. The FERMT1 gene provides the information needed to produce a protein called kindlin-1 where this protein plays an important role in attaching cells to the extracellular matrix which functions to hold, organize and connect cells in the body. Abnormalities in KS cause cells in the extracellular matrix to weaken so that the skin becomes brittle, prone to blisters and sores. Symptoms of SK are characterized by blisters that most often form on the backs of the hands and the tops of the feet, and thin, fragile skin. Mucosa of the eyes, intestines, esophagus, mouth, urinary tract and genitals may be affected. SK sufferers have a high sensitivity to light. Other symptoms can include discolored skin, thickened skin on the palms and soles and skin thatis atrophied or thin, dry and wrinkled. These symptoms appear in infancy and continue into adulthood, the risk of gingivitis (inflammation of the gums) which can lead to periodontitis or gum disease, throat, eye problems, higher risk of developing skin cancer and intestinal bleeding. Kindler syndrome management is basically preventive and symptomatic. Good wound care including the use of topical and systemic antibiotics for infected and ulcerated bullous lesions can reduce morbidity. Educating the patient to avoid trauma can help prevent blister formation.
Co-Authors Adniana Nareswari Arie Kusumawardani Budi Eko Prasetyorini Endra Yustin Ellistasari Indah Julianto Moerbono Mochtar