Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms. Hypolactasia is the term specifically for the small intestine producing little or no lactase enzyme. If a person with hypolactasia consumes lactose sugar, it results in lactose malabsorption. The digestive system is unable to process the lactose sugar, and the unprocessed sugars in the gut produce the symptoms of lactose intolerance. Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by a deficiency of lactase enzyme. Milk allergy, occurring in about 2% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction. Signs and symptoms
The principal manifestation of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after consumption. The severity of these signs and symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets without ill effects.Because lactose intolerance is not an allergy, it does not produce allergy symptoms (such as itching, hives, or anaphylaxis). Causes
Lactose intolerance is a consequence of lactase deficiency, which may be genetic (primary hypolactasia and primary congenital alactasia) or environmentally induced (secondary or acquired hypolactasia). In either case, symptoms are caused by insufficient levels of lactase in the lining of the duodenum.
The facial skin may be dry, exfoliative (flaking) or erythematous. Cervical lymphadenopathy (enlarged lymph nodes in the neck). Facial palsy (weakness and altered sensation of the face).The enlargement of the tissues of the mouth, lips and face seen in OFG is painless. Melkersson–Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve. The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression. Causes
The cause of the condition is unknown. The disease is characterized by non-caseating granulomatous inflammation. That is, the granulomas do not undergo the caseating ("cheese-like") necrosis typical of the granulomas of tuberculosis. There is disagreement as to whether OFG represents an early form of Crohn disease or sarcoidosis, or whether it is a distinct, but similar clinical entity. Crohn disease can affect any part of gastrointestinal tract, from mouth to anus. When it involves the mouth alone, some authors refer to this as "oral Crohn disease", distinguishing it from OFG, and others suggest that OFG is the same condition as Crohn disease when it presents in the oral cavity. OFG may represent a delayed hypersensitivity reaction, but the causative antigen(s) is not identified or varies form one individual to the next. Suspected sources of antigens include metals, e.g.